IN the past two decades, clinical and experimental studies have markedly expanded our understanding of the causes of renal disease. Enhanced understanding of the diverse pathogenetic mechanisms (vascular, metabolic, or immunologic disorders) involving the glomeruli, the interstitium, or both has not, however, resulted in commensurate therapeutic advances. Chronic renal insufficiency, once established, tends to progress to end-stage renal failure. Although there are some exceptions, efforts to halt or even slow the progression of chronic renal disease have been unsuccessful.

The mechanisms underlying the progression of renal disease have remained obscure for at least two reasons. First, the glomerulus and the . . .