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Charles F. Stewart, M.D.
JAMA. 1940;114(21):2099-2101. doi:10.1001/jama.1940.62810210002011a.
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In a recent discussion of experimental hypertension Goldblatt1 stated that "during the past year, in a few cases of hypertension without renal arteriosclerosis, severe sclerosis and narrowing of the orifice or lumen of the main renal arteries or the lumen of the larger extrarenal branches, obviously sufficient to cause renal ischemia, have been observed." Leiter2 reported a case of hypertension believed to be due to sclerosis of the main renal arteries (case 2). The patient's blood pressure varied from 240 to 180 systolic and from 160 to 88 diastolic; the kidneys were very small, one weighing 41, the other only 22 Gm. The glomeruli of the left kidney were hyalinized and numerous tubules were atrophied and obstructed. The main renal arterial branches had an extremely thickened, cellular and fibro-elastic intima; the internal elastica was degenerated. The medium and smaller arteries were the site of extensive degeneration of the


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