The biopsied kidneys from three patients with hepatitis Be antigen (HBeAg)‐associated nephropathy were observed by light microscopy, immunohistochemistry and electron microscopy. By an indirect technique utilizing horseradish peroxidase‐conjugated antisera, HBeAg was found to be deposited in a diffuse granular fashion along the glomerular capillary wall. No deposition of hepatitis Bs or hepatitis Be antigen was detected. The three cases were diagnosed as HBeAg‐associated nephropathy. Ultrastructurally, there were finely granular electron‐dense deposits in the subendothelial area, basement membrane, mesangial area and subepithelial area of the glomerular tufts. In all three cases, virus‐like particles between 30 and 70 nm in diameter were also found in such areas of the glomerular tufts, and rarely in the glomerular capillary lumen and space of Bowman. They occasionally formed clusters in the phagosomes of mesangial cells. In addition, tubulo‐reticular structures were noted in the cytoplasm of endothelial cells in the glomerular capillaries. The presence of HBeAg both in the serum and in the kidney and of virus‐like particles in the glomerular tufts suggests that HBeAg is causally related to the development of HBeAg‐associated nephropathy.
A 25-year-old man with a history of Kawasaki disease from the age of 7 had acute inferior myocardial infarction. Emergency right coronary arteriogram showed successive coronary aneurysms at the proximal to middle portion of the right coronary artery, and total occlusion at the proximal segment. Intracoronary thrombolysis was performed and the right coronary artery was recanalized. On left coronary arteriography, coronary aneurysms and mild localized stenoses at the inlet and outlet of the aneurysms were found. It was suggested that the myocardial infarction was caused by thrombotic occlusion of coronary aneurysms complicated with Kawasaki disease. (Internal Medicine 31: 774-777, 1992)
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