Component

Circulating calcitriol concentration

Circulating calcitriol concentration. Species, exposure and limitations are retained in each linked claim.

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. 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 FGF23 rise was associated with lower calcitriol and serum calcium and higher PTH concentrations.

    Circulating biologically active intact FGF23 → Circulating calcitriol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"}
    experimental_model
    Double-blind randomized comparison with physiological substudy
    exposure
    One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up
    limitations
    Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    1997 adults with iron-deficiency anemia; 185 in substudy
    plain_language
    The phosphate disturbance connected to active vitamin D and calcium-regulating hormones.
    primary_references
    [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    tissue_or_cell_type
    Blood and renal phosphate handling
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 979–990

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized comparison with physiological substudy · source_derived_draft · unverified_draft

    ### iron-fgf23-vitamin-d-calcium The FGF23 rise was associated with lower calcitriol and serum calcium and higher PTH concentrations. Condition category: nutrient_deficiency nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The phosphate disturbance connected to active vitamin D and calcium-regulating hormones. organism: 1997 adults with iron-deficiency anemia; 185 in substudy tissue_or_cell_type: Blood and renal phosphate handling experimental_model: Double-blind randomized comparison with physiological substudy limitations: Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow. exposure: One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up evidence_span: {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"} [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    Complete structured claim and evidence

  3. Ferric carboxymaltose-associated intact-FGF23 elevation accompanied lower circulating calcitriol in the substudy.

    Ferric carboxymaltose → Circulating calcitriol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/30518682.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d", "start_char": 0, "end_char": 2381, "text_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d"}
    experimental_model
    Randomized iron-formulation comparison with physiological substudy
    exposure
    One trial course of ferric carboxymaltose or ferumoxytol; follow-up five weeks
    limitations
    Formulation-specific drug effect, not dietary iron. FGF23 was associated with the downstream changes; the exact reason the formulations differ was not settled.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The phosphate-wasting pattern also reduced active vitamin D.
    primary_references
    [phosphorus-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    tissue_or_cell_type
    Iron-deficiency anemia; n=1997 parent trial, n=185 substudy
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 1011–1022

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized iron-formulation comparison with physiological substudy · source_derived_draft · unverified_draft

    ### phosphorus-iron-calcitriol Ferric carboxymaltose-associated intact-FGF23 elevation accompanied lower circulating calcitriol in the substudy. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The phosphate-wasting pattern also reduced active vitamin D. organism: Human tissue_or_cell_type: Iron-deficiency anemia; n=1997 parent trial, n=185 substudy experimental_model: Randomized iron-formulation comparison with physiological substudy limitations: Formulation-specific drug effect, not dietary iron. FGF23 was associated with the downstream changes; the exact reason the formulations differ was not settled. exposure: One trial course of ferric carboxymaltose or ferumoxytol; follow-up five weeks evidence_span: {"source_cache": "artifacts/phosphorus-research/30518682.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d", "start_char": 0, "end_char": 2381, "text_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d"} [phosphorus-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Diet-related FGF23 changes correlated inversely with maximal tubular phosphate reabsorption and calcitriol, and positively with urinary phosphate excretion.

    Phosphorus → Renal phosphate reabsorption source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/15613425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2", "start_char": 0, "end_char": 1563, "text_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2"}
    experimental_model
    Controlled sequential dietary intervention
    exposure
    Five-day low-phosphate diet plus binder, then phosphate loading; calcium adjusted to minimize PTH changes
    limitations
    Phosphate intake and calcium/binder cointerventions are explicit; correlation of hormones with renal handling does not independently prove each mediator.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The hormone, kidney and vitamin D responses moved together during the intervention.
    primary_references
    [phosphorus-p15613425] Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. (2005). https://pubmed.ncbi.nlm.nih.gov/15613425/ DOI: 10.1210/jc.2004-1039
    tissue_or_cell_type
    29 healthy young men; serum hormones and renal handling

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 920–931

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

    ### phosphorus-diet-renal-feedback Diet-related FGF23 changes correlated inversely with maximal tubular phosphate reabsorption and calcitriol, and positively with urinary phosphate excretion. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone, kidney and vitamin D responses moved together during the intervention. organism: Human tissue_or_cell_type: 29 healthy young men; serum hormones and renal handling experimental_model: Controlled sequential dietary intervention limitations: Phosphate intake and calcium/binder cointerventions are explicit; correlation of hormones with renal handling does not independently prove each mediator. exposure: Five-day low-phosphate diet plus binder, then phosphate loading; calcium adjusted to minimize PTH changes evidence_span: {"source_cache": "artifacts/phosphorus-research/15613425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2", "start_char": 0, "end_char": 1563, "text_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2"} [phosphorus-p15613425] Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. (2005). https://pubmed.ncbi.nlm.nih.gov/15613425/ DOI: 10.1210/jc.2004-1039
    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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