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J. D. E. PRICE, M.D.; R. A. PALMER, M.D.

AMA Arch Intern Med. 1960;105(1):90-98.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 others^2-4 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 . . . [Full Text PDF of this Article]

Author Affiliations
Vancouver, B.C., Canada

From the Departments of Medicine, The Vancouver General Hospital and the University of British Columbia, and the British Columbia Medical Research Institute.

Footnotes
Submitted for publication May 25, 1959.

Dr. Price can now be reached at the Toronto General Hospital.

Presented at the Annual Meeting of the Western Section of the American Federation for Clinical Research, Carmel, California, Jan. 29, 1959.

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