Do glomerular hemodynamic adaptations influence the progression of human renal disease?

Although experiments in the rat suggest that glomerular hemodynamic alterations following a reduction of renal mass may be implicated in the progression of chronic renal failure, we argue that the deleterious effects of similar adaptations in human renal disease are unproven. In the otherwise normal solitary kidney the supranormal glomerular filtration rate (GFR) remains stable over the longterm, and in early diabetic nephropathy which is also accompanied by hyperfiltration, renal deterioration cannot be dissociated from a rise in systemic blood pressure. In patients with miscellaneous renal diseases and a depressed basal GFR there is indirect evidence that hyperfiltration might occur in some of the remnant glomeruli. However, at present there is little conclusive evidence to indicate that therapies which might normalize glomerular hemodynamics, e.g., dietary protein restriction, have any effect on progression of renal disease, or that angiotensin converting-enzyme inhibitors, which lower glomerular capillary pressure, have any advantage over other antihypertensive agents which are equally efficacious in lowering systemic blood pressure.