In primary arterial hypertension the essential renal lesion is nephrosclerosis. In most cases, the nephrosclerosis is in itself benign. The chronic hypertension terminates in cardiac insufficiency, in a cerebrovascular accident, in a coronary accident or through some incidental cause. In the remaining cases, the nephrosclerosis itself is the malignant, lethal factor, and the hypertensive state is closed by uremia.
In most cases the clinical and morphologic distinction between benign and malignant nephrosclerosis is sharp. The group of chronic hypertensions that ends through some factor other than renal insufficiency almost always presents the well defined histologic picture of simple renal arteriosclerosis. The group that ends in uremia is usually associated with a marked and abrupt, but just as well defined, change in the histologic picture. Transitions are scanty, and so striking are the morphologic differences that in their original presentation of the subject, Volhard and Fahr1 postulated the addition of
SHAPIRO PF. MALIGNANT NEPHROSCLEROSIS: PATHOGENESIS. Arch Intern Med (Chic). 1931;48(2):199–233. doi:10.1001/archinte.1931.00150020030003
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