The term "accelerated" arteriosclerosis was first suggested by Löhlein1 to designate those vascular changes which differentiated the benign from the malignant form of nephrosclerosis. The concept of acceleration of the arteriosclerotic process was later supported by Klemperer and Otani.2 The characteristic arterial alterations which they emphasized consisted of cellular proliferation of the intima of the larger interlobular and arcuate arteries with associated narrowing of the lumen and coexistent necrosis of the arteriolar walls. Since these investigators were also able to demonstrate the usual arteriosclerotic process of elastica lamellation, intimal fibrosis and arteriolar hyalinization, they expressed the opinion that the addition of cellular intimal proliferations and necrotizing lesions evidenced a more rapid, or "accelerated," development of arteriosclerosis. The acute vascular alterations were ascribed to an ischemic mechanism incident to the accelerated arteriosclerotic changes in the medium-sized arteries and were considered to be degenerative rather than inflammatory in nature. It
HORN H, KLEMPERER P, STEINBERG MF. VASCULAR PHASE OF CHRONIC DIFFUSE GLOMERULONEPHRITIS: A CLINICOPATHOLOGIC STUDY. Arch Intern Med (Chic). 1942;70(2):260–283. doi:10.1001/archinte.1942.00200200080005
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