Component
Urinary loss of calcifediol
Urinary excretion of 25-hydroxyvitamin D3 after impaired tubular carrier retrieval.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Human patients with mutations causing cubilin dysfunction excreted calcifediol in urine, supporting the cubilin-dependent renal carrier-retrieval pathway.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Primary abstract, cubilin sequestration and human urinary loss.
- experimental_model
- Human inherited cubilin dysfunction; supporting receptor experiments
- exposure
- Inherited CUBN dysfunction; patient details/doses not specified in retrieved abstract.
- limitations
- This shared B12/D transport machinery does not mean dietary B12 deficiency causes urinary D loss. Genotype-phenotype evidence is observational.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- Cubilin defects can cause loss of vitamin D precursor through urine.
- primary_references
- [nykjaer2001] Cubilin dysfunction causes abnormal metabolism of the steroid hormone 25(OH) vitamin D(3). (2001). https://pubmed.ncbi.nlm.nih.gov/11717447/ DOI: 10.1073/pnas.241516998
- tissue_or_cell_type
- kidney proximal tubule and urine
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 257–270
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human inherited cubilin dysfunction; supporting receptor experiments · source_derived_draft · unverified_draft
### vd-act-cubilin-human-loss Human patients with mutations causing cubilin dysfunction excreted calcifediol in urine, supporting the cubilin-dependent renal carrier-retrieval pathway. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cubilin defects can cause loss of vitamin D precursor through urine. organism: Homo sapiens tissue_or_cell_type: kidney proximal tubule and urine experimental_model: Human inherited cubilin dysfunction; supporting receptor experiments limitations: This shared B12/D transport machinery does not mean dietary B12 deficiency causes urinary D loss. Genotype-phenotype evidence is observational. exposure: Inherited CUBN dysfunction; patient details/doses not specified in retrieved abstract. cross_nutrient: true evidence_location: Primary abstract, cubilin sequestration and human urinary loss. nutrient: Vitamin D2 and D3 [nykjaer2001] Cubilin dysfunction causes abnormal metabolism of the steroid hormone 25(OH) vitamin D(3). (2001). https://pubmed.ncbi.nlm.nih.gov/11717447/ DOI: 10.1073/pnas.241516998
Complete structured claim and evidenceMegalin-null mice failed to retrieve filtered calcifediol and lost the vitamin D precursor in urine.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Primary abstract, receptor-mediated uptake and knockout phenotype.
- experimental_model
- Targeted megalin knockout versus controls
- exposure
- Lrp2 gene disruption; no dietary restriction inferred.
- limitations
- The knockout affects other filtered ligands too; it is machinery impairment.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Mus musculus
- plain_language
- A broken kidney uptake receptor wastes vitamin D precursor.
- primary_references
- [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
- tissue_or_cell_type
- kidney and urine
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 242–255
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Targeted megalin knockout versus controls · source_derived_draft · unverified_draft
### vd-act-megalin-knockout-loss Megalin-null mice failed to retrieve filtered calcifediol and lost the vitamin D precursor in urine. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A broken kidney uptake receptor wastes vitamin D precursor. organism: Mus musculus tissue_or_cell_type: kidney and urine experimental_model: Targeted megalin knockout versus controls limitations: The knockout affects other filtered ligands too; it is machinery impairment. exposure: Lrp2 gene disruption; no dietary restriction inferred. cross_nutrient: false evidence_location: Primary abstract, receptor-mediated uptake and knockout phenotype. nutrient: Vitamin D2 and D3 [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.