Immunosuppression and proteinuria

Abstract

Proteinuria is an important marker for renal injury, not only in chronic kidney disease but also in kidney transplantation. In kidney transplant patients, proteinuria may have different causes, such as recurrence of the underlying disease, chronic allograft nephropathy, transplant glomerulopathy and de novo glomerulopathy. Immunosuppressive drugs used in transplantation interfere in the urinary excretion of proteins. Calcineurin inhibitors have important antiproteinuric effect, and they are being used to treat primary glomerulopathy. Antiproteinuric effect was also described using micophenolate. However, more recent studies have described the appearance and/or increase of proteinuria related to the use of proliferative signal inhibitors (PSIs). There are clinical evidences that proteinuria responds to the use of angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers. In this context, the study of the effect of PSIs on the molecules of the podocyte slit diaphragm as nephrin, podocin and synaptopodin (among others), and also on vascular endothelial growth factor (VEGF) is relevant. This review covers the above mentioned aspects.