In the past 18 years, there has been much progress in our knowledge of acute renal failure. However, despite the work of Jean Oliver1 and many others2-4 in the demonstration of the tubular lesions of this form or nephrosis, there is still uncertainty about the pathological physiology which occurs in renal shutdown. In the toxic nephroses, such as those caused by carbon tetrachloride, the failure of the kidney to excrete is not hard to understand as all nephrons tend to be involved uniformly. In the case of ischemic nephrosis, it is well known that the degree of oliguria is often out of all proportion to the tubular changes found morphologically. At the same time, in all follow-up studies which have been done, not only does there seem to be some permanent reduction in tubular function as measured by the P.A.H. clearance but also the glomerular filtration appears to
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