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November 13, 1943


Author Affiliations


Professor and Head, Department of Physiology, Chicago Colleges, University of Illinois.

JAMA. 1943;123(11):720. doi:10.1001/jama.1943.02840460054021

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To the Editor:—  In The Journal, October 2, page 277, Weiss and Chasis rightfully infer from the failure of the removal of a chronic atrophic pyelonephritic kidney to lower the blood pressure of a patient with hypertension that the diseased kidney probably was not causally related to the hypertension. From the fact that the other kidney showed normal blood flow, glomerular filtration rate and maximal tubular excretory capacity, however, they conclude that the remaining kidney was not diseased or ischemic and therefore not responsible for the hypertension. That the remaining kidney was not ischemic is obvious, but that it "cannot be indicted for this failure" [of the nephrectomy to reduce the blood pressure in the patient] is not necessarily true.The mechanism whereby constriction of the renal artery produces hypertension in experimental animals is still unsettled. Although a reduction in pulse pressure may be involved (Kohlstaedt, K. G., and Page,

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