The progression of chronic renal disease: immunological, nutritional and intrinsic renal mechanisms.

The majority of patients with any initial renal insult show progression of renal damage over time. The histological end-result is often the same, whatever the initial lesion, and consists of an increase in extracellular matrix (ECM) and ultimately glomerulosclerosis. The clinical rate of progression correlates mainly with the degree of interstitial, rather than with that of glomerular damage. The main culprits for the ultimate interstitial damage and the rate of progression of renal disease, are the type and degree of the initial (e.g. immunological) insult and the magnitude of the proteinuria. Hypertension (intraglomerular) is an independent risk factor. Control of hypertension with angiotension converting enzyme (ACE) inhibitors or angiotensin II (AII) receptor blockers, reduction of protein and fat intake, anti-oxidative therapy and a variety of experimental measures reduce the progression of renal damage in animal experiments. Some of these interventions have also been shown to be beneficial in a number of controlled clinical studies, in well-defined renal disease entities in humans. These new data provide insight into the pathogenesis of chronic renal damage and raise the hope that in the not too far future, effective strategies can be devised to attenuate the progression of acquired renal disease.