Rheumatic Nephrosclerosis

T HE occasional development of nephrosclerosis as a late sequel of rheumatic fever has been suggested by Fahr.1 2 But Fahr did not follow up this observation with detailed microscopic examinations, and the question remained unsettled as to the significance of the coarsely granular renal surface, often interrupted by deep depressions (infarcts). The histologic observations reported below revealed that nephrosclerosis in patients with rheumatic cardiac disease is the result of a widespread rheumatic obliterating endarteritis, involving particularly the mediumsized and small renal arteries.3 The term endarteritis rather than arteritis is preferred because the chronic vascular process is limited to the endothelium, in contrast to the acute type of rheumatic vascular disease with involvement of all the coats of the vessel wall.4 Blood vessels of the same size in other organs,8 especially in the brain9 10 and the myocardium, 11,12 may be similarly affected. Rheumatic occlusive vascular lesions were incidentally observed in 1890 by Krehl1' in the myocardium of patients with chronically diseased rheumatic heart valves. These observations were later confirmed by Karsner and Bayless'2 and Gross et al.,7 who described distinctive vascular lesions in active as well as inactive cases of rheumatic fever. Von Glahn and Pappenheimer8 systematically investigated all the peripheral vessels (except in the brain) of patients with rheumatic carditis, and described "specific" vascular lesions in various organs in 10 of 47 such cases. Usually, isolated vessels were affected, but in the kidneys the lesions were widespread. In the