Abstract
Arterial changes observed in the grafted kidney were studied from view point of the endothelial injury theory of atherosclerosis. Specimens were obtained by needle or open biopsy of transplanted kidneys from 15 patients with irreversible acute rejection, 6 from reversible acute rejection and 11 from chronic rejection.
Endothelial cells of the interlobular arteries were swollen, rounded and rather prominent, and desquamated at the early phase of the acute rejection as shown in Fig. 1. Denudation of the intima caused intraarterial coagulation and cortical necrosis in the patients with irreversible rejection. Fibrinolytic activities of the endothelium of the arteries and glomeruli examined with Todd's method were completely diminished in acute phase of rejection. These findings may indicate that the initial events of the arterial changes in the grafted kidney are endothelial injury by immunological processes.
Following changes after endothelial injury were appearance of foam cells in the intima (see Fig. 2). These foam cells were observed also in the capillary tuft of glomeruls as shown in Fig. 3. Electron microscopic observations revealed lipid droplets and cholesterol crystals in the cytoplasma of the cells as shown in Fig. 4. The foam cells were substituted with intimal and medial fibrosis. Fibrosis narrowed the lumina of the arteries in chronic phase of rejection (see Fig. 5).
Since several studies have reported that atherosclerosis is common cause of morbidity and mortality, and prevalence of hyperlipidemia in renal transplant patients, serum lipid alterations during the course of reversible rejection were studied. HDL cholesterol was significantly decreased at acute rejection as. compared that of prerejection or recovery phase. A tendency of hyperlipidemia was also observed in chronic phase of rejection (see Fig. 6).
From findings of the arterial lesion in the transplanted kidney, it may conclude that immunological injury of the endothelium induces enhanced permeability of the vascular wall with accumulation of foam cells and subsequently causes intimal and medial fibrosis. To resolve influences of hyperlipidemia on arterial lesions, further studies are required. Anyway, the arterial lesions in the transplanted kidney serves important informations in respect of immunological genesis of atherosclerosis.
