Nephrol Dial Transplant (2001) 16: 215-218
© 2001 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Albuminuria and renal injury—beware of proteins bearing gifts
1 Section of Nephrology, Department of Medicine, Robert Wood Johnson School of Medicine, New Brunswick, New Jersey, 2 Section of Nephrology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA
Keywords: albumin; apoptosis; chronic renal disease; oxidant injury; proteinuria
Introduction
Over the last two decades a shift in paradigm has taken place regarding the role of proteinuria in the progression of renal disease. Across a wide spectrum of glomerular and non-glomerular diseases (especially those characterized by tubulointerstitial fibrosis), the degree of proteinuria has been shown to correlate with the risk of progression to end-stage renal disease [1]. Initially, proteinuria was thought simply to be a marker of the severity of glomerular injury. Recent evidence, however, suggests that proteinuria, and particularly albuminuria, may itself promote tubular injury, with interstitial inflammation and eventual fibrosis [2,3].
While several mechanisms have been put forward to explain how albuminuria can produce renal injury, a direct causal relationship, even in animal models, has yet to be established. To complicate matters further, recent in vitro data indicate that albumin can inhibit apoptosis and promote the survival of primary cultures of mouse
Inhibition of apoptosis by albumin: carriage of non-cytokine survival factors
Inhibition of apoptosis by albumin: scavenging of reactive oxygen species
Structural modifications of albumin: oxidative and non-oxidative
Structurally modified albumin as inflammatory signalling intermediates
Hypothesis
Acknowledgments
Notes
References
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