Assessment of nephrotoxicity.

Prescott, L. F.

doi:10.1111/j.1365-2125.1982.tb01379.x

Cited by 28 publications

(7 citation statements)

References 63 publications

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“…Thus, changes occurring consistently in all experiments were also evaluated by significance of the paired t test as given in table 1. Creatinine clearance was somewhat higher than inulin clearance which is in agreement with the known tubular secretion of creatinine [ Prescott, 1982], Sulfinpyrazone decreased creatinine clearance signifi cantly which was not caused by a decrease of glomerular filtration. Despite the significant effect of sulfinpyrazone on creatinine clearance during the standardized clear ance periods, the effect of the drug on creatinine clear ance when determined from 24-hour collection periods was not significant.…”

Section: Discussionsupporting

confidence: 68%

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Effects of Sulfinpyrazone on Renal Function and Prostaglandin Formation in Man

Rosenkranz

Fejes-Tóth

Diener

et al. 1985

Nephron

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Sulfinpyrazone (800 mg/day for 6 days) significantly reduced the excretion of the main urinary prostaglandin E metabolite by 54% in 6 healthy female volunteers. While sulfinpyrazone did not affect inulin clearance, clearances of creatinine and PAH were significantly diminished by 18.0 and 44.7%, respectively. In the anaesthetized dog sulfinpyrazone decreased PAH clearance and PAH extraction concomitantly without affecting renal blood flow. These results show that clearances of creatinine and PAH do not reliably reflect glomerular filtration and renal perfusion, respectively, during sulfinpyrazone administration. Whereas sodium balance and body weight were not significantly different between the first control period and sulfinpyrazone administration, net sodium excretion significantly increased from 121.6 ± 5.4 mEq/day during sulfinpyrazone treatment to 139.3 ± 6.6 mEq/day during the following control period, while body weight significantly decreased indicating modest sodium retention during drug administration. Plasma renin activity, vascular sensitivity to angiotensin II, and urinary excretion of the enzymes N-acetylglucosaminidase and alanineaminopeptidase were not affected by sulfinpyrazone administration. In summary, sulfinpyrazone caused a decrease of total body prostaglandin E formation in healthy female volunteers together with a moderate sodium retention. Despite inhibition of prostaglandin synthesis, glomerular filtration rate, plasma renin activity, or pressor effects of angiotensin II were not altered.

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Section: Discussionsupporting

confidence: 68%

“…1982, including the inhibitors of PG synthesis acetylsalicylic acid or difiunisal [Dieppe et al, 1978;Prescott. 1982], In our acute study, sulfinpyrazone had no such effect.…”

Section: Discussionmentioning

confidence: 99%

Effects of Sulfinpyrazone on Renal Function and Prostaglandin Formation in Man

Rosenkranz

Fejes-Tóth

Diener

et al. 1985

Nephron

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“…Neither drug affected the urinary excretion of beta‐2‐microglobulin or N‐acetylglucosaminidase (NAG). The former is a sensitive test of proximal tubular integrity, 1 while increase in NAG excretion has also been shown to be associated with acute renal tubular injury 6 . The maintenance of normal urinary excretion of both these endogenous markers indicates that neither isoxicam nor piroxicam was associated with tubular damage in the course of this study.…”

Section: Discussionmentioning

confidence: 64%

The Effects of Isoxicam and Piroxicam on Renal Function in Healthy Subjects

Darragh

1985

Int J Clinical Practice

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Renal function before and after the random administration of isoxicam or piroxicam was studied in 20 healthy volunteers aged between 18 and 35. The Mann-Whitney test was used to compare pre-and post-treatment differences between the groups and the Wilcoxon Matched-Pairs Ranks test to compare post-treatment observations with baseline data.The most interesting finding was that, unlike piroxicam, isoxicam increased creatinine clearance during continuous administration. Neither drug appeared to be involved in tubular damage. Isoxicam resulted in a statistically significant reduction in serum uric acid levels, suggesting a possible application in the longterm management of gout.

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“…Anschließend an die glomeruläre Filtration erfolgt in den proximalen Tubuli eine Reabsorption und Katabolisierung zu 99,9% (3,9,21,30). Aus dieser Funktion der proximalen T ubuli im Stoffwechsel des ßz-Mikroglobulin ergibt sich die Anwendbarkeit des Nachweises einer vermehrten Ausscheidung dieser Substanz im Harn zur Früherkennung einer tubulären Nierenschädigung (21). In erster Linie sind es Schwermetalle und verschiedene Medikamenteinsbesondere die Aminoglykoside -bei denen bisher eine frühzeitige Erkennung einer Tubulopathie durch erhöhte ßz-Mikroglobulinausscheidung im Harn nachgewiesen wurde (8,23,29…”

Section: Importance Of ßRmicroglobulin In Rheumatoid Arthritis As a Punclassified