Component

Sodium-phosphate cotransporter NaPi-IIc / SLC34A3

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

6 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 it acts on

  1. The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23.

    Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Circulating calcitriol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
    experimental_model
    Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
    exposure
    SLC34A3 disease-associated mutations in five families
    limitations
    Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    A phosphate-handling defect can change the vitamin D environment.
    primary_references
    [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    tissue_or_cell_type
    Renal proximal tubule and systemic mineral phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 681–692

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft

    ### sodium-napi2c-calcitriol The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A phosphate-handling defect can change the vitamin D environment. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    Complete structured claim and evidence

  2. The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria.

    Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Urinary calcium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
    experimental_model
    Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
    exposure
    SLC34A3 disease-associated mutations in five families
    limitations
    Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    This phosphate disorder can also increase calcium loss into urine.
    primary_references
    [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    tissue_or_cell_type
    Renal proximal tubule and systemic mineral phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 694–705

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft

    ### sodium-napi2c-calcium The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This phosphate disorder can also increase calcium loss into urine. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    Complete structured claim and evidence

  3. SLC34A3 mutations segregated with renal phosphate wasting and hypophosphatemic rickets in the studied families.

    Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Renal phosphate reabsorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
    experimental_model
    Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
    exposure
    SLC34A3 disease-associated mutations in five families
    limitations
    Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    The kidney’s sodium/phosphate transporter is important for retaining phosphate.
    primary_references
    [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    tissue_or_cell_type
    Renal proximal tubule and systemic mineral phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 668–679

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft

    ### sodium-napi2c-phosphate SLC34A3 mutations segregated with renal phosphate wasting and hypophosphatemic rickets in the studied families. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney’s sodium/phosphate transporter is important for retaining phosphate. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    Complete structured claim and evidence

What acts on it

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

    Potassium → Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Magnesium deprivation decreased renal slc34a3-mrna abundance in the 21-day rat experiment.

    Magnesium → SLC34A3 mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium -> vitamin D/phosphate handling; transcript-level evidence.
    experimental_model
    Mg-free versus 0.05% Mg diet.
    limitations
    mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    A second phosphate-transporter message also fell.
    primary_references
    [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    tissue_or_cell_type
    Rat kidney
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1418–1428

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mg-free versus 0.05% Mg diet. · source_derived_draft · unverified_draft

    ### mg-deficiency-napi2c-transcript Magnesium deprivation decreased renal slc34a3-mrna abundance in the 21-day rat experiment. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second phosphate-transporter message also fell. organism: Rattus norvegicus tissue_or_cell_type: Rat kidney experimental_model: Mg-free versus 0.05% Mg diet. limitations: mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference. cross_nutrient: Magnesium -> vitamin D/phosphate handling; transcript-level evidence. [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    Complete structured claim and evidence

  2. The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux.

    SLC34A3-associated phosphate wasting in the 2016 ATP-flux patient → Human skeletal-muscle ATP synthetic flux by 31P-MRS source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"}
    experimental_model
    31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments
    exposure
    Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case
    limitations
    ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The study found a similar pattern in one person with inherited renal phosphate wasting.
    primary_references
    [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    tissue_or_cell_type
    Skeletal muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 607–618

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments · source_derived_draft · unverified_draft

    ### phosphorus-human-atp-defect The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study found a similar pattern in one person with inherited renal phosphate wasting. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments limitations: ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold. exposure: Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case evidence_span: {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"} [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    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.

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