THE PROGRESSION OF CHRONIC RENAL-DISEASE - IMMUNOLOGICAL, NUTRITIONALAND INTRINSIC RENAL MECHANISMS

The majority of patients with any initial renal insult show progressio n of renal damage over time. The histological end-result is often the same, whatever the initial lesion, and consists of an increase in extr acellular 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 th e ultimate interstitial damage and the rate of progression of renal di sease, are the type and degree of the initial (e.g. immunological) ins ult and the magnitude of the proteinuria. Hypertension (intraglomerula r) is an independent risk factor. Control of hypertension with angiote nsion converting enzyme (ACE) inhibitors or angiotensin II (All) recep tor blockers, reduction of protein and fat intake, anti-oxidative ther apy and a variety of experimental measures reduce the progression of r enal damage in animal experiments. Some of these interventions have al so been shown to be beneficial in a number of controlled clinical stud ies, in well-defined renal disease entities in humans. These new data provide insight into the pathogenesis of chronic renal damage and rais e the hope that in the not too far future, effective strategies can be devised to attenuate the progression of acquired renal disease.