High level of proteinuria during treatment with renin-angiotensin inhibitors is a strong predictor of renal outcome in nondiabetic kidney disease.

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.

[Advanced glycation end products induce expression of PAI-1 in cultured human proximal tubular epithelial cells through NADPH oxidase dependent pathway].

Aim: To investigate the effects of advanced glycation end products (AGES) on secretion of plasminogen activator inhibitor-1(PAI-1)by human proximal tubular epithelial cells and its NADPH oxidase dependent pathway.

Methods: Human proximal tubular epithelial cells were cultured in vitro with indicated concentration of AGES modified human serum albumin (AGES-HSA). NADPH oxidase activity were detected by lucigenin-enhanced chemiluminescence.