Component

Glomerular filtration rate measured by creatinine clearance

Glomerular filtration rate measured by creatinine clearance. Species, exposure and limitations are retained in each linked claim.

3 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. Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischaemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II, vasopressin or norepinephrine, indomethacin potentiates the renal actions of angiotensin II in vivo particularly the reduction of renal blood flow and filtration rate, and in dogs after chronic bile duct ligation cyclooxygenase inhibition by indomethacin, ibuprofen, naproxen or sulindac sulfide produced a comparable 50% decrease in both renal blood flow and filtration rate.

    The vasodilatory prostaglandin reserve that supports renal blood flow under stress → Glomerular filtration rate measured by creatinine clearance source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/6595999.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2", "start_char": 0, "end_char": 2422, "text_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2"}
    experimental_model
    Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data
    exposure
    Cyclooxygenase inhibition against a background of raised vasoconstrictor tone
    limitations
    A review assembling several models rather than one experiment. It states the conditional nature of the renal prostaglandin role, which is the point recorded here.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Rat, dog and human
    plain_language
    These prostaglandins are a reserve the kidney calls on under strain, which is why blocking them is harmless until it is not.
    primary_references
    [ibu-p6595999] Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. (1984). https://pubmed.ncbi.nlm.nih.gov/6595999/ DOI: 10.1007/978-3-642-69132-4_56
    tissue_or_cell_type
    Renal cortex and glomeruli

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 474–485

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data · source_derived_draft · unverified_draft

    ### ibu-a-reserve-not-a-baseline Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischaemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II, vasopressin or norepinephrine, indomethacin potentiates the renal actions of angiotensin II in vivo particularly the reduction of renal blood flow and filtration rate, and in dogs after chronic bile duct ligation cyclooxygenase inhibition by indomethacin, ibuprofen, naproxen or sulindac sulfide produced a comparable 50% decrease in both renal blood flow and filtration rate. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: These prostaglandins are a reserve the kidney calls on under strain, which is why blocking them is harmless until it is not. organism: Rat, dog and human tissue_or_cell_type: Renal cortex and glomeruli experimental_model: Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data limitations: A review assembling several models rather than one experiment. It states the conditional nature of the renal prostaglandin role, which is the point recorded here. exposure: Cyclooxygenase inhibition against a background of raised vasoconstrictor tone evidence_span: {"source_cache": "artifacts/ibuprofen-research/6595999.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2", "start_char": 0, "end_char": 2422, "text_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2"} [ibu-p6595999] Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. (1984). https://pubmed.ncbi.nlm.nih.gov/6595999/ DOI: 10.1007/978-3-642-69132-4_56
    Complete structured claim and evidence

  2. In 10 patients with chronic glomerular disease randomly assigned to one week of ibuprofen, urinary 6-keto-prostaglandin F1 alpha and prostaglandin E2 excretion fell by 80%, serum creatinine rose by 40% and creatinine and para-aminohippurate clearances fell by 28% and 35% respectively, with the reduction in both clearances inversely related to the basal urinary excretion of 6-keto-prostaglandin F1 alpha but not of prostaglandin E2, while no functional changes were detected in five healthy women despite a similar suppression of renal prostacyclin synthesis, and one week of sulindac did not affect renal prostacyclin synthesis or renal function despite marked inhibition of extrarenal cyclooxygenase.

    Ibuprofen → Glomerular filtration rate measured by creatinine clearance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/6361565.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b", "start_char": 0, "end_char": 1550, "text_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b"}
    experimental_model
    Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women
    exposure
    Ibuprofen for one week, against sulindac in a parallel group
    limitations
    The healthy comparison group is what makes this decisive: the same suppression of renal prostacyclin produced no functional change in them. Twenty patients, one week.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Human
    plain_language
    The same drop in kidney prostaglandins does nothing to a healthy kidney and takes a third of the function from a diseased one.
    primary_references
    [ibu-p6361565] Effects of sulindac and ibuprofen in patients with chronic glomerular disease. Evidence for the dependence of renal function on prostacyclin. (1984). https://pubmed.ncbi.nlm.nih.gov/6361565/ DOI: 10.1056/nejm198402023100502
    tissue_or_cell_type
    Kidney
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 461–472

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women · source_derived_draft · unverified_draft

    ### ibu-kidney-depends-on-what-is-blocked In 10 patients with chronic glomerular disease randomly assigned to one week of ibuprofen, urinary 6-keto-prostaglandin F1 alpha and prostaglandin E2 excretion fell by 80%, serum creatinine rose by 40% and creatinine and para-aminohippurate clearances fell by 28% and 35% respectively, with the reduction in both clearances inversely related to the basal urinary excretion of 6-keto-prostaglandin F1 alpha but not of prostaglandin E2, while no functional changes were detected in five healthy women despite a similar suppression of renal prostacyclin synthesis, and one week of sulindac did not affect renal prostacyclin synthesis or renal function despite marked inhibition of extrarenal cyclooxygenase. Condition category: biomarker_context nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The same drop in kidney prostaglandins does nothing to a healthy kidney and takes a third of the function from a diseased one. organism: Human tissue_or_cell_type: Kidney experimental_model: Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women limitations: The healthy comparison group is what makes this decisive: the same suppression of renal prostacyclin produced no functional change in them. Twenty patients, one week. exposure: Ibuprofen for one week, against sulindac in a parallel group evidence_span: {"source_cache": "artifacts/ibuprofen-research/6361565.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b", "start_char": 0, "end_char": 1550, "text_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b"} [ibu-p6361565] Effects of sulindac and ibuprofen in patients with chronic glomerular disease. Evidence for the dependence of renal function on prostacyclin. (1984). https://pubmed.ncbi.nlm.nih.gov/6361565/ DOI: 10.1056/nejm198402023100502
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A probable case of acute reversible renal failure with hyperkalaemia followed an increase in ibuprofen dose, and across reviewed cases the ability of these drugs to inhibit prostaglandin synthesis may explain the various renal consequences, with possible predisposing factors including the amount of drug consumed, compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations and high urinary prostaglandin excretion; renal failure with these drugs is generally acute and reversible although analgesic nephropathy with papillary necrosis and chronic failure are reported.

    Ibuprofen → Serum creatinine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/6420135.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7", "start_char": 0, "end_char": 957, "text_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7"}
    experimental_model
    Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity
    exposure
    An increase in ibuprofen dose in a susceptible patient
    limitations
    A single case with a narrative review. The predisposing factors listed are the authors’ synthesis rather than a measured risk model.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Human
    plain_language
    The kidney injury usually reverses when the drug stops, and the people at risk are the ones already leaning on prostaglandins.
    primary_references
    [ibu-p6420135] Reversible renal failure associated with ibuprofen: case report and review of the literature. (1984). https://pubmed.ncbi.nlm.nih.gov/6420135/ DOI: 10.1177/106002808401800103
    tissue_or_cell_type
    Kidney
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 552–563

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity · source_derived_draft · unverified_draft

    ### ibu-renal-failure-is-reversible A probable case of acute reversible renal failure with hyperkalaemia followed an increase in ibuprofen dose, and across reviewed cases the ability of these drugs to inhibit prostaglandin synthesis may explain the various renal consequences, with possible predisposing factors including the amount of drug consumed, compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations and high urinary prostaglandin excretion; renal failure with these drugs is generally acute and reversible although analgesic nephropathy with papillary necrosis and chronic failure are reported. Condition category: biomarker_context nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The kidney injury usually reverses when the drug stops, and the people at risk are the ones already leaning on prostaglandins. organism: Human tissue_or_cell_type: Kidney experimental_model: Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity limitations: A single case with a narrative review. The predisposing factors listed are the authors’ synthesis rather than a measured risk model. exposure: An increase in ibuprofen dose in a susceptible patient evidence_span: {"source_cache": "artifacts/ibuprofen-research/6420135.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7", "start_char": 0, "end_char": 957, "text_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7"} [ibu-p6420135] Reversible renal failure associated with ibuprofen: case report and review of the literature. (1984). https://pubmed.ncbi.nlm.nih.gov/6420135/ DOI: 10.1177/106002808401800103
    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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