Component

Plasma potassium concentration

Independent biological entity. Read linked claims for experimental scope and context.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Affected individuals had salt wasting with hyperkalemia and acidosis despite mineralocorticoid unresponsiveness.

    Epithelial sodium channel → Plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"}
    experimental_model
    Human family genetics and sodium-channel functional testing
    exposure
    Loss-of-function alpha- or beta-subunit variants in five kindreds
    limitations
    Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    Sodium-channel failure can impair the normal balance of potassium and acid as well as sodium.
    primary_references
    [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
    tissue_or_cell_type
    ENaC-dependent epithelia and systemic electrolyte phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 941–952

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and sodium-channel functional testing · source_derived_draft · unverified_draft

    ### sodium-enac-loss-potassium Affected individuals had salt wasting with hyperkalemia and acidosis despite mineralocorticoid unresponsiveness. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium-channel failure can impair the normal balance of potassium and acid as well as sodium. organism: Human tissue_or_cell_type: ENaC-dependent epithelia and systemic electrolyte phenotype experimental_model: Human family genetics and sodium-channel functional testing limitations: Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel. exposure: Loss-of-function alpha- or beta-subunit variants in five kindreds evidence_span: {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"} [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
    Complete structured claim and evidence

  2. Intestinal NHE3-null mice developed hyperkalemia.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
    experimental_model
    Inducible intestinal epithelial Slc9a3 deletion
    exposure
    Tamoxifen-induced NHE3 loss
    limitations
    Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Potassium can rise in this model; diarrhea does not impose one universal potassium pattern.
    primary_references
    [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
    tissue_or_cell_type
    Intestine with systemic electrolyte measurements
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 863–874

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft

    ### sodium-gut-potassium Intestinal NHE3-null mice developed hyperkalemia. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can rise in this model; diarrhea does not impose one universal potassium pattern. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
    Complete structured claim and evidence

  3. Affected CLCNKB families had hypokalemia alongside salt wasting.

    Chloride channel ClC-Kb → Plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/9326936.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e", "start_char": 0, "end_char": 1227, "text_sha256": "80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e"}
    experimental_model
    Genetics in seventeen kindreds
    exposure
    Loss-of-function CLCNKB variants
    limitations
    This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Human
    plain_language
    Potassium deficiency can be downstream of defective chloride transport.
    primary_references
    [chloride-p9326936] Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. (1997). https://pubmed.ncbi.nlm.nih.gov/9326936/ DOI: 10.1038/ng1097-171
    tissue_or_cell_type
    Renal salt handling
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 900–911

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

    ### chloride-clcnkb-potassium Affected CLCNKB families had hypokalemia alongside salt wasting. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium deficiency can be downstream of defective chloride transport. organism: Human tissue_or_cell_type: Renal salt handling experimental_model: Genetics in seventeen kindreds limitations: This cohort had normal magnesium and variable calciuria; do not universalize the full phenotype. exposure: Loss-of-function CLCNKB variants evidence_span: {"source_cache": "artifacts/chloride-research/9326936.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e", "start_char": 0, "end_char": 1227, "text_sha256": "80ade45b4ae654e5aa13b671daebab418640aa033aca3a74cae4ccf52d4e279e"} [chloride-p9326936] Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. (1997). https://pubmed.ncbi.nlm.nih.gov/9326936/ DOI: 10.1038/ng1097-171
    Complete structured claim and evidence

  4. Two weeks of KCl raised mean plasma potassium from 4.3 to 4.7 mmol/L; 21 of 191 CKD participants developed hyperkalemia.

    Potassium chloride → Plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Uncontrolled run-in; CKD G3b-4.
    exposure
    40 mmol/day KCl; 83% used RAAS inhibitors.
    limitations
    11% is this cohort rate, not general-population risk or a dose recommendation.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    Reduced kidney clearance changes the response to an added potassium load.
    primary_references
    [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
    tissue_or_cell_type
    Plasma

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1638–1648

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled run-in; CKD G3b-4. · source_derived_draft · unverified_draft

    ### k-ckd-kcl-plasma-rise Two weeks of KCl raised mean plasma potassium from 4.3 to 4.7 mmol/L; 21 of 191 CKD participants developed hyperkalemia. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced kidney clearance changes the response to an added potassium load. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Uncontrolled run-in; CKD G3b-4. limitations: 11% is this cohort rate, not general-population risk or a dose recommendation. exposure: 40 mmol/day KCl; 83% used RAAS inhibitors. [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
    Complete structured claim and evidence

  5. All three potassium salts increased plasma potassium despite their different acid-base effects.

    Potassium ion → Plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Same CKD crossover.
    limitations
    Cannot infer long-term food effects.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    An alkalizing potassium salt did not remove the potassium rise in this study.
    primary_references
    [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
    tissue_or_cell_type
    Plasma

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1674–1683

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

    ### k-ckd-salts-potassium-not-rescued-by-alkali All three potassium salts increased plasma potassium despite their different acid-base effects. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An alkalizing potassium salt did not remove the potassium rise in this study. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Same CKD crossover. limitations: Cannot infer long-term food effects. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards