Effects of nonsteroidal anti-inflammatory drugs on proteinuria

Vriesendorp, R.; Donker, A. J. M.; Zeeuw, Dick de; Jong, Paul E. de; Hem, G. K. van der; Brentjens, Jan R.

doi:10.1016/0002-9343(86)90910-1

Cited by 81 publications

(41 citation statements)

References 33 publications

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“…22,23 Different therapeutic strategies can reduce albuminuria, including a low-protein diet, 24 indomethacin, 25 and antihypertensive agents such as ACEIs 26 and AIIAs. 27 It is of interest to determine whether these or other interventions for the reduction of albuminuria also afford cardiac protection.…”

Section: Discussionmentioning

confidence: 99%

Albuminuria, a Therapeutic Target for Cardiovascular Protection in Type 2 Diabetic Patients With Nephropathy

et al. 2004

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Background-Albuminuria is an established risk marker for both cardiovascular and renal outcomes. Albuminuria can be reduced with drugs that block the renin-angiotensin system (RAS). We questioned whether the short-term drug-induced change in albuminuria would predict the long-term cardioprotective efficacy of RAS intervention. Methods and Results-We analyzed data from Reduction in Endpoints in Non-insulin dependent diabetes mellitus with the Angiotensin II Antagonist Losartan (RENAAL), a double-blind, randomized trial in 1513 type 2 diabetic patients with nephropathy, focusing on the relationship between the prespecified cardiovascular end point (composite) or hospitalization for heart failure and baseline or reduction in albuminuria. Patients with high baseline albuminuria (Ն3 g/g creatinine) had a 1.92-fold (95% CI, 1.54 to 2.38) higher risk for the cardiovascular end point and a 2.70-fold (95% CI, 1.94 to 3.75) higher risk for heart failure compared with patients with low albuminuria (Ͻ1.5 g/g). Among all available baseline risk markers, albuminuria was the strongest predictor of cardiovascular outcome. The association between albuminuria and cardiovascular outcome was driven by those patients who also had a renal event.Modeling of the initial 6-month change in risk parameters showed that albuminuria reduction was the only predictor for cardiovascular outcome: 18% reduction in cardiovascular risk for every 50% reduction in albuminuria and a 27% reduction in heart failure risk for every 50% reduction in albuminuria. Conclusions-Albuminuria is an important factor predicting cardiovascular risk in patients with type 2 diabetic nephropathy. Reducing albuminuria in the first 6 months appears to afford cardiovascular protection in these patients.

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Section: Discussionmentioning

confidence: 99%

Albuminuria, a Therapeutic Target for Cardiovascular Protection in Type 2 Diabetic Patients With Nephropathy

et al. 2004

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“…Albuminuria is a useful marker for evaluation of glomerular filtration barrier (GFB) damage. Conventionally, nonsteroidal anti-inflammatory drugs have been reported to reduce proteinuria (Vriesendorp et al, 1986), suggesting that prostanoids, derived from COX-1 or COX-2, may worsen GFB damage. The effect of EP4 receptor signaling on glomerular function has remained controversial, however.…”

Section: Other Immune Cellsmentioning

confidence: 99%

The Prostanoid EP4 Receptor and Its Signaling Pathway

Yokoyama

Iwatsubo²,

Umemura³

et al. 2013

Pharmacol Rev

227

257

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“…We therefore measured hydrolysis products and metabolites of TXA2 and PG12 in urine, to provide measures of biosynthesis of these eicosanoids in vivo. Cyclooxygenase-inhibition has been shown to be beneficial in reducing proteinuria in patients with nephrotic syndrome (Donker et al, 1978;Velosa & Torres, 1986;Vriesendorp et al, 1986). To study the role of prostaglandins in NTN, we have also studied the effect of ibuprofen, a cyclo-oxygenase inhibitor.…”

Section: Introductionmentioning

confidence: 99%

Excretion of metabolites of prostacyclin and thromboxane by rats with nephrotoxic nephritis: effects of interleukin‐1

Ward

Fuller

Ritter

et al. 1991

British J Pharmacology

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1 To obtain direct evidence of abnormal eicosanoid biosynthesis in rats injected with anti-glomerularbasement-membrane antibodies (a-GBM), products derived from thromboxane A2 (TXA2) and prostacyclin (PGO2) were measured in 24 h urine collections before and after a-GBM. 2 Administration of a-GBM (9.5 mg) caused albuminuria, decreased creatinine clearance, increased numbers of intra-glomerular neutrophils and increased excretion of TXB2, 2,3-dinor-TXB2 (products of TXA2) and 6-oxo-PGF1a and 2,3-dinor-6-oxo-PGF1. (products of PGO2) at 24 h. 3 Interleukin-1 (IL-I,,; 5ug) alone caused an increase in PGO2 metabolite excretion but had no effect on TXA2 metabolites. It had no effect on creatinine clearance but increased numbers of glomerular neutrophils by approximately 4-5 fold compared to a-GBM. 4 Pretreatment of rats with IL-1 before a-GBM synergistically increased albumin excretion but only additively increased eicosanoid excretion. Numbers of intra-glomerular neutrophils and creatinine clearance were unchanged compared to IL-1p alone.5 The cyclo-oxygenase inhibitor, ibuprofen (10mgkg-i.p., twice daily for 4 days) inhibited both serum TXB2 production and urinary prostaglandin excretion. It also caused an almost complete attenuation of albumin excretion. Creatinine clearance and glomerular neutrophils remained unchanged after a-GBM/ IL-1 . 6 We conclude that the 50% inhibition of thromboxane production induced by ibuprofen does not modify the fall in creatinine clearance of accumulation of neutrophils in the glomerulus caused by the a-GBM. This degree of inhibition of eicosanoid production was associated with a striking decrease in proteinuria, but this may reflect a haemodynamic rather than a disease modifying action.

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Effects of nonsteroidal anti-inflammatory drugs on proteinuria

Cited by 81 publications

References 33 publications

Albuminuria, a Therapeutic Target for Cardiovascular Protection in Type 2 Diabetic Patients With Nephropathy

Albuminuria, a Therapeutic Target for Cardiovascular Protection in Type 2 Diabetic Patients With Nephropathy

The Prostanoid EP4 Receptor and Its Signaling Pathway

Excretion of metabolites of prostacyclin and thromboxane by rats with nephrotoxic nephritis: effects of interleukin‐1

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