The prevalence of proteinuria at 1 year after renal transplantation ranges between 11% and 45% and is even higher in patients treated with inhibitors of the mammalian target of rapamycin (mTOR). Two main mechanisms can lead to proteinuria: an inadequate reabsorption of small proteins from proximal tubular cells damaged by ischemia-reperfusion injury, rejection, or toxic agents (tubular proteinuria) or an increased passage of albumin and/or protein with higher molecular weight (MW) because of a disruption of glomerular barrier caused by recurrent or de novo glomerulonephritis, transplant glomerulopathy, chronic rejection, or CNI toxicity (glomerular proteinuria). Proteinuric patients have worse patient and graft survival rates in comparison to non proteinuric patients. The amount of proteinuria is a reliable predictor of the allograft outcome. However, even microalbuminuria may be associated with a poor outcome. Treatment of proteinuria mainly rests on the management of the etiologic cause. Inhibitors of renin-angiotensin system (RAS) are useful in reversing microalbuminuria and can reduce proteinuria, but their efficacy in interfering with patient or graft survival is not demonstrated.
- angiotensin-converting enzyme inhibitors
- mTOR inhibitors and proteinuria
- post-transplant proteinuria
- tubular proteinuria
ASJC Scopus subject areas