Nephrol Dial Transplant (2002) 17: 363-368
© 2002 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
The inflammatory component in progressive renal disease—are interventions possible?
Renal Pathophysiology Laboratory, Renal Division, Department of Clinical Medicine, Faculty of Medicine, University of São Paulo, Brazil
Introduction
The pathogenesis of progressive renal diseases leading to end-stage renal failure is still largely unknown and is therefore the subject of intense investigation. Some features have been well recognized such as the development of glomerulosclerosis, tubulointerstital injury, and the accumulation of extracellular matrix leading to fibrosis and scarring of the renal structures.
It is now clear that major events, which determine the outcome of progressive renal disease, regardless of the initial insult, are related to the tubulointerstitial compartment. Even in primary glomerulonephritis the degree of tubulointerstitial damage correlates more closely with the long-term outcome than to the extent of glomerular involvement [1,2].
Although mechanical factors such as glomerular hypertension and hypertrophy are likely to contribute to the initiation of some forms of progressive renal disease, tubulointerstitial lesions cannot be simply interpreted as an ischaemic sequela of glomerular sclerosis. There is growing evidence that the participation of
Cellular and molecular events involved in the progression of renal disease
The fibrogenic process in progressive renal disease
Possible therapeutic interventions
Pharmacological blockade of the RAS
A role for anti-inflammatory interventions?
What is the role of mycophenolate mofetil?
Notes
References
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