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High Level of Proteinuria During Treatment With Renin–Angiotensin Inhibitors Is a Strong Predictor of Renal Outcome in Nondiabetic Kidney Disease.
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- Author(s): Xie, Di; Hou, Fan Fan; Fu, Bi Ling; Zhang, Xun; Liang, Min
- Source:
Journal of Clinical Pharmacology; Jul2011, Vol. 51 Issue 7, p1025-1034, 10p- Subject Terms:
CHRONIC diseases; BIOMARKERS; BLOOD pressure; CHINESE people; CHRONIC kidney failure; COMPUTER software; CONFIDENCE intervals; CREATININE; DIABETES; ANTIHYPERTENSIVE agents; KIDNEY diseases; MULTIVARIATE analysis; HEALTH outcome assessment; PROTEINS; PROTEINURIA; RESEARCH funding; STATISTICAL sampling; STATISTICS; SURVIVAL analysis (Biometry); TIME; URINALYSIS; RENIN-angiotensin system; DATA analysis; SECONDARY analysis; TREATMENT effectiveness; PROPORTIONAL hazards models; DISEASE progression; LOSARTAN; PROGNOSIS; THERAPEUTICS - Source:
- Additional Information
- Abstract: This study investigated whether proteinuria not only could serve as a marker of renal outcome but also could monitor the renoprotection of renin–angiotensin system (RAS) inhibitor treatment in patients with nondiabetic chronic kidney disease (CKD). Data from the Renoprotection of Optimal Antiproteinuric Doses (ROAD) trial were used to examine the contribution of the antiproteinuric effect of benazepril and losartan on renal outcome (the primary composite end point of doubling of serum creatinine and end-stage renal disease or death) in 339 Chinese nondiabetic CKD patients with overt proteinuria and renal insufficiency. The degree of proteinuria at month 6 of treatment (residual proteinuria) and during follow-up (time-average proteinuria) showed a close relationship with renal end points. Lowering of proteinuria reduced the risk of renal progression in patients with high, as well as low, proteinuria at baseline. After adjustment for baseline risk markers, therapy-induced change in these variables at month 6 and during follow-up—high residual proteinuria and time-average proteinuria (≥1.0 g/d)—remained the independent predictors for renal end points. Therefore, minimization of proteinuria at least to less than 1.0 g/d should be a therapeutic goal in the management of nondiabetic patients with heavy proteinuria and renal insufficiency. [ABSTRACT FROM PUBLISHER]
- Abstract: Copyright of Journal of Clinical Pharmacology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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