Fumihiko Tamada

An outbreak of fulminant hepatitis B in immunocompromised hemodialysis patients

BackgroundWe aimed to clarify the pathogenesis of an outbreak of fulminant hepatitis B in hemodialysis (HD) patients whose compromised cell-mediated immunity in turn contributed to chronic hepatitis B virus (HBV) carriage.MethodsFive consecutive adult HD patients with acute hepatitis B were evaluated. Viral genotype, mutations, and HBV-DNA levels were studied in relation to viral clearance, liver disease severity, and liver histology by immunostaining.ResultsAll five patients had hepatitis B surface antigen (HBsAg) genotype C, a G-to-A stop codon mutation at nucleotide (nt) 1896 in the precore region, an A-to-T mutation at nt 1762 and an G-to-A mutation at nt 1764 in the basal core promoter. The possible index patient, who suffered from liver cirrhosis, had HBsAg genotype C, anti-hepatitis B envelope (HBe), and these mutations. The level of HBV-DNA declined by about 10 percent per week and no difference in viral kinetics between the patients who died and the survivor was found, irrespective of therapies. The amount of liver cell apoptosis, as assessed by single-stranded DNA, was scarce. The risk of fulminant hepatic failure did not correlate with the preexistent liver histopathological changes. Acute HBV superinfection was associated with hepatitis C virus (HCV) elimination and increased mortality.ConclusionsThis outbreak of fulminant hepatitis B suggests that HD patients can foster highly virulent HBV strains (possibly owing to their compromised immune responses), which may place others at risk of severe, life-threatening acute liver damage and at increased risk of mortality if chronic carriers of HCV should be infected.

The beneficial effect of effective control of anemia on hyperinsulinemia and hypoxemia in a hemodialysis patient with corrected transposition of the great arteries

We report the beneficial effect of control of anemia on hyperinsulinemia and hypoxemia in a hemodialysis patient with corrected transposition of the great arteries. The patient’s hemoglobin (Hb) level of 10.3 g/dl on admission represents good control for hemodialysis (HD) patients, but it was too low for this patient with secondary polycythemia because of a right-to-left shunt. Control of anemia for a 10-month period was followed by a marked increase in Hb level (from 10.3 g/dl to 13.9 g/dl) and in aerobic work capacity, while the fasted insulin level decreased from 36.7 µU/ml to 8.0 µU/ml, without changes in leptin level, body mass index (BMI), fat mass, Kt/V, or protein catabolic rate (PCR). Additionally, hypoxemia was ameliorated, from PO2 33.1 mmHg to PO2 56.2 mmHg, and the hyperdynamic cardiac state was improved. The degree of anemia, together with deteriorating tissue oxygenation, may have predisposed this patient to developing insulin resistance and consequent hyperinsulinemia. The most appropriate target Hb concentration should be tailored for the clinical condition of each individual patient, bearing in mind an insulin-resistance state, especially in hemodialysis patients with hypoxemia. A more complete understanding of what regulates insulin resistance and consequent hyperinsulinemia in endstage renal disease (ESRD) awaits the elucidation of carbohydrate and insulin metabolism.

Deep venous thrombosis, myocardial infarction, and occlusion of vascular access associated with heparin-induced thrombocytopenia in a diabetic hemodialysis patient

We report a patient with diabetic endstage renal disease with an initial platelet count of 17.6 × 104/mm3 who developed type-II heparin-induced thrombocytopenia (HIT) during the induction period of hemodialysis (HD) when unfractionated heparin was used. Because the recognition of the condition and the treatment of this patient with HIT was unsatisfactory, she developed deep venous thrombosis, myocardial infarction, and occlusion of vascular access, at times of platelet counts of 4.1 × 104, 7.7 × 104, and 6.4 × 104/mm3, respectively, with antibodies to heparin/platelet factor 4 complex. Unfortunately, we misjudged in our belief that the thromboembolic events might be associated with an underlying procoagulant state in diabetic nephrotic syndrome, rather than being associated with the clinical picture of HIT. This case report suggests that the clinician must consider HIT in the differential diagnosis for thromboembolic complications during the induction period of HD, because unfractionated heparin is the major anticoagulant used in HD.

Acute renal failure in a case of Waldenstroem's macroglobulinemia

症例は66歳,男性.主訴は全身倦怠感.精査の結果M蛋白を認め,原発性マクログロブリン血症(Waldenstroms macroglobulinemia)と診断.入院後急性腎不全を呈したため,各種血液浄化を施行しつつ化学療法を併用するも不幸の転帰をとった.原発性マクログロブリン血症に急性腎障害を併発する症例は稀であり報告する.

Diabetic end-stage renal failure with autonomic dysfunction and spontaneous hypoglycemia during fasting

Abstract Spontaneous hypoglycemia during fasting was frequently observed in a 53-year old man with diabetic end-stage renal failure. On fasting, despite being managed on dietary therapy, this patient developed hypoglycemia (independent of hemodialysis), at which time he was lethargic. He showed severe autonomic dysfunction for a long period. No significant transient increase in catecholamines was not observed in response to the Schellong test or during the hypoglycemic episodes. During the oral glucose tolerance test (OGTT) and intravenous glucose tolerance test (IVGTT), basal insulin level was not detectable, and insulin response was absent. Glucagon loading test and epinephrine loading test suggested that the glycogen store in the liver was maintained, but that glycogenolysis was impaired. Lack of catecholamine response and diminished glucagon response to hypoglycemia because of autonomic disinnervation may suppress hepatic glycogenolysis and renal gluconeogenesis, thereby resulting in fasting hypoglycemia in pathologic situations such as diabetes mellitus and renal insufficiency.