Component
Urinary phosphate excretion
Independent biological entity. Read linked claims for experimental scope and context.
3 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
Urinary phosphate rose from 21.6 to 28.8 mmol/day during the higher-phosphate/calcium regimen.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/21030580.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e", "start_char": 0, "end_char": 1603, "text_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e"}
- experimental_model
- Paired 36-hour dietary interventions
- exposure
- Low/high phosphate and calcium diets, separated by a week
- limitations
- Both calcium and phosphate changed; phosphate alone cannot be assigned the full effect. Timing and circadian variation matter.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Human
- plain_language
- The kidneys excreted more phosphate.
- primary_references
- [phosphorus-p21030580] Effects of dietary phosphate and calcium intake on fibroblast growth factor-23. (2011). https://pubmed.ncbi.nlm.nih.gov/21030580/ DOI: 10.2215/cjn.04730510
- tissue_or_cell_type
- Ten healthy adults; serial serum measurements and 24-hour urine
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 959–970
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Paired 36-hour dietary interventions · source_derived_draft · unverified_draft
### phosphorus-mixed-diet-urine Urinary phosphate rose from 21.6 to 28.8 mmol/day during the higher-phosphate/calcium regimen. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys excreted more phosphate. organism: Human tissue_or_cell_type: Ten healthy adults; serial serum measurements and 24-hour urine experimental_model: Paired 36-hour dietary interventions limitations: Both calcium and phosphate changed; phosphate alone cannot be assigned the full effect. Timing and circadian variation matter. exposure: Low/high phosphate and calcium diets, separated by a week evidence_span: {"source_cache": "artifacts/phosphorus-research/21030580.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e", "start_char": 0, "end_char": 1603, "text_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e"} [phosphorus-p21030580] Effects of dietary phosphate and calcium intake on fibroblast growth factor-23. (2011). https://pubmed.ncbi.nlm.nih.gov/21030580/ DOI: 10.2215/cjn.04730510
Complete structured claim and evidenceTenapanor decreased urinary phosphorus in the four-day healthy-volunteer study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/30158152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e6950931f538331a62ce1a6b35ba66ddf0a6bcaec7fe4b4f8f81e8fd952ee0e", "start_char": 0, "end_char": 1701, "text_sha256": "6e6950931f538331a62ce1a6b35ba66ddf0a6bcaec7fe4b4f8f81e8fd952ee0e"}
- experimental_model
- Rodent physiology, human enteroid transport and healthy-volunteer intervention
- exposure
- Enteroid NHE3 perturbation; healthy volunteers 15 mg tenapanor twice daily for four days
- limitations
- Tenapanor inhibits NHE3 rather than binding phosphate. TEER is an epithelial assay measure, not a direct clinical permeability score.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Human
- plain_language
- The urinary result was consistent with less intestinal absorption, not direct proof of renal-transporter inhibition.
- primary_references
- [phosphorus-p30158152] Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability. (2018). https://pubmed.ncbi.nlm.nih.gov/30158152/ DOI: 10.1126/scitranslmed.aam6474
- tissue_or_cell_type
- Intestinal epithelium; stool and urinary balance
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 386–397
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent physiology, human enteroid transport and healthy-volunteer intervention · source_derived_draft · unverified_draft
### phosphorus-tenapanor-urine Tenapanor decreased urinary phosphorus in the four-day healthy-volunteer study. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The urinary result was consistent with less intestinal absorption, not direct proof of renal-transporter inhibition. organism: Human tissue_or_cell_type: Intestinal epithelium; stool and urinary balance experimental_model: Rodent physiology, human enteroid transport and healthy-volunteer intervention limitations: Tenapanor inhibits NHE3 rather than binding phosphate. TEER is an epithelial assay measure, not a direct clinical permeability score. exposure: Enteroid NHE3 perturbation; healthy volunteers 15 mg tenapanor twice daily for four days evidence_span: {"source_cache": "artifacts/phosphorus-research/30158152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e6950931f538331a62ce1a6b35ba66ddf0a6bcaec7fe4b4f8f81e8fd952ee0e", "start_char": 0, "end_char": 1701, "text_sha256": "6e6950931f538331a62ce1a6b35ba66ddf0a6bcaec7fe4b4f8f81e8fd952ee0e"} [phosphorus-p30158152] Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability. (2018). https://pubmed.ncbi.nlm.nih.gov/30158152/ DOI: 10.1126/scitranslmed.aam6474
Complete structured claim and evidence
Where it participates (unsigned role)
The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Potassium -> calcium/phosphate/PTH observations.
- experimental_model
- Concurrent mineral and hormone measurements.
- limitations
- Co-occurrence does not establish that PTH caused every excretion change.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Homo sapiens
- plain_language
- Potassium depletion affected calcium-phosphate regulation alongside sodium handling.
- primary_references
- [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
- tissue_or_cell_type
- Plasma and urine
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1534–1544
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concurrent mineral and hormone measurements. · source_derived_draft · unverified_draft
### k-depletion-human-mineral-pth-response The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion affected calcium-phosphate regulation alongside sodium handling. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Concurrent mineral and hormone measurements. limitations: Co-occurrence does not establish that PTH caused every excretion change. cross_nutrient: Potassium -> calcium/phosphate/PTH observations. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
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.