Renal functional reserve in experimental chronic glomerulonephritis

Loss of renal functional reserve, that is, absence of the glomerularvasodilatory response to amino-acid infusion, has been interpretedas equivalent to glomerular hyperperfusion/hypertension, andthere fore proposed as a marker of high risk for progressiveglomerular sclerosis. To substantiate the validity of this hypothesiswe evaluated the renal response to glycine and the extent ofglomerular damage 10–12 weeks after induction of anti-glomerularbasement membrane glomerulonephritis with or without superimposedclip hypertension. Untreated rats and rats chronically treatedwith quinapril, a converting-enzyme inhibitor, were studied.In untreated groups, loss of renal functional reserve was demonstratedsince GFR, single-nephron GFR (SNGFR) and plasma flow (SNPF)did not increase during glycine infusion. The absence of renalreserve was associated with glomerular hyperfusion/hypertension,and development of proteinuria and glomerulosclerosis. Quinaprilreduced proteinuria and diffuse sclerosis in anti-glomerularbasement membrane GN, and decreased blood pressure and segmentalglomeruloscierosis in anti glomerular basement membrane GN withsuperimposed clip hypertension. Both treated groups demonstrateda restoration of renal functional reserve, as depicted by increasesin GFR, SNGFR, and SNPF after glycine, despite persistence ofglomerular hyperperfusion/hypertension. These data demonstrthat renal functional reserve testing, although it does notdetect glomerular hyperperfusion/hypertension, can provide informationon the progression of glomerular damage.