title: Renal functional reserve in experimental chronic glomerulonephritis.
abstract: Loss of renal functional reserve, that is, absence of the glomerular vasodilatory response to amino-acid infusion, has been interpreted as equivalent to glomerular hyperperfusion/hypertension, and therefore proposed as a marker of high risk for progressive glomerular sclerosis. To substantiate the validity of this hypothesis we evaluated the renal response to glycine and the extent of glomerular damage 10-12 weeks after induction of anti-glomerular basement membrane glomerulonephritis with or without superimposed clip hypertension. Untreated rats and rats chronically treated with quinapril, a converting-enzyme inhibitor, were studied. In untreated groups, loss of renal functional reserve was demonstrated since GFR, single-nephron GFR (SNGFR) and plasma flow (SNPF) did not increase during glycine infusion. The absence of renal reserve was associated with glomerular hyperfusion/hypertension, and development of proteinuria and glomerulosclerosis. Quinapril reduced proteinuria and diffuse sclerosis in anti-glomerular basement membrane GN, and decreased blood pressure and segmental glomerulosclerosis in antiglomerular basement membrane GN with superimposed clip hypertension. Both treated groups demonstrated a restoration of renal functional reserve, as depicted by increases in GFR, SNGFR, and SNPF after glycine, despite persistence of glomerular hyperperfusion/hypertension. These data demonstrate that renal functional reserve testing, although it does not detect glomerular hyperperfusion/hypertension, can provide information on the progression of glomerular damage.
authors: Division of Nephrology-Hypertension, University of California, San Diego School of Medicine.
authors: L
authors: L
authors: De Nicola
authors: O W
authors: OW
authors: Peterson
authors: S
authors: S
authors: Obagi
authors: J A
authors: JA
authors: Kaiser
authors: C B
authors: CB
authors: Wilson
authors: F B
authors: FB
authors: Gabbai
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000906:Antibodies / Q000276:immunology; D000959:Antihypertensive Agents / Q000494:pharmacology; D001485:Basement Membrane / Q000276:immunology; D002908:Chronic Disease; D005921:Glomerulonephritis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D005998:Glycine / Q000009:adverse effects; D006978:Hypertension, Renovascular / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D007546:Isoquinolines / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology*; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D008297:Male; D000077583:Quinapril; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000502:physiology; D044005:Tetrahydroisoquinolines
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000906:Antibodies; D000959:Antihypertensive Agents; D007546:Isoquinolines; D044005:Tetrahydroisoquinolines; D000077583:Quinapril; D005998:Glycine