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Nephrol Dial Transplant (2004) 19: 301-305
© ERA–EDTA 2004; all rights reserved

Editorial Review

Proteinuria after renal transplantation: pathogenesis and management

Helmut Reichel1, Martin Zeier2 and Eberhard Ritz2

1Nephrological Center, Villingen-Schwenningen and 2Department of Internal Medicine, University of Heidelberg, Germany

Correspondence and offprint requests to: Dr Helmut Reichel, Nephrological Center, Schramberger Strasse 28, D-78054 Schwenningen, Germany. Email: helmut.reichel@dialyse-schwenningen.de

Keywords: chronic allograft rejection; hypertension; proteinuria; renal transplantation

The first 150 words of the full text of this article appear below.

Proteinuria: marker or culprit?

The amount of protein excreted in the urine was previously shown to be a powerful predictor of renal outcome [1]. More recently it has been proposed that proteinuria per se promotes progression of renal disease by conferring to proximal tubular epithelial cells, after uptake of proteins by endocytosis, an inflammatory phenotype with increased production of ANG II, endothelin 1, cytokines and chemokines. All these agonists, preferentially secreted in an upluminal direction [2] stimulate interstitial fibroblasts, and potentially cause trans-differentiation of epithelial cells into fibroblasts, thus promoting interstitial fibrosis. Direct evidence that proteinuria leads to interstitial fibrosis of the kidney has recently been provided by studies on the amphibian kidneys of axolotl [3]. These kidneys have two types of nephrons: closed nephrons like the mammalian kidney, and open nephrons that communicate with the peritoneal cavity via an orifice. Injection of protein into the peritoneal cavity . . . [Full Text of this Article]

How frequent is microalbuminuria/proteinuria after renal transplantation?

Does proteinuria predict graft loss in patient survival?

What are the pathomechanisms underlying post-transplant proteinuria?

Which interventions affect proteinuria after transplantation?

Conclusions


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