Pathological changes in the cerebral medullary arteries of five autopsy cases of malignant nephrosclerosis: observation by morphometry and reconstruction of serial sections.
Hypertension (HT) is a serious risk factor of not only cerebral infarction and bleeding, but also Binswanger's encephalopathy (BE). In BE especially, severe stiffening of the cerebral medullary arteries because of hypertensive changes with loss of medial smooth muscle cells (SMC) occurs, which induces diffuse atrophy of the cerebral white matter. But, it is not yet ascertained whether HT is particularly severe in BE. Therefore, a spectrum of the pathological changes of the cerebral arteries were investigated by reconstruction of serial sections and morphometry of the medial thickness in five autopsied patients with malignant nephrosclerosis (MN) of exacerbated form. Each presented clinically acute progression of long-standing HT at the terminal stage and pathologically typical renal changes. The heartweight was 380-900 g. Morphometry of the medial thickness of the arachnoid arteries presented significant medial hypertrophy in four cases of MN, but in the medullary arteries it presented in only two cases with marked cardiomegaly of 700 g and 900 g. In four cases of MN, only a few medullary arteries showed slight pathological changes. However, in another case with cardiomegaly of 900 g, all 10 medullary arteries showed multiple segments of atheroma, medial SMC loss, and prominent dilatation; edematous concentric intimal fibrosis with luminal obstruction and atrophy of the white matter were absent. In conclusion, only one case of MN showing marked cardiomegaly of 900 g presented severe pathological changes of the cerebral medullary arteries comparable with those of BE, although other MN-cases showing severe cardiac hypertrophy presented only trivial arterial changes. Therefore, the cerebral medullary artery seems to be protected from HT, yet it is involved in a case of severe and long-standing HT inducing an extreme cardiomegaly.
Okeda
Riki
R
Department of Neuropathology, Medical Research Institute, Tokyo Medical & Dental University, Tokyo, Japan.
D000328:Adult; D001099:Arachnoid / Q000098:blood supply*; D001158:Arteries / Q000473:pathology*; D006332:Cardiomegaly / Q000209:etiology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications*; D008297:Male; D008526:Medulla Oblongata / Q000098:blood supply*; D008875:Middle Aged; D009400:Nephrosclerosis / Q000209:etiology / Q000473:pathology*; D017540:Tunica Media / Q000473:pathology