Nephrol Dial Transplant (2004) 19: 277-281
© ERA–EDTA 2004; all rights reserved
Editorial Comments
Proteinuria and interstitial injury
Children's Hospital and Regional Medical Center, Department of ediatrics, University of Washington, Seattle, WA, USA
Correspondence and offprint requests to: Allison Eddy, Children's Hospital and Regional Medical Center, Division of Nephrology, Mail Stop M1-5, 4800 Sand Point Way NE, Seattle, WA 98105, USA. Email: allison.eddy@seattlechildrens.org
Keywords: chemokines; fibrosis; inflammation; proteinuria; macrophages
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Introduction: proteinuria as a risk factor for progressive renal disease
It has long been recognized that patients with high-grade proteinuria due to chronic glomerular disease are more likely to develop chronic renal failure than a matched group of patients with low-grade or no proteinuria [1,2]. Although this association may seem intuitively obvious, suggesting correlation with the severity of glomerular damage, two important observations promote an alternative compelling hypothesis. First is the fact that renal functional outcome for patients with chronic glomerulopathy is best predicted histologically by the severity of chronic extraglomerular damage—peritubular capillary loss, tubular atrophy and interstitial fibrosis. Second is research evidence that urinary proteins themselves may elicit pro-inflammatory and pro-fibrotic effects that directly contribute to chronic tubulointerstitial damage. For example, rodents injected daily with large doses of albumin develop ‘overload proteinuria’ that consists of both the exogenous albumin as well as several endogenous plasma proteins [3,4]. Although there does not
The proteinuria–interstitial inflammation–fibrosis connection
Effects of proteinuria on renal tubules
Other pathways from the glomerulus to the interstitium
Why is the inflamed interstitium a concern?
Conclusion
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Connotea 
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