1985 Volume 18 Issue 3 Pages 319-322
A 36-year-old female hemodialysis patient with chronic renal failure due to chronic glomerulonephritis was admitted to our hospital. Since the predialysis period, she had suffered from severe renal anemia which did not respond to anabolic steroid or protein permeable hemodiafiltration.
In November 1983, her serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) levels rose to 64 and 53 KU respectively, and continued to rise during the next three weeks, when she was admitted. On admission, the tests for hepatitis B surface antigen and hepatitis A antibody were negative, and no elevation of other viral titers was noted. The tests for hepatitis B surface antibody had been consistently positive since 1981. Drug-induced hepatic injury could be ruled out. Based on these findings, she was diagnosed as having non-A, non-B hepatitis induced by a blood transfusion which had been performed in September because of genital bleeding.
Her hepatic enzyme levels increased gradually and reached peak values (SGOT 224KU, SGPT 223KU) four weeks after admission. The levels of these enzymes returned to normal eight weeks later. Her hematocrit value, which had been around 16% before the onset of acute hepatitis, showed a rise associated with the liver damage and reached 30% at the peak of the liver enzyme abnormalities. Then her hematocrit value decreased slowly with the improvement in liver function, and was down to 21% sixteen weeks later. The circulating erythropoietin (Ep) level and reticulocyte count increased with the deterioration of the liver damage, and returned to the initial levels after normalization of the hepatic enzyme.
The clinical course of this patient strongly suggests a relationship between acute hepatitis and improvement in the anemia. The presumed mechanism of the improvement is that hepatic erythropoietic factor (HEF) produced by the liver damage stimulated hepatic Ep production, which increased erythropoiesis in the bone marrow. Furthermore the elimination, by protein permeable hemodiafiltration, of renal inhibitory factor and accumulated uremic substances, which inhibit HEF and erythropoiesis in the bone marrow, may have contributed to the marked improvement in her anemia.
