Component

Urinary magnesium excretion

Urinary magnesium loss, interpreted relative to circulating availability.

12 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. Claudin-16 RNAi mice developed renal magnesium wasting.

    Claudin-16 RNAi mouse genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Calcium wasting accompanied magnesium loss after shared tight-junction impairment.
    evidence-system
    Transgenic Cldn16 RNAi with renal mineral phenotyping
    experimental_model
    Transgenic Cldn16 RNAi with renal mineral phenotyping
    limitations
    This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Reducing this tight-junction component made the kidneys lose magnesium.
    primary_references
    [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    tissue
    Kidney; urine
    tissue_or_cell_type
    Kidney; urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1111–1123

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic Cldn16 RNAi with renal mineral phenotyping · source_derived_draft · unverified_draft

    ### cldn16-rnai-magnesium-loss Claudin-16 RNAi mice developed renal magnesium wasting. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing this tight-junction component made the kidneys lose magnesium. organism: Mouse tissue_or_cell_type: Kidney; urine experimental_model: Transgenic Cldn16 RNAi with renal mineral phenotyping limitations: This organismal endpoint accompanies selectivity changes; the experiment does not isolate every intervening transport step. cross_nutrient: Calcium wasting accompanied magnesium loss after shared tight-junction impairment. evidence-system: Transgenic Cldn16 RNAi with renal mineral phenotyping tissue: Kidney; urine [hou-2007-cldn16] Transgenic RNAi depletion of claudin-16 and the renal handling of magnesium. (2007). https://pubmed.ncbi.nlm.nih.gov/17442678/ DOI: 10.1074/jbc.M700632200
    Complete structured claim and evidence

  2. Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss.

    Pro-EGF P1070L → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Human pedigree and serum/urine phenotyping
    experimental_model
    Human pedigree and serum/urine phenotyping
    limitations
    Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    The inherited EGF defect was linked to failure of the kidneys to conserve magnesium.
    primary_references
    [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1043–1054

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pedigree and serum/urine phenotyping · source_derived_draft · unverified_draft

    ### egf-variant-human-magnesium-wasting Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inherited EGF defect was linked to failure of the kidneys to conserve magnesium. organism: Human tissue_or_cell_type: Kidney; serum and urine experimental_model: Human pedigree and serum/urine phenotyping limitations: Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo. evidence-system: Human pedigree and serum/urine phenotyping tissue: Kidney; serum and urine [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    Complete structured claim and evidence

  3. Human CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study.

    CLDN16 loss-of-function genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Human familial positional genetics and kidney localization
    experimental_model
    Human familial positional genetics and kidney localization
    limitations
    Establishes essential machinery; does not by itself identify a Mg-selective pore.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    A renal tight-junction protein is necessary for the kidney to retain magnesium normally.
    primary_references
    [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
    tissue
    Renal thick ascending limb
    tissue_or_cell_type
    Renal thick ascending limb
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1056–1067

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human familial positional genetics and kidney localization · source_derived_draft · unverified_draft

    ### human-cldn16-magnesium-wasting Human CLDN16 mutations were linked to renal magnesium wasting in the positional-cloning study. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A renal tight-junction protein is necessary for the kidney to retain magnesium normally. organism: Human tissue_or_cell_type: Renal thick ascending limb experimental_model: Human familial positional genetics and kidney localization limitations: Establishes essential machinery; does not by itself identify a Mg-selective pore. evidence-system: Human familial positional genetics and kidney localization tissue: Renal thick ascending limb [simon-1999-cldn16] Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999). https://pubmed.ncbi.nlm.nih.gov/10390358/ DOI: 10.1126/science.285.5424.103
    Complete structured claim and evidence

  4. Pathogenic CLDN19 variants were identified in families with renal magnesium loss and hypomagnesemia.

    CLDN19 loss-of-function genotype → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    The disorder also includes abnormal calcium handling; shared renal machinery is implicated rather than competition for dietary absorption.
    curation_notes
    Existing catalog claim fb9278a2-5be5-5e4b-92f3-e02f00f3cfc7 covers the same families with urinary-calcium-excretion endpoint. This magnesium endpoint is deliberately separate.
    evidence-system
    Human family genetics with trafficking and assembly support
    experimental_model
    Human family genetics with trafficking and assembly support
    limitations
    Associated retinal abnormalities are not assigned solely to low Mg.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    Claudin-19 failure can make the kidneys lose magnesium.
    primary_references
    [konrad-2006-cldn19] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pubmed.ncbi.nlm.nih.gov/17033971/ DOI: 10.1086/508617
    tissue
    Renal tubules
    tissue_or_cell_type
    Renal tubules
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1069–1082

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics with trafficking and assembly support · source_derived_draft · unverified_draft

    ### human-cldn19-magnesium-wasting Pathogenic CLDN19 variants were identified in families with renal magnesium loss and hypomagnesemia. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Claudin-19 failure can make the kidneys lose magnesium. organism: Human tissue_or_cell_type: Renal tubules experimental_model: Human family genetics with trafficking and assembly support limitations: Associated retinal abnormalities are not assigned solely to low Mg. cross_nutrient: The disorder also includes abnormal calcium handling; shared renal machinery is implicated rather than competition for dietary absorption. curation_notes: Existing catalog claim fb9278a2-5be5-5e4b-92f3-e02f00f3cfc7 covers the same families with urinary-calcium-excretion endpoint. This magnesium endpoint is deliberately separate. evidence-system: Human family genetics with trafficking and assembly support tissue: Renal tubules [konrad-2006-cldn19] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pubmed.ncbi.nlm.nih.gov/17033971/ DOI: 10.1086/508617
    Complete structured claim and evidence

  5. Two of three adults with homozygous PCBD1 mutations had hypomagnesemia with renal magnesium loss.

    Human pterin-4-alpha-carbinolamine dehydratase / PCBD1 → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Small human case series, three adults with homozygous PCBD1 mutations.
    limitations
    Two also had MODY-like diabetes regardless of magnesium status; neither finding establishes that phenylalanine supplements cause or correct the disorder.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A genetic defect can connect abnormal phenylalanine handling with magnesium wasting.
    primary_references
    Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24204001/ · DOI 10.1681/ASN.2013040337
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 94–100

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Small human case series, three adults with homozygous PCBD1 mutations. · source_derived_draft · unverified_draft

    ## l-phenylalanine-pcbd-magnesium A genetic defect can connect abnormal phenylalanine handling with magnesium wasting. Two of three adults with homozygous PCBD1 mutations had hypomagnesemia with renal magnesium loss. Model: Small human case series, three adults with homozygous PCBD1 mutations. Limitations: Two also had MODY-like diabetes regardless of magnesium status; neither finding establishes that phenylalanine supplements cause or correct the disorder. Evidence access: Primary abstract Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24204001/ · DOI 10.1681/ASN.2013040337
    Complete structured claim and evidence

  6. Boron supplementation reduced urinary magnesium in the 1987 postmenopausal feeding study, apparently more strongly in the low-magnesium group.

    Boron → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/boron-research/3678698.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7", "start_char": 0, "end_char": 1373, "text_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7"}
    experimental_model
    Sequential controlled feeding in a metabolic unit; 12 postmenopausal women
    exposure
    About 0.25 mg boron/day for 119 days, then 3 mg/day supplement; seven low-magnesium and five adequate-magnesium participants
    limitations
    Small sequential study, not a fracture or bone-density trial. Diet and magnesium status matter. Later studies did not consistently reproduce the reported effects.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human
    plain_language
    The measured magnesium loss in urine decreased; this does not by itself demonstrate correction of magnesium deficiency.
    primary_references
    [boron-p3678698] Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. (1987). https://pubmed.ncbi.nlm.nih.gov/3678698/ DOI: 10.1096/fasebj.1.5.3678698
    tissue_or_cell_type
    Systemic mineral balance and circulating hormones
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 612–623

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequential controlled feeding in a metabolic unit; 12 postmenopausal women · source_derived_draft · unverified_draft

    ### boron-human-magnesium-sparing-1987 Boron supplementation reduced urinary magnesium in the 1987 postmenopausal feeding study, apparently more strongly in the low-magnesium group. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured magnesium loss in urine decreased; this does not by itself demonstrate correction of magnesium deficiency. organism: Human tissue_or_cell_type: Systemic mineral balance and circulating hormones experimental_model: Sequential controlled feeding in a metabolic unit; 12 postmenopausal women limitations: Small sequential study, not a fracture or bone-density trial. Diet and magnesium status matter. Later studies did not consistently reproduce the reported effects. exposure: About 0.25 mg boron/day for 119 days, then 3 mg/day supplement; seven low-magnesium and five adequate-magnesium participants evidence_span: {"source_cache": "artifacts/boron-research/3678698.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7", "start_char": 0, "end_char": 1373, "text_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7"} [boron-p3678698] Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. (1987). https://pubmed.ncbi.nlm.nih.gov/3678698/ DOI: 10.1096/fasebj.1.5.3678698
    Complete structured claim and evidence

  7. Later nighttime conservation did not fully offset earlier loss; net 24-hour urinary excretion increased by 0.16 mmol.

    Caffeine → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial.
    limitations
    Two-day urinary balance is not total body mineral balance or a long-term deficiency diagnosis.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Later compensation reduced, but did not erase, the measured daily loss.
    primary_references
    Effect of caffeine on circadian excretion of urinary calcium and magnesium. · 1994 · https://pubmed.ncbi.nlm.nih.gov/7836625/ · DOI 10.1080/07315724.1994.10718436

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 348–354

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial. · source_derived_draft · unverified_draft

    ## caf-mg24 Later compensation reduced, but did not erase, the measured daily loss. Later nighttime conservation did not fully offset earlier loss; net 24-hour urinary excretion increased by 0.16 mmol. Model: 17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial. Limitations: Two-day urinary balance is not total body mineral balance or a long-term deficiency diagnosis. Evidence access: Primary abstract Effect of caffeine on circadian excretion of urinary calcium and magnesium. · 1994 · https://pubmed.ncbi.nlm.nih.gov/7836625/ · DOI 10.1080/07315724.1994.10718436
    Complete structured claim and evidence

  8. Urinary magnesium/creatinine rose from 70 to 110 mg/g.

    Caffeine → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection.
    limitations
    Acute renal handling. The exact tubular mechanism was unresolved; no long-term deficiency, bone loss or replacement requirement measured.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    The acute urine measurement increased.
    primary_references
    Effects of dietary caffeine on renal handling of minerals in adult women. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2402180/ · DOI 10.1016/0024-3205(90)90616-y

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 308–314

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection. · source_derived_draft · unverified_draft

    ## caf-urine-mg The acute urine measurement increased. Urinary magnesium/creatinine rose from 70 to 110 mg/g. Model: 37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection. Limitations: Acute renal handling. The exact tubular mechanism was unresolved; no long-term deficiency, bone loss or replacement requirement measured. Evidence access: Primary abstract Effects of dietary caffeine on renal handling of minerals in adult women. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2402180/ · DOI 10.1016/0024-3205(90)90616-y
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The tested citrate oral load produced a larger urinary Mg increment than the oxide load in healthy volunteers.

    Magnesium citrate → Magnesium oxide source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Magnesium chemical form -> absorption proxy.
    experimental_model
    Healthy-volunteer oral-load comparison.
    exposure
    25 mmol Mg experimental oral loads; historical study exposure, not dosage advice.
    limitations
    Urinary response is not tissue restoration or proof of superior clinical outcomes.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    A formulation difference was reflected in a short-term absorption proxy.
    primary_references
    [mg-lindberg1990] Magnesium bioavailability from magnesium citrate and magnesium oxide (1990). https://pubmed.ncbi.nlm.nih.gov/2407766/ DOI: 10.1080/07315724.1990.10720349
    tissue_or_cell_type
    Simulated gastric solutions or human urinary Mg response, as specified in model

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1640–1651

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Healthy-volunteer oral-load comparison. · source_derived_draft · unverified_draft

    ### mg-citrate-oxide-urinary-response The tested citrate oral load produced a larger urinary Mg increment than the oxide load in healthy volunteers. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A formulation difference was reflected in a short-term absorption proxy. organism: Homo sapiens tissue_or_cell_type: Simulated gastric solutions or human urinary Mg response, as specified in model experimental_model: Healthy-volunteer oral-load comparison. limitations: Urinary response is not tissue restoration or proof of superior clinical outcomes. cross_nutrient: Magnesium chemical form -> absorption proxy. exposure: 25 mmol Mg experimental oral loads; historical study exposure, not dosage advice. [mg-lindberg1990] Magnesium bioavailability from magnesium citrate and magnesium oxide (1990). https://pubmed.ncbi.nlm.nih.gov/2407766/ DOI: 10.1080/07315724.1990.10720349
    Complete structured claim and evidence

  2. Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice.

    Kidney-specific Trpm6-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Ksp-Cre conditional deletion; six-month-old male mice
    experimental_model
    Ksp-Cre conditional deletion; six-month-old male mice
    limitations
    Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    These mice maintained circulating magnesium after kidney-specific TRPM6 loss.
    primary_references
    [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 936–947

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ksp-Cre conditional deletion; six-month-old male mice · source_derived_draft · unverified_draft

    ### renal-trpm6-loss-serum-preserved Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: These mice maintained circulating magnesium after kidney-specific TRPM6 loss. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Ksp-Cre conditional deletion; six-month-old male mice limitations: Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans. evidence-system: Ksp-Cre conditional deletion; six-month-old male mice tissue: Kidney; serum and urine [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    Complete structured claim and evidence

  3. Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets.

    Slc41a1-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Constitutive knockout with dietary Mg restriction challenge
    experimental_model
    Constitutive knockout with dietary Mg restriction challenge
    limitations
    Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance.
    primary_references
    [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1195–1206

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Constitutive knockout with dietary Mg restriction challenge · source_derived_draft · unverified_draft

    ### slc41a1-null-mouse-magnesium-preserved Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Constitutive knockout with dietary Mg restriction challenge limitations: Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope. evidence-system: Constitutive knockout with dietary Mg restriction challenge tissue: Kidney; serum and urine [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
    Complete structured claim and evidence

  4. Low versus high dietary K increased calcium excretion in both salt-sensitive and salt-resistant Dahl rats on high NaCl.

    Potassium → Urinary calcium excretion source_derived_draftungraded
    Experimental context and source evidence
    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
    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