AJP - Renal Physiology, Vol 259, Issue 2 239-F245, Copyright © 1990 by American Physiological Society
Hypertension and progressive glomerular injury caused by focal glomerular ischemia
P. L. Miller, H. G. Rennke and T. W. Meyer
Department of Medicine, Stanford University, California 94305.
Sprague-Dawley rats received infusions of 55-microns microspheres (groups 1
and 3) or dextrose (groups 2 and 4) into both renal arteries. Groups 1 and
2 rats were studied over 7 mo. In group 1 rats renal embolization increased
the mean arterial pressure (group 1, 140 +/- 4 mmHg; group 2, 118 +/- 2
mmHg) without reducing the glomerular filtration rate (GFR; group 1, 4.69
+/- 0.16 ml/min; group 2, 4.57 +/- 0.22 ml/min). Micropuncture studies
showed that systemic hypertension was accompanied by an increase in the
glomerular capillary pressure of functioning nephrons in group 1 rats.
Morphological studies showed that renal embolization caused both glomerular
ischemia (group 1, 11.8 +/- 1.9% of glomeruli; group 2, 0.1 +/- 0.1% of
glomeruli) and glomerular segmental sclerosis (group 1, 15.0 +/- 1.0% of
glomeruli; group 2, 3.3 +/- 0.2% of glomeruli). Groups 3 and 4 rats were
studied over 2 mo. Renal embolization again increased the mean arterial
pressure without reducing the GFR in group 3 rats. Morphological studies
showed that at 2 mo renal embolization caused glomerular ischemia without
glomerular segmental sclerosis. These studies show that focal glomerular
ischemia can cause systemic and glomerular capillary hypertension in the
absence of a reduction in the GFR. They further show that focal glomerular
ischemia can cause progressive sclerotic injury in the remaining,
nonischemic portion of the glomerular population.
