RENAL FUNCTIONAL RESERVE IN EXPERIMENTAL CHRONIC GLOMERULONEPHRITIS

Loss of renal functional reserve, that is, absence of the glomerular v asodilatory response to amino-acid infusion, has been interpreted as e quivalent to glomerular hyperperfusion/hypertension, and therefore pro posed as a marker of high risk for progressive glomerular sclerosis. T o substantiate the validity of this hypothesis we evaluated the renal response to glycine and the extent of glomerular damage 10-12 weeks af ter induction of anti-glomerular basement membrane glomerulonephritis with or without superimposed clip hypertension. Untreated rats and rat s chronically treated with quinapril, a converting-enzyme inhibitor, w ere studied. In untreated groups, loss of renal functional reserve was demonstrated since GFR, single-nephron GFR (SNGFR) and plasma flow (S NPF) did not increase during glycine infusion. The absence of renal re serve was associated with glomerular hyperfusion/hypertension, and dev elopment of proteinuria and glomerulosclerosis. Quinapril reduced prot einuria and diffuse sclerosis in anti-glomerular basement membrane GN, and decreased blood pressure and segmental glomerulosclerosis in anti glomerular basement membrane GN with super-imposed clip hypertension. Both treated groups demonstrated a restoration of renal functional res erve, as depicted by increases in GFR, SNGFR, and SNPF after glycine, despite persistence of glomerular hyperperfusion/hypertension. These d ata demonstrate that renal functional reserve testing, although it doe s not detect glomerular hyperperfusion/hypertension, can provide infor mation on the progression of glomerular damage.