Improvement of Anemia Associated with Constrictive Pericarditis in a Hemodialised Patient

Chikashi Kitoh, Division of Nephrology, Fukui Prefectural Hospital, Yotsui 2-8-1, Fukui City (Japan) Dear Sir, We read with great interest Brunois’s report on the relationship between acute hepatitis and erythropoiesis in chronically hemodialysed patients [Nephron 28: 152–153 (1981)]. We observed the same relationship. Furthermore, we found that incomprehensible erythropoiesis seen on rare occasions exists. We here report on a patient whose anemia recovered spontaneously during the end stage of uremic constrictive pericarditis. The important finding concerning this case is that reticulocytosis with erythropoiesis was not recognized in a period of acute hepatitis but during liver congestion. Observations similar to ours have not been found in the past literature. This erythropoiesis could impossibly be explained by means of the known mechanism, such as erythropoietin induced by viral hepatitis. As the pathogenesis of anemia in hemodialyzed patients remains uncertain, we would like to report this rare phenomenon which might give some suggestions on the mechanism of erythropoiesis in chronic renal failure. Case Report In March 1980, a 44-year-old man was admitted to our hospital because of fever. For 2 years, he had been receiving hemodialysis treatment (12 h a week using a coil dialyzer) against diabetic nephro-pathy. Physical examination discolsed a temperature of 39 °C and a blood pressure of 150/94 mm Hg. The other objective findings were unremarkable. Laboratory data on admission were as follows: WBC count 14,500/mm3, RBC count 208 × 104/mm3, hemoglobin 6.2 g/dl, reticulocyte count 1.4%, ESR 150 mm/h, BUN 98 mg/dl, creatinine 12.8 mg/dl, SGOT 10 mU/ml, SGPT 14 mU/ml, LDH 160 m/U/ml and FBS 138 mg/dl. Chest roentgenogram and ECG on admission showed no specific findings. Although we closely examined the cause of the patient’s fever, no particular findings were detected. 2 months after administration of antibiotics the fever was under control. By June 1980, however, hepatomegaly (2–3 fb below right costal margin) and refractory hypotension began to appear and in August ECG findings supported constrictive pericarditis. From September until the patient’s death, heart failure progressed rapidly and at the same time the reticulocyte count increased (0.8> 15.0%) and anemia spontaneously improved (RBC count 234 × 104→366 × 104/mm3, hemoglobin: 7.0→10.8 g/dl). He was never subject to blood transfusion nor to administration of an anabolic steroid. Hepatitis B surface antigen was constantly negative and significant hypoxemia was not observed in his clinical course, except during his last 2 days of life. The schedule of hemodialysis treatment was not changed during this time. Liver function studies carried out each month were constantly within normal limits. At autopsy it was found that the heart was encased by a thick, leathery pericardium measuring 6–8 mm. The parietal and visceral layers were firm,