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Steven Chrysant
Kansas City, Mo

Arch Intern Med. 1984;144(11):2282.

	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 Reply.—Bursztyn et al present evidence contrary to the current belief regarding renal blood flow autoregulation in the ischemic kidney. Several studies, including ours,^1-5 have shown that interference with angiotensin II formation in patients with critical, and I emphasize critical renal artery stenosis either to both kidneys or to a solitary kidney, leads to severe reversible azotemia.^3-5 The explanation is that angiotensin II is necessary to maintain adequate glomerular filtration pressure in the face of poststenotic drop in mean arterial pressure. This has been attributed to preferential constriction of the efferent arteriole by angiotensin II.⁶ If that does not happen, then one has to assume that the renal artery stenosis is not critical. The authors do not provide any functional evidence, besides anatomic, as to whether the renal arte[ill] stenosis was critical. The response [ill] arterial pressure to converting [ill] zyme inhibitors cannot be taken [ill] evidence for critical renal . . . [Full Text PDF of this Article]

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