title: Effect of renovascular hypertension on experimental glomerulonephritis in rats.
abstract: Systemic hypertension is a major risk factor that determines the rate of progression of kidney disease. The underlying mechanisms, however, are incompletely understood. To gain insight into these mechanisms, the present study was undertaken to characterize the effects of renovascular hypertension on the course of anti-thymocyte antibody-induced glomerulonephritis. Glomerulonephritis was induced in rats 6 weeks after the initiation of two-kidney, one-clip hypertension, when blood pressure was already increased. Structure and function of the clipped and the nonclipped kidney were examined 5 days later. Glomerular filtration rate (GFR) was measured by inulin clearance. The induction of nephritis did not alter the blood pressure in either hypertensive rats or normotensive controls. Albuminuria increased slightly in normotensive rats after the induction of nephritis, whereas no significant differences were found between hypertensive rats with or without nephritis. No significant differences were found for the GFR values of normotensive controls and nephritic animals or for values in the clipped kidney with or without nephritis. However, the GFR of the nonclipped kidney was significantly reduced in nephritic animals as compared with all other groups. Morphologic evaluation revealed that hypertensive rats with nephritis exhibited a combination of characteristics of nephritis and hypertensive glomerular injury. Histologic findings of nephritis, such as glomerular binding of rabbit IgG and glomerular proliferation and mesangial matrix expansion, were similar after the induction of nephritis in controls and in the clipped and nonclipped kidneys of hypertensive animals. However, intraglomerular microaneurysms were significantly more often found in the non-clipped kidneys after the induction of nephritis. Hypertension-induced deterioration of glomerular function was not associated with marked morphologic deterioration but rather with a combination of the characteristics of nephritis and hypertensive glomerular injury.
authors.affiliation: Department of Medicine, University of Hamburg, Germany.
authors.forename: U O
authors.initials: UO
authors.lastname: Wenzel
authors.forename: F
authors.initials: F
authors.lastname: Thaiss
authors.forename: U
authors.initials: U
authors.lastname: Panzer
authors.forename: A
authors.initials: A
authors.lastname: Schneider
authors.forename: G
authors.initials: G
authors.lastname: Schwietzer
authors.forename: U
authors.initials: U
authors.lastname: Helmchen
authors.forename: R A
authors.initials: RA
authors.lastname: Stahl
mesh_terms: D000419:Albuminuria / Q000209:etiology; D000783:Aneurysm / Q000473:pathology; D000818:Animals; D000961:Antilymphocyte Serum / Q000008:administration & dosage; D001794:Blood Pressure; D002455:Cell Division; D003176:Complement C3 / Q000378:metabolism; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006978:Hypertension, Renovascular / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D007074:Immunoglobulin G / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D011817:Rabbits; D051381:Rats; D017207:Rats, Sprague-Dawley; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000961:Antilymphocyte Serum; D003176:Complement C3; D007074:Immunoglobulin G