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AMA Arch Surg. 1951;63(2):272-278. doi:10.1001/archsurg.1951.01250040276017.
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HYPERTENSION in some instances has been shown by clinical and experimental studies to result from various renal lesions or diseases. Since the classical observations of Bright1 in 1836 on this subject, a great many investigators have added their evidence incriminating the kidney as the sole factor responsible for hyperpiesis under certain conditions or diseases of this organ.2 Among this group of diseases are polycystic kidney, chronic pyelonephritis, nephrosclerosis, glomerulonephritis, and conditions producing prolonged urinary obstruction. Periarteritis nodosa involving the renal arteries, amyloidosis of the kidney, mercury poisoning, renal hypoplasia, and Wilms's tumor in children have been reported as playing an etiologic role in hypertension.2h

Many experiments were carried out by Hartman and his colleagues,2b Cash,3 Bell and Pedersen,4 Janeway,5 and others in which they showed that destruction and changes in the renal parenchyma either from direct attack on the kidney tissue or from


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