Component

Renal magnesium reabsorption

Recovery of filtered magnesium by renal tubular transport.

4 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. Renal magnesium loss is a well-known effect of cyclosporine treatment in people, and in this rat model the authors attribute it to downregulation of TRPM6 in the distal convoluted tubule.

    Cyclosporine → Renal magnesium reabsorption source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Rat model of cyclosporine nephrotoxicity, with the human observation as the stated background
    exposure
    Cyclosporine, dose and duration not stated here
    limitations
    The human magnesium loss is cited as established background in this report rather than measured in it. The rat measurement is the transporter expression and the fractional excretion, and the causal attribution between them is the authors' reading.
    organism
    Rat model of cyclosporine nephrotoxicity, with the human observation as the stated background
    plain_language
    Renal magnesium loss is a well-known effect of cyclosporine treatment in people, and in this rat model the authors attribute it to downregulation of TRPM6 in the distal convoluted tubule.
    primary_references
    Expression of renal distal tubule transporters TRPM6 and NCC in a rat model of cyclosporine nephrotoxicity and effect of EGF treatment. (2011). https://pubmed.ncbi.nlm.nih.gov/21653632/ DOI: 10.1152/ajprenal.00116.2011
    route
    In vivo
    tissue
    Renal magnesium handling

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 300–300

    Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Rat model of cyclosporine nephrotoxicity, with the human observation as the stated background · source_derived_draft · unverified_draft

    Renal magnesium loss is a well-known effect of cyclosporine treatment in people, and in this rat model the authors attribute it to downregulation of TRPM6 in the distal convoluted tubule.
    Complete structured claim and evidence

  2. Magnesium reabsorption fell from 97.0% to 94.2%, with no significant change in filtered magnesium load.

    Caffeine → Renal magnesium reabsorption 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 kidneys retained a smaller fraction of the filtered mineral.
    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 292–298

    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-renal-mg The kidneys retained a smaller fraction of the filtered mineral. Magnesium reabsorption fell from 97.0% to 94.2%, with no significant change in filtered magnesium load. 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. 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

  2. Overexpressed wild-type PCBD1 bound HNF1B and increased FXYD2 promoter activity in a human kidney cell line.

    Human pterin-4-alpha-carbinolamine dehydratase / PCBD1 → Human sodium/potassium ATPase regulatory subunit / FXYD2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human kidney-cell overexpression and promoter assay.
    limitations
    Promoter activity is not a direct measurement of magnesium flux or proof that phenylalanine intake regulates magnesium.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A protein used in phenylalanine metabolism also helps control a kidney transport regulator.
    primary_references
    Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24204001/ · DOI 10.1681/ASN.2013040337

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 78–84

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human kidney-cell overexpression and promoter assay. · source_derived_draft · unverified_draft

    ## l-phenylalanine-pcbd-transcription A protein used in phenylalanine metabolism also helps control a kidney transport regulator. Overexpressed wild-type PCBD1 bound HNF1B and increased FXYD2 promoter activity in a human kidney cell line. Model: Human kidney-cell overexpression and promoter assay. Limitations: Promoter activity is not a direct measurement of magnesium flux or proof that phenylalanine intake regulates magnesium. 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

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