Nephrol Dial Transplant (2001) 16: 885-888
© 2001 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Modulation of the renin–angiotensin system in proteinuric renal disease: are there added benefits?
Department of Nephrology, Leicester General Hospital and University of Leicester, Leicester, UK
Keywords: ACE inhibitors; AIIRA; profibrogenic pathways; proteinuria; renin–angiotensin system
Introduction
Most forms of progressive renal disease follow a final common pathway resulting in tubular atrophy, interstitial scarring and an interstitial inflammatory cell infiltrate [1]. The onset and degree of proteinuria is associated with a poor prognosis and has recently led to an increased interest in characterizing the pathogenic role proteinuria plays in the progression of renal damage. Evidence is accumulating that the filtration of excessive proteins by the glomerulus together with their subsequent reabsorption exerts a toxic effect on the proximal tubular epithelial cell in the manner of a signalling molecule [2,3]. This protracted over-reabsorption of protein results in the activation of pro-inflammatory pathways, which trigger inflammation in the interstitium. It is the severity of the resultant interstitial fibrosis that correlates most closely with the degree of renal impairment and subsequent prognosis. Studies performed using angiotensin converting enzyme (ACE) inhibitors have demonstrated the beneficial
The role of the RAS in the development of tubulointerstitial disease
The role of proteinuria in the development of tubulointerstitial disease
The beneficial effects of AIIRA vs ACE inhibition in proteinuric renal disease
Conclusion
Notes
References
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  M. A J Devonald and F. E Karet Targeting the renin-angiotensin system in patients with renal disease J R Soc Med, January 8, 2002; 95(8): 391 - 397. [Full Text] [PDF]
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