Component
Renal apical sodium-citrate cotransport
Functional sodium-dependent citrate uptake in renal brush-border membrane vesicles; older activity assays do not prove an isoform identity.
1 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
Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry.
- endpoint
- Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles.
- experimental-exposure
- Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
- experimental_model
- Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
- limitations
- Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Rattus norvegicus
- plain_language
- The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling.
- primary_references
- [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
- tissue_or_cell_type
- renal proximal-tubule apical membrane
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1190–1202
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. · source_derived_draft · unverified_draft
### k-depletion-increases-na-citrate-transport Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling. organism: Rattus norvegicus tissue_or_cell_type: renal proximal-tubule apical membrane experimental_model: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. limitations: Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested. cross_nutrient: Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry. experimental-exposure: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. endpoint: Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
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.