Potassium

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells.

experimental-exposure

Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding.

experimental_model

Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding.

limitations

Autophagy inhibition was not performed; colocalization and recovery do not establish that autophagic AQP2 degradation alone caused polyuria.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

Water-channel disposal began early, alongside AQP2 loss.

primary_references

[khositseth-2015-aqp2] Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus (2015). https://www.nature.com/articles/srep18311 DOI: 10.1038/srep18311

tissue_or_cell_type

inner medullary collecting duct

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1399–1410

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. · source_derived_draft · unverified_draft

### early-k-deprivation-aqp2-autophagic-localization After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Water-channel disposal began early, alongside AQP2 loss. organism: Rattus norvegicus tissue_or_cell_type: inner medullary collecting duct experimental_model: Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. limitations: Autophagy inhibition was not performed; colocalization and recovery do not establish that autophagic AQP2 degradation alone caused polyuria. experimental-exposure: Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. endpoint: After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells. [khositseth-2015-aqp2] Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus (2015). https://www.nature.com/articles/srep18311 DOI: 10.1038/srep18311

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation increases renal calcium loss in a controlled human dietary model.

endpoint

Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3.

experimental-exposure

Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.

experimental_model

Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.

limitations

Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation.

primary_references

[lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123

tissue_or_cell_type

kidney and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1274–1286

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. · source_derived_draft · unverified_draft

### human-k-withdrawal-increases-calciuria Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. limitations: Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links. cross_nutrient: Potassium deprivation increases renal calcium loss in a controlled human dietary model. experimental-exposure: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. endpoint: Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. [lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate.

endpoint

In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone.

experimental-exposure

Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.

experimental_model

Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.

limitations

Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

Potassium depletion and mineralocorticoid exposure can act together on renal acid handling.

primary_references

[eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471

tissue_or_cell_type

collecting tubule and systemic blood

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1137–1149

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. · source_derived_draft · unverified_draft

### k-aldosterone-joint-bicarbonate In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion and mineralocorticoid exposure can act together on renal acid handling. organism: Rattus norvegicus tissue_or_cell_type: collecting tubule and systemic blood experimental_model: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. limitations: Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently. cross_nutrient: Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate. experimental-exposure: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. endpoint: In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. [eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471

experimental_model

FMD subgroup, 22-24 usable measurements per comparison.

limitations

Same parent trial; no direct demonstration of nitric oxide or a particular channel as mediator.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

A vessel-response measurement improved in this subgroup.

primary_references

[k-gijsbers2015-fmd] Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/26343780/ DOI: 10.1017/s0007114515002986

tissue_or_cell_type

Brachial artery

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1557–1566

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FMD subgroup, 22-24 usable measurements per comparison. · source_derived_draft · unverified_draft

### k-controlled-feeding-fmd The endothelial substudy found a 1.16-percentage-point increase in flow-mediated dilation with potassium. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A vessel-response measurement improved in this subgroup. organism: Homo sapiens tissue_or_cell_type: Brachial artery experimental_model: FMD subgroup, 22-24 usable measurements per comparison. limitations: Same parent trial; no direct demonstration of nitric oxide or a particular channel as mediator. [k-gijsbers2015-fmd] Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/26343780/ DOI: 10.1017/s0007114515002986

experimental_model

Four-week crossover; 36 completers.

limitations

Untreated elevated-pressure adults with relatively low baseline sodium/potassium intake; no detected pulse-wave-velocity benefit.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

The blood-pressure effect was measured directly in this trial.

primary_references

[k-gijsbers2015-bp] Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/25673113/ DOI: 10.1038/jhh.2015.3

tissue_or_cell_type

Systemic circulation

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1546–1555

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week crossover; 36 completers. · source_derived_draft · unverified_draft

### k-controlled-feeding-pressure Potassium supplementation reduced 24-hour pressure by approximately 3.9/1.6 mmHg under controlled feeding. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood-pressure effect was measured directly in this trial. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Four-week crossover; 36 completers. limitations: Untreated elevated-pressure adults with relatively low baseline sodium/potassium intake; no detected pulse-wave-velocity benefit. [k-gijsbers2015-bp] Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/25673113/ DOI: 10.1038/jhh.2015.3

cross_nutrient

Potassium -> endocrine regulation; sodium/volume context retained.

experimental_model

35 participants from the same feeding trial.

limitations

Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

A hormone response can accompany a pressure reduction rather than imply the opposite outcome.

primary_references

[k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786

tissue_or_cell_type

Plasma

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1568–1578

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 35 participants from the same feeding trial. · source_derived_draft · unverified_draft

### k-controlled-feeding-regulatory-hormones Potassium increased aldosterone, renin and copeptin in the post-hoc hormone analysis while blood pressure fell. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone response can accompany a pressure reduction rather than imply the opposite outcome. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: 35 participants from the same feeding trial. limitations: Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response. cross_nutrient: Potassium -> endocrine regulation; sodium/volume context retained. [k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.

endpoint

Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport.

experimental-exposure

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

experimental_model

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

limitations

Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus; Mus musculus where specified

plain_language

More of one transporter did not mean greater overall phosphate recovery.

primary_references

[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

tissue_or_cell_type

renal proximal-tubule brush border

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1372–1384

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft

### k-deficiency-napi2a-abundance Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More of one transporter did not mean greater overall phosphate recovery. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.

endpoint

Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice.

experimental-exposure

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

experimental_model

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

limitations

Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus; Mus musculus where specified

plain_language

A sodium-phosphate uptake protein was depleted from the membrane.

primary_references

[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

tissue_or_cell_type

renal proximal-tubule brush border

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1344–1356

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft

### k-deficiency-napi2c-abundance Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-phosphate uptake protein was depleted from the membrane. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.

endpoint

Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice.

experimental-exposure

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

experimental_model

Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.

limitations

Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus; Mus musculus where specified

plain_language

A second, distinct sodium-phosphate transporter declined.

primary_references

[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

tissue_or_cell_type

renal proximal-tubule brush border

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1358–1370

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft

### k-deficiency-pit2-abundance Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second, distinct sodium-phosphate transporter declined. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts.

experimental-exposure

Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding.

experimental_model

Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding.

limitations

Parallel changes and refeeding support reversibility, but no AQP2-specific rescue isolated its complete contribution.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

Less water-channel protein accompanied the concentrating defect.

primary_references

[marples-1996-aqp2] Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex (1996). https://pubmed.ncbi.nlm.nih.gov/8621781/ DOI: 10.1172/JCI118628

tissue_or_cell_type

cortical and inner medullary collecting ducts

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1386–1397

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. · source_derived_draft · unverified_draft

### k-depletion-aqp2-abundance Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less water-channel protein accompanied the concentrating defect. organism: Rattus norvegicus tissue_or_cell_type: cortical and inner medullary collecting ducts experimental_model: Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. limitations: Parallel changes and refeeding support reversibility, but no AQP2-specific rescue isolated its complete contribution. experimental-exposure: Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. endpoint: Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts. [marples-1996-aqp2] Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex (1996). https://pubmed.ncbi.nlm.nih.gov/8621781/ DOI: 10.1172/JCI118628

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium -> calcium/phosphate/PTH observations.

experimental_model

Concurrent mineral and hormone measurements.

limitations

Co-occurrence does not establish that PTH caused every excretion change.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

Potassium depletion affected calcium-phosphate regulation alongside sodium handling.

primary_references

[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

tissue_or_cell_type

Plasma and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1534–1544

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concurrent mineral and hormone measurements. · source_derived_draft · unverified_draft

### k-depletion-human-mineral-pth-response The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion affected calcium-phosphate regulation alongside sodium handling. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Concurrent mineral and hormone measurements. limitations: Co-occurrence does not establish that PTH caused every excretion change. cross_nutrient: Potassium -> calcium/phosphate/PTH observations. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium/sodium balance -> pressure.

experimental_model

Same cohort and intervention.

limitations

Not an independent replication or proof of one molecular mediator.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

In this setting, lowering potassium raised blood pressure.

primary_references

[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

tissue_or_cell_type

Systemic circulation

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1522–1532

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same cohort and intervention. · source_derived_draft · unverified_draft

### k-depletion-human-pressure Low potassium increased systolic/diastolic pressure by about 7/6 mmHg in the same crossover. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this setting, lowering potassium raised blood pressure. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Same cohort and intervention. limitations: Not an independent replication or proof of one molecular mediator. cross_nutrient: Potassium/sodium balance -> pressure. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium -> sodium balance.

experimental_model

12 hypertensive adults; ten-day periods.

exposure

16 versus 96 mmol/day K; sodium 120 mmol/day.

limitations

Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

A potassium shortage changed how the kidney handled sodium.

primary_references

[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

tissue_or_cell_type

Kidney and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1509–1520

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 12 hypertensive adults; ten-day periods. · source_derived_draft · unverified_draft

### k-depletion-human-sodium-retention At fixed sodium intake, potassium depletion reduced urinary sodium from 110 to 83 mmol/day in this crossover. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A potassium shortage changed how the kidney handled sodium. organism: Homo sapiens tissue_or_cell_type: Kidney and urine experimental_model: 12 hypertensive adults; ten-day periods. limitations: Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain. cross_nutrient: Potassium -> sodium balance. exposure: 16 versus 96 mmol/day K; sodium 120 mmol/day. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats.

experimental-exposure

Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats.

experimental_model

Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats.

limitations

ATP hydrolysis and inhibitor sensitivity establish activity class, not a specific protein isoform or whole-animal flux.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The distal kidney increased an ATP-consuming activity compatible with potassium recovery.

primary_references

[doucet-1987-hka] Characterization of K-ATPase activity in distal nephron: stimulation by potassium depletion (1987). https://pubmed.ncbi.nlm.nih.gov/2957926/ DOI: 10.1152/ajprenal.1987.253.3.F418

tissue_or_cell_type

collecting tubule

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1124–1135

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. · source_derived_draft · unverified_draft

### k-depletion-increases-hka-activity Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The distal kidney increased an ATP-consuming activity compatible with potassium recovery. organism: Rattus norvegicus tissue_or_cell_type: collecting tubule experimental_model: Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. limitations: ATP hydrolysis and inhibitor sensitivity establish activity class, not a specific protein isoform or whole-animal flux. experimental-exposure: Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. endpoint: Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats. [doucet-1987-hka] Characterization of K-ATPase activity in distal nephron: stimulation by potassium depletion (1987). https://pubmed.ncbi.nlm.nih.gov/2957926/ DOI: 10.1152/ajprenal.1987.253.3.F418

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium depletion changes mitochondrial glutamine nitrogen metabolism; enzyme capacity and substrate entry need separate accounting.

endpoint

Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding.

experimental-exposure

Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding.

experimental_model

Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding.

limitations

Isolated mitochondrial assay, not whole-body bicarbonate balance. Glutaminase activity rose earlier than ammonia flux; mitochondrial glutamine entry was proposed as a limiting step.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The kidney adaptation included greater ammonia production, beyond changes in enzyme abundance.

primary_references

[sastrasinh-1986-mitochondrial-ammonia] Renal mitochondrial glutamine metabolism during K+ depletion (1986). https://pubmed.ncbi.nlm.nih.gov/3963205/ DOI: 10.1152/ajprenal.1986.250.4.F667

tissue_or_cell_type

renal mitochondria

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1041–1053

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. · source_derived_draft · unverified_draft

### k-depletion-increases-mitochondrial-ammonia Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney adaptation included greater ammonia production, beyond changes in enzyme abundance. organism: Rattus norvegicus tissue_or_cell_type: renal mitochondria experimental_model: Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. limitations: Isolated mitochondrial assay, not whole-body bicarbonate balance. Glutaminase activity rose earlier than ammonia flux; mitochondrial glutamine entry was proposed as a limiting step. cross_nutrient: Potassium depletion changes mitochondrial glutamine nitrogen metabolism; enzyme capacity and substrate entry need separate accounting. experimental-exposure: Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. endpoint: Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding. [sastrasinh-1986-mitochondrial-ammonia] Renal mitochondrial glutamine metabolism during K+ depletion (1986). https://pubmed.ncbi.nlm.nih.gov/3963205/ DOI: 10.1152/ajprenal.1986.250.4.F667

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry.

endpoint

Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles.

experimental-exposure

Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.

experimental_model

Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.

limitations

Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling.

primary_references

[levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767

tissue_or_cell_type

renal proximal-tubule apical membrane

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1190–1202

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. · source_derived_draft · unverified_draft

### k-depletion-increases-na-citrate-transport Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling. organism: Rattus norvegicus tissue_or_cell_type: renal proximal-tubule apical membrane experimental_model: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. limitations: Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested. cross_nutrient: Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry. experimental-exposure: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. endpoint: Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells.

experimental-exposure

Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.

experimental_model

Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.

limitations

Cell-specific regulation is not a contradiction of the proximal-tubule result; neither establishes net flux in an intact human kidney.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Different kidney cells adjusted the same ammonia-recycling enzyme in opposite directions.

primary_references

[verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013

tissue_or_cell_type

type A intercalated cells of cortical and outer medullary collecting duct

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1055–1066

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. · source_derived_draft · unverified_draft

### k-depletion-intercalated-glul The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different kidney cells adjusted the same ammonia-recycling enzyme in opposite directions. organism: Mus musculus tissue_or_cell_type: type A intercalated cells of cortical and outer medullary collecting duct experimental_model: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. limitations: Cell-specific regulation is not a contradiction of the proximal-tubule result; neither establishes net flux in an intact human kidney. experimental-exposure: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. endpoint: The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells. [verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Citrate affects urinary calcium chemistry, but this depletion experiment measured citrate handling rather than stones.

endpoint

The potassium-depleted rats had reduced fractional urinary citrate excretion.

experimental-exposure

Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.

experimental_model

Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.

limitations

The transport and excretion measurements were parallel; downstream stone formation was not tested.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

Less filtered citrate remained in urine during depletion.

primary_references

[levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767

tissue_or_cell_type

kidney and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1204–1216

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. · source_derived_draft · unverified_draft

### k-depletion-lowers-citrate-excretion The potassium-depleted rats had reduced fractional urinary citrate excretion. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less filtered citrate remained in urine during depletion. organism: Rattus norvegicus tissue_or_cell_type: kidney and urine experimental_model: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. limitations: The transport and excretion measurements were parallel; downstream stone formation was not tested. cross_nutrient: Citrate affects urinary calcium chemistry, but this depletion experiment measured citrate handling rather than stones. experimental-exposure: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. endpoint: The potassium-depleted rats had reduced fractional urinary citrate excretion. [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium status alters machinery that also controls sodium transport.

experimental_model

Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models.

limitations

Diet, diuretic and resin models differ; abstract does not provide each regimen duration.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rat and mouse

plain_language

Depleted muscle had fewer functional sodium-potassium pumps.

primary_references

[norgaard-1981-muscle] Potassium depletion decreases the number of 3H-ouabain binding sites and the active Na-K transport in skeletal muscle (1981). https://www.nature.com/articles/293739a0 DOI: 10.1038/293739a0

tissue_or_cell_type

Soleus/extensor digitorum longus

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 739–749

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models. · source_derived_draft · unverified_draft

### k-depletion-muscle-pump-loss Rodent potassium depletion reversibly reduced muscle ouabain-binding sites and pump-mediated potassium uptake capacity. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleted muscle had fewer functional sodium-potassium pumps. organism: Rat and mouse tissue_or_cell_type: Soleus/extensor digitorum longus experimental_model: Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models. limitations: Diet, diuretic and resin models differ; abstract does not provide each regimen duration. cross_nutrient: Potassium status alters machinery that also controls sodium transport. [norgaard-1981-muscle] Potassium depletion decreases the number of 3H-ouabain binding sites and the active Na-K transport in skeletal muscle (1981). https://www.nature.com/articles/293739a0 DOI: 10.1038/293739a0

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule.

experimental-exposure

Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.

experimental_model

Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.

limitations

Expression and localization were measured; the quantitative contribution of GLUL to total flux was not isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Less ammonia-recycling enzyme was present in this compartment, potentially leaving more ammonia available for excretion.

primary_references

[verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013

tissue_or_cell_type

renal proximal tubule

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1028–1039

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. · source_derived_draft · unverified_draft

### k-depletion-proximal-glul Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less ammonia-recycling enzyme was present in this compartment, potentially leaving more ammonia available for excretion. organism: Mus musculus tissue_or_cell_type: renal proximal tubule experimental_model: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. limitations: Expression and localization were measured; the quantitative contribution of GLUL to total flux was not isolated. experimental-exposure: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. endpoint: Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule. [verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.

endpoint

Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats.

experimental-exposure

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

experimental_model

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

limitations

Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The kidney changed nitrogen and acid excretion before blood potassium fell.

primary_references

[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

tissue_or_cell_type

renal proximal tubule and whole-kidney excretion

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 958–970

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

### k-deprivation-early-ammonium Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney changed nitrogen and acid excretion before blood potassium fell. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.

endpoint

Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats.

experimental-exposure

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

experimental_model

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

limitations

Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The first glutamine-deaminating enzyme increased; glutamate and ammonium are separate products in this pathway.

primary_references

[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

tissue_or_cell_type

renal proximal tubule and whole-kidney excretion

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 986–998

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

### k-deprivation-gls Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The first glutamine-deaminating enzyme increased; glutamate and ammonium are separate products in this pathway. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.

endpoint

Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats.

experimental-exposure

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

experimental_model

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

limitations

Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

A second ammonia-producing enzyme increased; this connects glutamate nitrogen to ammonium and its carbon skeleton to 2-oxoglutarate.

primary_references

[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

tissue_or_cell_type

renal proximal tubule and whole-kidney excretion

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1000–1012

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

### k-deprivation-glud1 Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second ammonia-producing enzyme increased; this connects glutamate nitrogen to ammonium and its carbon skeleton to 2-oxoglutarate. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.

endpoint

Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats.

experimental-exposure

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

experimental_model

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

limitations

Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes.

primary_references

[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

tissue_or_cell_type

renal proximal tubule and whole-kidney excretion

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1014–1026

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

### k-deprivation-pck1 Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.

endpoint

Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course.

experimental-exposure

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

experimental_model

Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.

limitations

Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

More glutamine transporter was detected in the kidney, supporting substrate delivery to the ammonia pathway.

primary_references

[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

tissue_or_cell_type

renal proximal tubule and whole-kidney excretion

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 972–984

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft

### k-deprivation-snat3 Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glutamine transporter was detected in the kidney, supporting substrate delivery to the ammonia pathway. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

experimental_model

Rabbit dietary experiment, four weeks.

limitations

Animal dietary finding does not establish human intake targets or a sole QT mechanism.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rabbit

plain_language

Sustained dietary restriction affected a cardiac recovery current.

primary_references

[guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027

tissue_or_cell_type

Ventricular myocardium

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 704–713

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rabbit dietary experiment, four weeks. · source_derived_draft · unverified_draft

### k-diet-rabbit-ikr Four weeks of 0.1% versus 0.62% dietary K produced hypokalemia, reduced ventricular IKr and prolonged corrected QT in rabbits. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sustained dietary restriction affected a cardiac recovery current. organism: Rabbit tissue_or_cell_type: Ventricular myocardium experimental_model: Rabbit dietary experiment, four weeks. limitations: Animal dietary finding does not establish human intake targets or a sole QT mechanism. [guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation regulates sodium-bicarbonate transport machinery.

endpoint

Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice.

experimental-exposure

NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.

experimental_model

NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.

limitations

Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

A sodium-bicarbonate transporter adapted during potassium conservation.

primary_references

[lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019

tissue_or_cell_type

cortical proximal tubule

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1068–1080

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. · source_derived_draft · unverified_draft

### k-free-diet-increases-nbce1a Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-bicarbonate transporter adapted during potassium conservation. organism: Mus musculus tissue_or_cell_type: cortical proximal tubule experimental_model: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. limitations: Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux. cross_nutrient: Potassium deprivation regulates sodium-bicarbonate transport machinery. experimental-exposure: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. endpoint: Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium depletion altered carbohydrate handling; the precise cellular link remains unmeasured.

experimental_contrast

{"combination": "single", "comparator": "Before depletion in the reported clamp study", "conditions": [{"entity_slug": "potassium", "state": "Experimentally depleted"}], "effect_direction": "decrease", "endpoint": "Clamp insulin response", "intervention": "Experimental potassium depletion"} Comparison extracted from the existing source-pinned Rowe 1980 claim (PMID 6991855); no new primary full-text access in this pass. The raw supports/positive relationship is retained independently.

experimental_model

Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline.

limitations

Seven men; diet-plus-resin exposure. No direct beta-cell channel measurement.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Human

plain_language

Depletion impaired glucose handling alongside a smaller insulin response.

primary_references

[rowe-1980-depletion] Effect of experimental potassium deficiency on glucose and insulin metabolism (1980). https://www.sciencedirect.com/science/article/pii/0026049580900748 DOI: 10.1016/0026-0495(80)90074-8

tissue_or_cell_type

Systemic glucose/insulin response

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 834–844

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline. · source_derived_draft · unverified_draft

### k-human-depletion-insulin Experimental depletion lowered clamp insulin response by 26% and glucose disposal by 27.4%; estimated tissue insulin sensitivity was unchanged. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depletion impaired glucose handling alongside a smaller insulin response. organism: Human tissue_or_cell_type: Systemic glucose/insulin response experimental_model: Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline. limitations: Seven men; diet-plus-resin exposure. No direct beta-cell channel measurement. cross_nutrient: Potassium depletion altered carbohydrate handling; the precise cellular link remains unmeasured. [rowe-1980-depletion] Effect of experimental potassium deficiency on glucose and insulin metabolism (1980). https://www.sciencedirect.com/science/article/pii/0026049580900748 DOI: 10.1016/0026-0495(80)90074-8

availability_state

nutrient_deficiency Imported condition classification; unverified.

experimental_model

Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion.

limitations

Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Human

plain_language

The measured glucose effect depended on the test and was mild.

primary_references

[gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544

tissue_or_cell_type

Systemic glucose regulation

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 846–855

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. · source_derived_draft · unverified_draft

### k-human-depletion-route-boundary Five depleted subjects had impaired oral glucose tolerance; two tested intravenously did not, and insulin-resistance tests were negative. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured glucose effect depended on the test and was mild. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. limitations: Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result. [gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544

experimental_model

Five-day feeding periods.

exposure

Added 20, 40 or 60 mEq/day; fries evaluated separately.

limitations

Specific foods and healthy participants; does not rank all foods or establish long-term outcomes.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

Potassium in the tested food and salt both reached the body.

primary_references

[k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225

tissue_or_cell_type

Gastrointestinal tract; modeled balance

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1452–1462

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-day feeding periods. · source_derived_draft · unverified_draft

### k-potato-gluconate-absorption Modeled potassium absorption was high and not detectably different between potatoes and gluconate in the short feeding comparison. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium in the tested food and salt both reached the body. organism: Homo sapiens tissue_or_cell_type: Gastrointestinal tract; modeled balance experimental_model: Five-day feeding periods. limitations: Specific foods and healthy participants; does not rank all foods or establish long-term outcomes. exposure: Added 20, 40 or 60 mEq/day; fries evaluated separately. [k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225

availability_state

nutrient_deficiency Imported condition classification; unverified.

endpoint

Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice.

experimental-exposure

Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.

experimental_model

Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.

limitations

Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The channel activation/trafficking state changed even where total protein loss was less marked.

primary_references

[al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020

tissue_or_cell_type

cortical and medullary collecting duct

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1412–1423

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. · source_derived_draft · unverified_draft

### k-restriction-lowers-aqp2-ser256 Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The channel activation/trafficking state changed even where total protein loss was less marked. organism: Mus musculus tissue_or_cell_type: cortical and medullary collecting duct experimental_model: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. limitations: Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase. experimental-exposure: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. endpoint: Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. [al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.

endpoint

Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments.

experimental-exposure

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

experimental_model

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

limitations

Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The kidneys lost more calcium when dietary potassium was restricted.

primary_references

[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

tissue_or_cell_type

kidney, blood and trabecular skeleton

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1288–1300

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft

### mouse-k-restriction-calciuria Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys lost more calcium when dietary potassium was restricted. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.

endpoint

Dietary potassium restriction reduced measured plasma total calcium in the male mice.

experimental-exposure

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

experimental_model

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

limitations

Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Blood total calcium fell alongside increased urinary calcium loss.

primary_references

[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

tissue_or_cell_type

kidney, blood and trabecular skeleton

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1302–1314

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft

### mouse-k-restriction-low-calcium Dietary potassium restriction reduced measured plasma total calcium in the male mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood total calcium fell alongside increased urinary calcium loss. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Dietary potassium restriction reduced measured plasma total calcium in the male mice. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.

endpoint

The potassium-restricted male mice showed increased plasma parathyroid hormone.

experimental-exposure

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

experimental_model

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

limitations

Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The calcium-regulating hormone response accompanied altered calcium balance.

primary_references

[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

tissue_or_cell_type

kidney, blood and trabecular skeleton

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1316–1328

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft

### mouse-k-restriction-pth The potassium-restricted male mice showed increased plasma parathyroid hormone. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium-regulating hormone response accompanied altered calcium balance. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: The potassium-restricted male mice showed increased plasma parathyroid hormone. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.

endpoint

Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study.

experimental-exposure

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

experimental_model

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

limitations

Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The mineral imbalance extended to a measured skeletal endpoint.

primary_references

[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

tissue_or_cell_type

kidney, blood and trabecular skeleton

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1330–1342

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft

### mouse-k-restriction-trabecular-bone Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mineral imbalance extended to a measured skeletal endpoint. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

evidence_location

Primary abstract; meal-plus-K and eplerenone comparisons.

experimental_model

Controlled meal challenges and MR-blockade comparison; 32 participants

limitations

Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

People can increase potassium excretion after a meal before a measurable blood rise.

primary_references

[preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243

tissue_or_cell_type

Gastrointestinal-renal axis

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 472–482

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled meal challenges and MR-blockade comparison; 32 participants · source_derived_draft · unverified_draft

### renal-human-meal-k-excretion-without-serum-rise A potassium-containing meal increased K excretion without a detected serum K rise in the human study; the response persisted with eplerenone. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: People can increase potassium excretion after a meal before a measurable blood rise. organism: Homo sapiens tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Controlled meal challenges and MR-blockade comparison; 32 participants limitations: Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference. evidence_location: Primary abstract; meal-plus-K and eplerenone comparisons. [preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Dietary K adjusts the balance controlling Na/Cl transporter activation.

evidence_location

Figure 1; Figures 4-5; Discussion.

experimental_model

Four-day dietary K loading in CA-SPAK mice

limitations

Response required higher plasma K than controls; not a general claim that kinase state is irrelevant.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

With adaptation, the phosphate-removing response can overcome a continuously active kinase.

primary_references

[grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498

tissue_or_cell_type

DCT

trigger_kind

machinery_impairment Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 281–292

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-day dietary K loading in CA-SPAK mice · source_derived_draft · unverified_draft

### renal-k-adaptation-overcomes-active-spak After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With adaptation, the phosphate-removing response can overcome a continuously active kinase. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Four-day dietary K loading in CA-SPAK mice limitations: Response required higher plasma K than controls; not a general claim that kinase state is irrelevant. cross_nutrient: Dietary K adjusts the balance controlling Na/Cl transporter activation. evidence_location: Figure 1; Figures 4-5; Discussion. [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_location

Primary abstract; K/Rb comparisons with buffer and secretion manipulation.

experimental_model

Clearance studies with amiloride and buffer-delivery manipulation

limitations

Clearance evidence does not identify the H,K-ATPase isoform or directly localize all transport.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The depleted kidney can increase potassium recovery; rubidium does not track it perfectly.

primary_references

[1992-k-reabsorption] Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption (1992). https://pubmed.ncbi.nlm.nih.gov/1405312/ DOI: 10.1038/ki.1992.286

tissue_or_cell_type

Kidney; distal absorptive pathway inferred

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 523–533

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clearance studies with amiloride and buffer-delivery manipulation · source_derived_draft · unverified_draft

### renal-k-depletion-activates-reabsorption K-depleted rats preferentially retained K over Rb, especially when distal buffer delivery increased and residual secretion was inhibited. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The depleted kidney can increase potassium recovery; rubidium does not track it perfectly. organism: Rattus norvegicus tissue_or_cell_type: Kidney; distal absorptive pathway inferred experimental_model: Clearance studies with amiloride and buffer-delivery manipulation limitations: Clearance evidence does not identify the H,K-ATPase isoform or directly localize all transport. evidence_location: Primary abstract; K/Rb comparisons with buffer and secretion manipulation. [1992-k-reabsorption] Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption (1992). https://pubmed.ncbi.nlm.nih.gov/1405312/ DOI: 10.1038/ki.1992.286

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Low K availability increases signaling for sodium/chloride reabsorption.

evidence_location

Results; dietary NCC immunoblots.

experimental_model

Diet manipulation

limitations

pNCC is an activity-associated proxy; this is not a universal dietary threshold.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

With little dietary potassium, the kidney increases a sodium-chloride transporter signal.

primary_references

[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006

tissue_or_cell_type

Distal convoluted tubule

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 99–110

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diet manipulation · source_derived_draft · unverified_draft

### renal-low-k-activates-ncc High-salt/low-potassium feeding increased renal NCC phosphorylation in mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With little dietary potassium, the kidney increases a sodium-chloride transporter signal. organism: Mus musculus tissue_or_cell_type: Distal convoluted tubule experimental_model: Diet manipulation limitations: pNCC is an activity-associated proxy; this is not a universal dietary threshold. cross_nutrient: Low K availability increases signaling for sodium/chloride reabsorption. evidence_location: Results; dietary NCC immunoblots. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Low K increases urinary calcium output under the tested sodium background.

evidence_location

Primary abstract; final-week balance results.

experimental_model

Four-week 0.2% versus 4% K diet; both 8% NaCl

limitations

Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

In this high-salt setting, lower potassium intake increased calcium loss in urine.

primary_references

[wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647

tissue_or_cell_type

Kidney/urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 510–521

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week 0.2% versus 4% K diet; both 8% NaCl · source_derived_draft · unverified_draft

### renal-low-k-increases-calcium-loss-high-salt Low versus high dietary K increased calcium excretion in both salt-sensitive and salt-resistant Dahl rats on high NaCl. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this high-salt setting, lower potassium intake increased calcium loss in urine. organism: Rattus norvegicus tissue_or_cell_type: Kidney/urine experimental_model: Four-week 0.2% versus 4% K diet; both 8% NaCl limitations: Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven. cross_nutrient: Low K increases urinary calcium output under the tested sodium background. evidence_location: Primary abstract; final-week balance results. [wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_location

Abstract; early/late endosomal marker colocalization.

experimental_model

Dietary restriction; confocal localization

limitations

Localization supports internalization/degradation; microscopy does not directly measure secretion.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The kidney removes potassium exit channels from the surface when potassium is scarce.

primary_references

[chu-2003-romk-endocytosis] Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct (2003). https://journals.physiology.org/doi/10.1152/ajprenal.00150.2003 DOI: 10.1152/ajprenal.00150.2003

tissue_or_cell_type

Cortical collecting duct

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 320–330

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction; confocal localization · source_derived_draft · unverified_draft

### renal-low-k-romk-internalization After 48 hours of dietary K deficiency, rat CCD ROMK shifted from apical membrane toward endosomal/lysosomal locations. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney removes potassium exit channels from the surface when potassium is scarce. organism: Rattus norvegicus tissue_or_cell_type: Cortical collecting duct experimental_model: Dietary restriction; confocal localization limitations: Localization supports internalization/degradation; microscopy does not directly measure secretion. evidence_location: Abstract; early/late endosomal marker colocalization. [chu-2003-romk-endocytosis] Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct (2003). https://journals.physiology.org/doi/10.1152/ajprenal.00150.2003 DOI: 10.1152/ajprenal.00150.2003

cross_nutrient

K loading suppresses a Na/Cl transporter before some hormonal adaptations.

evidence_location

Primary abstract; early NCC time course and aldosterone-deficient mice.

experimental_model

Gastric K load; aldosterone-deficient comparison

limitations

Early response differs from later ENaC activation; acute gavage is not a chronic diet.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The earliest NCC response to potassium does not require a new aldosterone signal in this model.

primary_references

[sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14

tissue_or_cell_type

Kidney DCT

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 294–305

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gastric K load; aldosterone-deficient comparison · source_derived_draft · unverified_draft

### renal-oral-k-aldosterone-independent-ncc-off Oral K rapidly dephosphorylated NCC in mice, including aldosterone-deficient animals. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The earliest NCC response to potassium does not require a new aldosterone signal in this model. organism: Mus musculus tissue_or_cell_type: Kidney DCT experimental_model: Gastric K load; aldosterone-deficient comparison limitations: Early response differs from later ENaC activation; acute gavage is not a chronic diet. cross_nutrient: K loading suppresses a Na/Cl transporter before some hormonal adaptations. evidence_location: Primary abstract; early NCC time course and aldosterone-deficient mice. [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14

evidence_location

Study 1 and primary abstract.

experimental_model

Meal comparison with plasma-profile-matched KCl infusion

limitations

The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

The meal-associated signal adds to the effect of potassium measured in blood.

primary_references

[oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011

tissue_or_cell_type

Gastrointestinal-renal axis

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 460–470

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Meal comparison with plasma-profile-matched KCl infusion · source_derived_draft · unverified_draft

### renal-rat-meal-k-excretion-beyond-plasma Potassium-containing meals produced more renal K excretion than K-free meals plus intravenous KCl despite matched plasma K profiles in rats. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The meal-associated signal adds to the effect of potassium measured in blood. organism: Rattus norvegicus tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Meal comparison with plasma-profile-matched KCl infusion limitations: The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal. evidence_location: Study 1 and primary abstract. [oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

magnesium -> potassium

experimental_model

Within-person dietary depletion and repletion

limitations

Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK.

nutrient_topic

Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

organism

Homo sapiens

plain_language

Supplying potassium became less effective at maintaining potassium status as Mg depletion progressed.

primary_references

[shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133

tissue_or_cell_type

Blood and whole-body potassium pool

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 217–227

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person dietary depletion and repletion · source_derived_draft · unverified_draft

### human-mg-depletion-increases-k-replacement-needs Prolonged experimental Mg depletion caused hypokalemia requiring substantial extra potassium intake to maintain serum K, alongside decreased exchangeable potassium. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying potassium became less effective at maintaining potassium status as Mg depletion progressed. organism: Homo sapiens tissue_or_cell_type: Blood and whole-body potassium pool experimental_model: Within-person dietary depletion and repletion limitations: Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK. cross_nutrient: magnesium -> potassium [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133

evidence_span

{"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"}

experimental_model

Human CTR1 expression and radiocopper transport assays

exposure

CTR1 expression; pH and potassium changes in culture

limitations

Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status.

nutrient_topic

Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper

organism

Human protein in human HEK293 cells

plain_language

The chemical surroundings changed transport speed; this is not a dietary potassium recommendation.

primary_references

[copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200

tissue_or_cell_type

Plasma membrane

transport_effect

raises The object already names cellular copper uptake.

transport_pool

the cytosol The object already names cellular copper uptake.

Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 260–271

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CTR1 expression and radiocopper transport assays · source_derived_draft · unverified_draft

### copper-ctr1-energy-ph CTR1-mediated radiocopper transport was energy independent and increased at acidic extracellular pH and high extracellular potassium in the assay. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chemical surroundings changed transport speed; this is not a dietary potassium recommendation. organism: Human protein in human HEK293 cells tissue_or_cell_type: Plasma membrane experimental_model: Human CTR1 expression and radiocopper transport assays limitations: Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status. exposure: CTR1 expression; pH and potassium changes in culture evidence_span: {"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"} [copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

magnesium -> potassium

experimental_model

Within-person dietary depletion and repletion

limitations

Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK.

nutrient_topic

Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

organism

Homo sapiens

plain_language

Restoring Mg improved potassium status in these depleted individuals; the experiment does not show that every low potassium result has this cause.

primary_references

[shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133

tissue_or_cell_type

Blood and whole-body potassium pool

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 229–239

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person dietary depletion and repletion · source_derived_draft · unverified_draft

### human-mg-repletion-restores-serum-k Serum potassium rose after Mg repletion in both men studied during prolonged experimental Mg depletion. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring Mg improved potassium status in these depleted individuals; the experiment does not show that every low potassium result has this cause. organism: Homo sapiens tissue_or_cell_type: Blood and whole-body potassium pool experimental_model: Within-person dietary depletion and repletion limitations: Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK. cross_nutrient: magnesium -> potassium [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

magnesium -> potassium

experimental_model

Double-blind placebo-controlled randomized surgical-ICU trial

limitations

Usual K/Mg treatment continued in both groups; 30 completers; hypokalemia enrollment did not establish intracellular Mg depletion in every patient.

nutrient_topic

Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

organism

Homo sapiens

plain_language

The Mg group retained more of the potassium supplied even though blood potassium looked similar. This supports retention, not a directly proven human ROMK mechanism.

primary_references

[hamill-ruth-1996-potassium-balance] Magnesium repletion and its effect on potassium homeostasis in critically ill adults: results of a double-blind, randomized, controlled trial. (1996). https://pubmed.ncbi.nlm.nih.gov/8565536/ DOI: 10.1097/00003246-199601000-00009

tissue_or_cell_type

Blood and timed urine collections

trigger_kind

biomarker_context Imported condition classification; unverified.

Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 241–251

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind placebo-controlled randomized surgical-ICU trial · source_derived_draft · unverified_draft

### icu-mg-repletion-improves-potassium-balance Randomized additional Mg sulfate improved 48-hour potassium input-minus-urine balance in hypokalemic ICU adults despite similar serum K; between-group total potassium replacement was not significantly different. Condition category: biomarker_context nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The Mg group retained more of the potassium supplied even though blood potassium looked similar. This supports retention, not a directly proven human ROMK mechanism. organism: Homo sapiens tissue_or_cell_type: Blood and timed urine collections experimental_model: Double-blind placebo-controlled randomized surgical-ICU trial limitations: Usual K/Mg treatment continued in both groups; 30 completers; hypokalemia enrollment did not establish intracellular Mg depletion in every patient. cross_nutrient: magnesium -> potassium [hamill-ruth-1996-potassium-balance] Magnesium repletion and its effect on potassium homeostasis in critically ill adults: results of a double-blind, randomized, controlled trial. (1996). https://pubmed.ncbi.nlm.nih.gov/8565536/ DOI: 10.1097/00003246-199601000-00009

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

magnesium -> sodium -> potassium

experimental_model

Dietary restriction in C57BL/6J mice with renal transport assays

limitations

Model-specific non-sufficiency; not a claim that isolated Mg restriction can never lower K at other durations or in humans.

nutrient_topic

Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

organism

Mus musculus

plain_language

A low Mg blood value alone did not guarantee falling potassium: sodium transport and the rest of the kidney response mattered.

primary_references

[maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704

tissue_or_cell_type

Kidney distal nephron

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 166–176

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft

### mg-restriction-alone-not-sufficient-hypokalemia Isolated Mg restriction produced hypomagnesemia without the hypokalemia observed under combined Na/Mg restriction in the tested mice. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low Mg blood value alone did not guarantee falling potassium: sodium transport and the rest of the kidney response mattered. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Model-specific non-sufficiency; not a claim that isolated Mg restriction can never lower K at other durations or in humans. cross_nutrient: magnesium -> sodium -> potassium [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704

availability_state

biomarker_context Imported condition classification; unverified.

experimental_model

Prediabetes pilot, 40 mEq/day KCl, 27 completers.

limitations

Underpowered pilot; absence of significance is not proof of no effect.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Human

plain_language

The trial did not establish better glucose tolerance.

primary_references

[chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570

tissue_or_cell_type

Systemic glucose regulation

trigger_kind

biomarker_context Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 924–933

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prediabetes pilot, 40 mEq/day KCl, 27 completers. · source_derived_draft · unverified_draft

### k-pilot-ogtt-null The 12-week KCl pilot found no significant between-group improvement in primary glucose AUC or OGTT insulin measures. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not establish better glucose tolerance. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Prediabetes pilot, 40 mEq/day KCl, 27 completers. limitations: Underpowered pilot; absence of significance is not proof of no effect. [chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

Potassium and accompanying alkali cannot be treated as an identical intervention.

experimental_model

Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each.

limitations

Eleven subjects, short duration and surrogate estimates; no established molecular pathway or prevention effect.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Human

plain_language

The accompanying anion changed the observed metabolic response.

primary_references

[conen-2016-pilot] Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study (2016). https://www.sciencedirect.com/science/article/abs/pii/S105687271630054X DOI: 10.1016/j.jdiacomp.2016.03.017

tissue_or_cell_type

Systemic glucose regulation

trigger_kind

biomarker_context Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 946–956

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each. · source_derived_draft · unverified_draft

### k-salt-glycemic-anion-boundary Both potassium salts improved beta-cell-function estimates; only citrate improved insulin-sensitivity estimates in this small normokalemic pilot. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The accompanying anion changed the observed metabolic response. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each. limitations: Eleven subjects, short duration and surrogate estimates; no established molecular pathway or prevention effect. cross_nutrient: Potassium and accompanying alkali cannot be treated as an identical intervention. [conen-2016-pilot] Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study (2016). https://www.sciencedirect.com/science/article/abs/pii/S105687271630054X DOI: 10.1016/j.jdiacomp.2016.03.017

evidence_location

Abstract; binding motif experiments and renal Arh-null comparison.

experimental_model

Binding, knockdown and Arh-null dietary experiments

limitations

Cell uptake mechanism and mouse dietary phenotype are complementary experiments.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Chlorocebus-derived COS-7 cells; Mus musculus

plain_language

An adaptor helps pull ROMK from the membrane and contributes to potassium-dependent channel adjustment.

primary_references

[fang-2009-arh-romk] The ARH adaptor protein regulates endocytosis of the ROMK potassium secretory channel in mouse kidney (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2769171/ DOI: 10.1172/JCI37950

tissue_or_cell_type

Cell system and distal nephron

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 332–342

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Binding, knockdown and Arh-null dietary experiments · source_derived_draft · unverified_draft

### renal-arh-targets-romk-endocytosis ARH bound the ROMK internalization motif and promoted endocytosis in COS-7 cells; Arh deletion altered dietary regulation of renal ROMK. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An adaptor helps pull ROMK from the membrane and contributes to potassium-dependent channel adjustment. organism: Chlorocebus-derived COS-7 cells; Mus musculus tissue_or_cell_type: Cell system and distal nephron experimental_model: Binding, knockdown and Arh-null dietary experiments limitations: Cell uptake mechanism and mouse dietary phenotype are complementary experiments. evidence_location: Abstract; binding motif experiments and renal Arh-null comparison. [fang-2009-arh-romk] The ARH adaptor protein regulates endocytosis of the ROMK potassium secretory channel in mouse kidney (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2769171/ DOI: 10.1172/JCI37950

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Defective K sensing prevents appropriate sodium/chloride transporter adjustment.

evidence_location

Results and primary abstract; dietary electrophysiology and NCC assays.

experimental_model

Kir5.1 knockout with high/low K diets

limitations

Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes.

primary_references

[wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025

tissue_or_cell_type

DCT

trigger_kind

machinery_impairment Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 203–214

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kir5.1 knockout with high/low K diets · source_derived_draft · unverified_draft

### renal-kir5-loss-prevents-diet-ncc-response Kcnj16-null mice failed to change NCC abundance/phosphorylation with high- or low-K diets despite persistent Kir4.1 conductance. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Kir5.1 knockout with high/low K diets limitations: Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion. cross_nutrient: Defective K sensing prevents appropriate sodium/chloride transporter adjustment. evidence_location: Results and primary abstract; dietary electrophysiology and NCC assays. [wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium restriction changes sodium handling through NCC.

evidence_location

Figure 2A-C.

experimental_model

Wild-type versus Slc12a3-null dietary study

limitations

Knockout tests pathway contribution, not exclusive control of pressure.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Potassium scarcity can make sodium retention easier through NCC.

primary_references

[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006

tissue_or_cell_type

Kidney

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 112–123

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type versus Slc12a3-null dietary study · source_derived_draft · unverified_draft

### renal-low-k-ncc-salt-retention Low-potassium feeding on high salt reduced sodium excretion; NCC deletion blunted the blood-pressure response. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium scarcity can make sodium retention easier through NCC. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Wild-type versus Slc12a3-null dietary study limitations: Knockout tests pathway contribution, not exclusive control of pressure. cross_nutrient: Potassium restriction changes sodium handling through NCC. evidence_location: Figure 2A-C. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006

cross_nutrient

K loading can increase sodium excretion through NCC regulation.

evidence_location

Primary abstract; NCC-deficient natriuresis comparison.

experimental_model

NCC knockout and control K gavage

limitations

This does not establish that increased distal sodium delivery alone explains all kaliuresis.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Turning NCC down contributes to the sodium loss caused by potassium loading.

primary_references

[sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14

tissue_or_cell_type

Kidney

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 307–318

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NCC knockout and control K gavage · source_derived_draft · unverified_draft

### renal-ncc-loss-blunts-k-natriuresis NCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Turning NCC down contributes to the sodium loss caused by potassium loading. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: NCC knockout and control K gavage limitations: This does not establish that increased distal sodium delivery alone explains all kaliuresis. cross_nutrient: K loading can increase sodium excretion through NCC regulation. evidence_location: Primary abstract; NCC-deficient natriuresis comparison. [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_location

Abstract; high-K channel-number and localization comparison.

experimental_model

Isoform-specific knockout; high-K diet

limitations

Baseline channel gating and NKCC2 phenotype were preserved; not equivalent to pan-ROMK deletion.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

This ROMK splice isoform helps increase potassium exit-channel availability when intake rises.

primary_references

[romk1-2016-isoform] Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4777858/ DOI: 10.1074/jbc.M115.707877

tissue_or_cell_type

Collecting tubule

trigger_kind

machinery_impairment Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 344–354

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform-specific knockout; high-K diet · source_derived_draft · unverified_draft

### renal-romk1-needed-high-k-adaptation Romk1-specific deletion blunted high-K-induced collecting-tubule ROMK surface recruitment and caused hyperkalemia during that challenge. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This ROMK splice isoform helps increase potassium exit-channel availability when intake rises. organism: Mus musculus tissue_or_cell_type: Collecting tubule experimental_model: Isoform-specific knockout; high-K diet limitations: Baseline channel gating and NKCC2 phenotype were preserved; not equivalent to pan-ROMK deletion. evidence_location: Abstract; high-K channel-number and localization comparison. [romk1-2016-isoform] Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4777858/ DOI: 10.1074/jbc.M115.707877

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Impaired ENaC sodium-channel adaptation accompanies defective K clearance.

evidence_location

Results Figure 2; two-day versus five-day dietary comparison.

experimental_model

Inducible tubular deletion; two-day high-K citrate diet

limitations

Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

Removing kidney SGK1 impairs the initial ability to clear a potassium load.

primary_references

[al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016

tissue_or_cell_type

Kidney tubules

trigger_kind

machinery_impairment Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 434–445

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible tubular deletion; two-day high-K citrate diet · source_derived_draft · unverified_draft

### renal-sgk1-loss-impairs-high-k-excretion Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing kidney SGK1 impairs the initial ability to clear a potassium load. organism: Mus musculus tissue_or_cell_type: Kidney tubules experimental_model: Inducible tubular deletion; two-day high-K citrate diet limitations: Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased. cross_nutrient: Impaired ENaC sodium-channel adaptation accompanies defective K clearance. evidence_location: Results Figure 2; two-day versus five-day dietary comparison. [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women

exposure

Approximately 118 versus 318 mg Mg/day and 0.25 versus 3.25 mg B/day; 42-day periods

limitations

Boron had no obvious overall effect on the response to magnesium deprivation. Results cannot establish boron as a treatment for hypomagnesemia or a substitute for magnesium.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human

plain_language

Low boron intake changed potassium loss in this experiment; this does not establish clinical potassium deficiency.

primary_references

[boron-p15724868] The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation. (2004). https://pubmed.ncbi.nlm.nih.gov/15724868/

tissue_or_cell_type

Mineral balance and endocrine measurements

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 729–740

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women · source_derived_draft · unverified_draft

### boron-potassium-low-boron Experimental boron deprivation increased urinary potassium excretion in the 2004 feeding study, whereas magnesium deprivation decreased it. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low boron intake changed potassium loss in this experiment; this does not establish clinical potassium deficiency. organism: Human tissue_or_cell_type: Mineral balance and endocrine measurements experimental_model: Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women limitations: Boron had no obvious overall effect on the response to magnesium deprivation. Results cannot establish boron as a treatment for hypomagnesemia or a substitute for magnesium. exposure: Approximately 118 versus 318 mg Mg/day and 0.25 versus 3.25 mg B/day; 42-day periods evidence_span: {"source_cache": "artifacts/boron-research/15724868.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24", "start_char": 0, "end_char": 2138, "text_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24"} [boron-p15724868] The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation. (2004). https://pubmed.ncbi.nlm.nih.gov/15724868/

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/42581205.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "616a276982b68c86769b127edd0b346732467698b8da80259d093b842708aa4b", "start_char": 0, "end_char": 1953, "text_sha256": "616a276982b68c86769b127edd0b346732467698b8da80259d093b842708aa4b"}

experimental_model

Cross-sectional diet records and 24-hour urine study; 89 adults

exposure

28 lacto-ovo-vegetarians, 29 vegans and 32 omnivores in Germany

limitations

Observational diet-pattern comparisons cannot show that boron causes potassium loss; shared food sources, intake estimation and renal handling can affect correlations. No diagnostic deficiency cutoff was validated.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human

plain_language

People excreting more boron also tended to excrete more potassium; this does not mean boron caused potassium wasting.

primary_references

[boron-p42581205] Boron Intake and 24-hour Urinary Excretion in Long-term Omnivores, Vegetarians and Vegans: a Cross-sectional Study. (2026). https://pubmed.ncbi.nlm.nih.gov/42581205/ DOI: 10.1007/s12011-026-05297-x

tissue_or_cell_type

Diet intake estimates and urine

trigger_kind

biomarker_context Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 1132–1143

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cross-sectional diet records and 24-hour urine study; 89 adults · source_derived_draft · unverified_draft

### boron-urine-potassium-correlation Higher urinary boron was associated with higher urinary potassium across the three dietary groups. Condition category: biomarker_context nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: People excreting more boron also tended to excrete more potassium; this does not mean boron caused potassium wasting. organism: Human tissue_or_cell_type: Diet intake estimates and urine experimental_model: Cross-sectional diet records and 24-hour urine study; 89 adults limitations: Observational diet-pattern comparisons cannot show that boron causes potassium loss; shared food sources, intake estimation and renal handling can affect correlations. No diagnostic deficiency cutoff was validated. exposure: 28 lacto-ovo-vegetarians, 29 vegans and 32 omnivores in Germany evidence_span: {"source_cache": "artifacts/boron-research/42581205.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "616a276982b68c86769b127edd0b346732467698b8da80259d093b842708aa4b", "start_char": 0, "end_char": 1953, "text_sha256": "616a276982b68c86769b127edd0b346732467698b8da80259d093b842708aa4b"} [boron-p42581205] Boron Intake and 24-hour Urinary Excretion in Long-term Omnivores, Vegetarians and Vegans: a Cross-sectional Study. (2026). https://pubmed.ncbi.nlm.nih.gov/42581205/ DOI: 10.1007/s12011-026-05297-x

evidence_access

Primary abstract

experimental_model

15 healthy adults; about 19 mmol extra potassium over 24 hours at the higher dose.

limitations

Not evidence that every lithium user develops potassium depletion.

nutrient_topic

Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium

plain_language

The potassium response depended on exposure.

primary_references

Effect of a single test dose of lithium carbonate on sodium and potassium excretion in man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1649725/ · DOI 10.1042/cs0810059

Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 360–366

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 15 healthy adults; about 19 mmol extra potassium over 24 hours at the higher dose. · source_derived_draft · unverified_draft

## lithium-potassium-excretion The potassium response depended on exposure. Potassium excretion increased after 600 mg lithium carbonate but not after 300 mg in the volunteer study. Model: 15 healthy adults; about 19 mmol extra potassium over 24 hours at the higher dose. Limitations: Not evidence that every lithium user develops potassium depletion. Evidence access: Primary abstract Effect of a single test dose of lithium carbonate on sodium and potassium excretion in man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1649725/ · DOI 10.1042/cs0810059

evidence_span

{"source_cache": "artifacts/pectin-research/6307932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1", "start_char": 0, "end_char": 1593, "text_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1"}

experimental_model

Within-person ileostomy balance study; six participants

exposure

15 g/day citrus pectin on days 5-7 of a 10-day low-fiber feeding protocol

limitations

Ileal apparent absorption and output are not whole-body status or clinical deficiency; the colon was bypassed.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

The potassium finding belongs to people with an ileostomy in this study.

primary_references

[pectin-p6307932] The effect of citrus pectin on the absorption of nutrients in the small intestine. (1983). https://pubmed.ncbi.nlm.nih.gov/6307932/

tissue_or_cell_type

Small intestine; ileal effluent

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 568–579

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person ileostomy balance study; six participants · source_derived_draft · unverified_draft

### pectin-ileal-potassium Pectin increased potassium output in ileal effluent. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The potassium finding belongs to people with an ileostomy in this study. organism: Homo sapiens tissue_or_cell_type: Small intestine; ileal effluent experimental_model: Within-person ileostomy balance study; six participants limitations: Ileal apparent absorption and output are not whole-body status or clinical deficiency; the colon was bypassed. exposure: 15 g/day citrus pectin on days 5-7 of a 10-day low-fiber feeding protocol evidence_span: {"source_cache": "artifacts/pectin-research/6307932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1", "start_char": 0, "end_char": 1593, "text_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1"} [pectin-p6307932] The effect of citrus pectin on the absorption of nutrients in the small intestine. (1983). https://pubmed.ncbi.nlm.nih.gov/6307932/