Reversible hemodynamic defect in glomerular filtration rate after ischemic injury.

In Wistar rats with surface glomeruli 3 h of nearly complete occlusion of the left renal artery resulted in uniform falls (similar to50%) in ipsilateral whole-kidney glomerular filtration rate (GFR) and single-nephron GFR (SNGFR) and in urinary findings consistent with impaired water reabsorption. Since the fall in SNGFR was accompanied by a proportional fall in glomerular plasma flow rate (GPF), and since net ultrafiltration pressure at afferent and efferent ends of the glomerular capillary was unchanged from preischemic levels, these findings suggest that the fall in SNGFR was a hemodynamic consequence of the fall in GPF. To test this hypothesis, GPF was restored to preischemic levels by means of acute infusion of homologous, isoncotic plasma. GPF and SNGFR uniformly increased, on average to preischemic levels, whereas net ultrafiltration pressure at afferent and efferent ends of the glomerular capillary again remained essentially unchanged. These studies demonstrate that the fall in SNGFR in this model of ischemic injury is causally related to the accompanying fall in GPF. Of interest, despite this reversal of the defect in GFR, fractional water reabsorption remained impaired. This restoration of GFR but not reabsorption by plasma infusion abruptly converts this ischemic lesion from nondiuretic to diuretic.