Renal plasma flow measured by para-aminohippurate clearance

Where it participates (unsigned role)

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

3. Indomethacin produced severe acute mesenteric vasoconstriction by intravenous infusion and by intra-arterial injection with rapid tachyphylaxis, whereas ibuprofen did not alter mesenteric blood flow even when a large 50 milligram bolus was rapidly injected, and the indomethacin response was not modified when prostaglandin synthesis was inhibited nor significantly mediated by alpha adrenergic agents or serotonin, while both drugs raised aortic pressure and reduced renal blood flow by small but significant amounts.

   Ibuprofen → Mesenteric vascular resistance source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/ibuprofen-research/7299691.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d", "start_char": 0, "end_char": 1542, "text_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d"}

   experimental_model

   Regional vascular resistance measurement in pentobarbital-anaesthetised dogs

   exposure

   Indomethacin and ibuprofen given intravenously and intra-arterially, including a 50 milligram intravenous bolus

   limitations

   A direct head-to-head between two drugs of the same class in the same animals, with a negative result for ibuprofen. Anaesthetised dogs.

   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

   Dog

   plain_language

   One drug of this class strangles the gut circulation and the other does not, and it is not a prostaglandin effect.

   primary_references

   [ibu-p7299691] Differential effects of ibuprofen and indomethacin in the regional circulation of the dog. (1981). https://pubmed.ncbi.nlm.nih.gov/7299691/ DOI: 10.1016/s0022-3565(25)32861-2

   tissue_or_cell_type

   Mesenteric and renal circulations

   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 487–498

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional vascular resistance measurement in pentobarbital-anaesthetised dogs · source_derived_draft · unverified_draft

   ### ibu-not-a-class-effect Indomethacin produced severe acute mesenteric vasoconstriction by intravenous infusion and by intra-arterial injection with rapid tachyphylaxis, whereas ibuprofen did not alter mesenteric blood flow even when a large 50 milligram bolus was rapidly injected, and the indomethacin response was not modified when prostaglandin synthesis was inhibited nor significantly mediated by alpha adrenergic agents or serotonin, while both drugs raised aortic pressure and reduced renal blood flow by small but significant amounts. 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: One drug of this class strangles the gut circulation and the other does not, and it is not a prostaglandin effect. organism: Dog tissue_or_cell_type: Mesenteric and renal circulations experimental_model: Regional vascular resistance measurement in pentobarbital-anaesthetised dogs limitations: A direct head-to-head between two drugs of the same class in the same animals, with a negative result for ibuprofen. Anaesthetised dogs. exposure: Indomethacin and ibuprofen given intravenously and intra-arterially, including a 50 milligram intravenous bolus evidence_span: {"source_cache": "artifacts/ibuprofen-research/7299691.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d", "start_char": 0, "end_char": 1542, "text_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d"} [ibu-p7299691] Differential effects of ibuprofen and indomethacin in the regional circulation of the dog. (1981). https://pubmed.ncbi.nlm.nih.gov/7299691/ DOI: 10.1016/s0022-3565(25)32861-2

   Complete structured claim and evidence