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Leonard B. Berman, MD

JAMA. 1975;231(10):1067-1069.

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

FEW syndromes have had as many names and periodic rediscoveries as acute tubular necrosis. The 1940s produced "lower nephron nephrosis," and after that "hemoglobinuric nephrosis," "crush kidney," and "acute tubular necrosis"; all made their debut. Recently, "vasomotor nephropathy" was proposed, thus completing a circle back to 1917 when the same syndrome was studied by German investigators and called "vasomotor nephritis." This parade of names clearly illustrates changing concepts of pathogenesis. Specifically, we are now leaving the era of acute tubular necrosis, a term that emphasized minor morphological changes in the tubules as pathogenetic, and we are entering an era in which persistent renal cortical vasoconstriction (angiotensin-induced?) is regarded as the central defect. In any case, and by whatever name, we are speaking of the reversible acute renal failure, which follows various kinds of shock or certain other insults and is accompanied by relatively minor morphological change in the kidney. A . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Nephrology, Mt. Sinai Hospital, Cleveland.

Footnotes
Reprint requests to Mt. Sinai Hospital, University Circle, Cleveland, OH 44106 (Dr. Berman).

Edited by Samuel Vaisrub, MD, Senior Editor.

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