Effect of renovascular hypertension on experimental glomerulonephritis in rats

Citation
Uo. Wenzel et al., Effect of renovascular hypertension on experimental glomerulonephritis in rats, J LA CL MED, 134(3), 1999, pp. 292-303
Citations number
27
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
ISSN journal
00222143 → ACNP
Volume
134
Issue
3
Year of publication
1999
Pages
292 - 303
Database
ISI
SICI code
0022-2143(199909)134:3<292:EORHOE>2.0.ZU;2-2
Abstract
Systemic hypertension is a major risk factor that determines the rate of pr ogression of kidney disease. The underlying mechanisms, however, are incomp letely 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. Glomerul onephritis 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 hyper tensive rats or normotensive controls. Albuminuria increased slightly in no rmotensive rats after the induction of nephritis, whereas no significant di fferences were found between hypertensive rats with or without nephritis. N o significant differences were found for the GFR values of normotensive con trols and nephritic animals or for values in the clipped kidney with or wit hout nephritis. However, the GFR of the nonclipped kidney was significantly reduced in nephritic animals as compared with all other groups. Morphologi c evaluation revealed that hypertensive rats with nephritis exhibited a com bination of characteristics of nephritis and hypertensive glomerular injury . Histologic findings of nephritis, such as glomerular binding of rabbit Ig G and glomerular proliferation and mesangial matrix expansion, were similar after the induction of nephritis in controls and in the clipped and noncli pped kidneys of hypertensive animals. However, intraglomerular microaneurys ms were significantly more often found in the nonclipped kidneys after the induction of nephritis. Hypertension-induced deterioration of glomerular fu nction was not associated with marked morphologic deterioration but rather with a combination of the characteristics of nephritis and hypertensive glo merular injury.