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.