PROLIFERATIVE endarteritis and arteriolar necrosis are known to be the classical vascular lesions of malignant nephrosclerosis (Fahr, 19 19; Klemperer and Otani, 1931; Kimmelstiel and Wilson, 1936; Ellis, 1938; Heptinstall, 1953), but the full range of the arteriolonecrotic lesions has not been clearly defined in the literature and doubts still remain about the relationship between the arteriolar necrosis and the proliferative endarteritis.

Arteriolar spasm is generally believed to be the cause of arteriolar necrosis in malignant hypertension. Injection of such vasoconstrictive drugs as vasopressin (Byrom, 1937) and adrenaline (Penner and Bernheim, 1940) is known to produce vascular necrosis, and Byrom (1954) has directly visualised intense and often obliterative spasm of the small cerebral arteries in experimental acute hypertensive encephalopathy, with subsequent histological demonstration of focal arterial necroses and cerebral micro-infarcts. Doubts about the pathogenesis of arteriolar necrosis have, however, been raised by Kincaid-Smith, McMichael and Murphy (1958) and reiterated by Heptinstall (1966). Kincaid-Smith et aE. believed that the most characteristic vascular change in malignant hypertension was proliferative endarteritis of the interlobular arteries, and suggested that some new and unknown factor might be implicated in addition to a high level of blood pressure. They pointed out that arteriolar necrotic changes could be intense in vessels distal to narrowed interlobular arteries and stated that, if narrowing reduces pressure in the vessels beyond, high pressure could hardly be responsible for the necrosis of such “protected” vessels.