Late consequences of acute ischemic injury to a solitary kidney

The sequelae of acute ischemic injury to a solitary kidney were assessed in rats subjected to right nephrectomy and transient occlusion of the left re nal artery, control rats underwent right nephrectomy alone. Incomplete reco very from ischemic injury at 2 wk (serum creatinine levels of 1.1 +/- 0.2 v ersus 0.5 +/- 0.1 mg/dl, P < 0.05 for ischemia versus control) was followed by deterioration of renal function at 20 wk (serum creatinine levels of 1. 7 +/- 0.4 versus 0.7 +/- 0.1 mg/dl, P < 0.05 for ischemia versus control). Morphologic studies showed that impairment of function after ischemic injur y was associated with widespread tubulointerstitial disease. Some tubule se gments were atrophic and others exhibited cystic dilation, so that the tubu lar cell volume fraction was reduced (37 +/- 4 versus 53 +/- 2%, P < 0.05), while the tubular lumen and interstitial volume fractions were increased ( 31 +/- 4 versus 23 +/- 2% and 29 +/- 2 versus 20 +/- 1%, respectively, both P < 0.05). Many glomeruli retained open capillary loops but were no longer connected to normal tubule segments (63 +/- 8 versus 15 +/- 7% of glomerul i, P < 0.05). There was a strong inverse correlation between the prevalence of such glomeruli and the GFR at 20 wk after ischemia (r(2) = 0.79, P < 0. 001). Tubulointerstitial disease at that time was accompanied by proteinuri a and widespread segmental glomerular tuft injury. The occurrence of simila r processes in human patients could contribute to the loss of graft kidneys that suffer ischemic injury during transplantation.