Recent development of hematopoietic stem cell transplantation (HSCT) has remarkably contributed to improvement of the quality and life span of patients. However, acute renal failure (ARF), which is considered to occur frequently after HSCT, is often critical and most relevant to survival of patients. We attempted to examine the clinical characteristics of ARF in patients who were treated with allogeneic HSCT, using our own database that had been accumulated from 1998 to 2006. A retrospective analysis of 402 adult patients (239 males and 163 females) receiving transplants at Komagome Hospital was undertaken. Mean patient age was 39.9±12.5 years. ARF was defined as serum creatinine (Cr) elevation more than 1.2 mg/dL or two-fold rise in serum Cr levels. Incidence of ARF was 8.9% (36 out of 402 patients) and mortality rate of ARF patients was 52.8% (19 out of 36 patients). Mean age of ARF patients was 47.4±9.25 years, which was significantly higher than that of all HSCT patients. ARF occurred 17±14.7 days after HSCT. It was very difficult to determine a specific cause of ARF because most patients had coexisting diseases, such as drug-induced tubulo-interstitial nephritis, infections including sepsis, and acute graft versus host disease. Advanced age and high serum Cr levels at the time of HSCT were relevant to the mortality of ARF patients. Dialysis treatment was required in 9 ARF patients (9 of 36 patients : 25.0%) all of whom concomitantly developed several organ failures including heart, lung, and liver. Therefore, their mortality rate was quite high (89%). In conclusion, the incidence of ARF after HSCT was approximately 9% and its mortality rate was 52.8%. Patients who developed serious multiple organ failure required dialysis therapy and their mortality rate was extremely high.

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Bacterial numbers during each of 5 steps in the production process of RO water, which dialysis fluid was made from, were measured using fluorescent staining methods (DAPI and 6CFDA staining, and microcolony methods). And measured values were compared with those obtained by conventional methods (existing culture method and measurement of endotoxin activity). According to the results of the comparison, we confirmed that bacterial number in the production process of RO water was not measured precisely by the existing culture methods and combination with fluorescent staining methods was effective for monitoring, as indicated in related reports. As a result of the measurements of the bacterial number at these 5 stages using various methods, we confirmed that the bacterial number required attention at these points from tap water to RO tank in order to ensure the safety of dialysis fluid.

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A 63 year-old Japanese man on long-term hemodialysis therapy (for 25 years) developed fever, erythropoietin-resistant anemia, and elevated C-reactive protein (CRP) in March 2005. Empiric antibiotic therapy failed to improve the clinical symptoms, and he was admitted to our hospital for fever of unknown origin (FUO) in June 2005. On admission, he showed painless swelling of the left shoulder joint. Both bone scintigraphy and galium scintigraphy demonstrated strong uptake to the left shoulder joint. A synovial membrane biopsy of the left shoulder joint demonstrated positive β₂ microglobulin (β₂-MG) immunostaining, and he was diagnosed as having arthropathy due to dialysis-related amyloidosis (DRA). He received β₂-MG adsorption therapy using a β₂-MG adsorption column (Lixelle^®) and corticosteroid therapy (prednisolone 10 mg/day). Thereafter, his symptoms and laboratory data such as anemia and elevated CRP dramatically improved. The main causes of FUO are generally considered due to malignancy, chronic infection, or collagen diseases. However, in cases of FUO on long-term hemodialysis therapy, DRA should also be examined as a possible cause of FUO.

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A 55-year-old man who had been undergoing hemodialysis at our hospital with diabetes mellitus and alcohol abuse was admitted with consciousness loss. Blood sugar on initial examination was 1,086 mg/dL, and computed tomography and magnetic resonance imaging (MRI) did not demonstrate any abnormalities. These findings indicated a diagnosis of hyperglycemic coma. Although treatment with insulin was immediately started, his consciousness level was not improved. MRI performed after eight weeks demonstrated hyperintense lesions in the bilateral basal ganglia on T1-weighted images. Two and half months after his admission, he suddenly died and the autopsy findings exhibited ischemic change in the bilateral basal ganglia. Recently, cases of hyperintense changes in basal ganglia on T1-weighted MRI have been reported in hyperglycemic diabetic patients with hemichorea-hemiballism. These cases were not associated with long-standing disturbance of consciousness, and the prognosis was excellent. The clinical course in our case may have been affected by alcohol abuse, renal anemia and hemodialysis, added to hyperglycemia.

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We report a case of heparin-induced thrombocytopenia (HIT) complicated by anaphylaxis in a patient undergoing chronic hemodialysis. A 58-year-old man with polycystic kidney disease had received maintenance hemodialysis since 2001 using heparin without any complications. On Jan. 11, 2006, he had sweating, dyspnea and abdominal pain immediately after initiating hemodialysis. Since his arterial pressure and pO₂ was decreased, hemodialysis was discontinued. Hematology test showed decreased platelet count from 36.8×10⁴/mm³ to 11.4×10⁴/mm³. There was blood coagulation in both arterial and venous chambers of circuit. Similar episode occurred when low-molecular heparin but not nafamostat mesilate was used as an anticoagulant during hemodialysis. HIT was highly suspected from these clinical manifestations. However, Anti-PF4/heparin antibodies were not detected and heparin-induced platelet activation assay was negative. Regarding the heparin allergy, the open patch test with heparin was positive. We diagnosed with HIT complicated with anaphylaxis induced by heparin on the basis of clinical symptoms. This is a rare case of HIT since it suddenly develops with anaphylaxis after long term use of heparin without the detection of HIT antibodies.

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