SCANNING ELECTRON-MICROSCOPIC STUDY OF GLYCEROL MODEL OF ACUTE RENAL-FAILURE

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  • 1 January 1976
    • journal article
    • research article
    • Vol. 34  (4) , 406-414
Abstract
Previous studies have implicated both intrarenal vasoconstriction and reduced glomerular permeability in the pathogenesis of acute renal failure. The role of vasoconstriction and glomerular structural abnormalities in this syndrome was studied. Six rats (group I) given angiotensin II (180 ng./100 g per min) did not develop acute renal failure (blood urea N 28.6 mg./100 ml. at 24 h). Twenty-five rats (group II), allowed free access to water and given glycerol i.m. (8 ml./kg.), developed mild acute renal failure (blood urea N 41.6 mg./100 ml. at 24 h). Ten nondehydrated rats (group III), given both glycerol and angiotensin II, developed a more severe form of acute renal failure (blood urea N 120.4 mg./100 ml. at 24 h P < 0.001): this value was not significantly different from that of 14 rats (group IV) dehydrated 24 h prior to glycerol administration (blood urea nitrogen 137 mg./100 ml. at 24 h). Kidneys from 8 control rats and 17 rats randomly selected from the 4 groups were examined with the scanning EM. Rats in groups I and III showed glomerular capillary loop constriction not seen in groups II or IV. Rats in groups III and IV-A (2-8 h after glycerol) showed the fenestrated glomerular endothelium to be obscured by a dense covering of amorphous particulate material. This material also covered the filtering areas of the external surface of the glomeruli and formed casts in the tubules. In addition, glomerular capillaries of group III rats (6 h after glycerol) were filled with twisted strands of fibrin-like material not seen in the other groups. In group IV-B rats (24 h after glycerol), the particulate debris was no longer present and glomerular architecture was entirely normal, although surrounding tubules were filled by casts. Early in the course of the disease the accumulation of foreign matter in the glomeruli may initiate the syndrome. Acute renal failure after glycerol administration persists in the presence of normal glomerular architecture. This observation lends no further support to the hypothesis that glomerular filtration rate remains low because of reduced glomerular permeability, and suggests a tubular rather than a glomerular mechanism to explain continued renal failure in this model.