In hemodialysis therapy, blood-material contact during extracorporeal circulation can cause various biological reactions. Intradialytic activation of leukocytes is one of the major causes of hemodialysis-associated complications. Platelets and coagulation system are also activated by blood-membrane contact. The activation of platelets and coagulation system results in platelet adhesion on the dialyzer membrane, a release of growth and activating factors, platelet aggregation and consequently clotting in the extracorporeal circuit. Such reactions can play an important role not only in dialysis-related side-effects, but also various complications in patients on hemodialysis. We report two cases of severe thrombocytopenia developed by maintenance hemodialysis. Significant decreases in the platelet count were observed and considered a dialysis-related complication. The platelet counts decreased after we changed their dialyzers to FPX^®(Fresenius Medical Care Japan, Tokyo, Japan), a novel high-flux polysulfone dialyzer membrane. The platelet counts were improved to the normal range after we changed these dialyzers to different polysulfone membranes. The medications were not changed before or after the onset of thrombocytopenia. Heparin induced thrombocytopenia (HIT) and disseminated intravascular coagulation (DIC) were ruled out. Activation coagulating time was also evaluated. Although FPX^® is one of the most efficient and clinically well-tolerated membrane polymers used for hemodialysis treatment, our findings suggest that FPX^® may cause severe thrombocytopenia in some patients.

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The patient is a 56-year-old male undergoing hemodialysis since 1993. He was admitted to our hospital for the evaluation of erythrocytosis in 1997. His serum erythropoietin concentration was high. After some diagnostic investigations, the main causes of erythrocytosis were evaluated as sleep apnea syndrome, smoking, and hypotension during hemodialysis. Since sleep apnea syndrome had already been treated by otorhinological surgery, he was only prescribed weight control by dietary restriction and it was temporarily effective for controlling erythrocytosis. The evaluation of sleep apnea syndrome by apnomonitor was repeated in 2003, and the patient was classified as having severe disease. He, however, was again prescribed only weight control without continuous positive airway pressure (CPAP) therapy, because weight control had been effective. The patient was subsequently involved in a motor vehicle crash due to excessive daytime sleepiness. In this case, we should have initiated CPAP therapy earlier.

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Heparin-induced thrombocytopenia (HIT) is a relatively common complication of heparin treatment among the patients who are newly treated by hemodialysis. We herein describe an 81-year-old woman with polycythemia vera (PV) who developed HIT associated with respiratory failure. She developed uremia due to diabetic nephropathy and hemodialysis was therefore initiated. Ten days after the first hemodialysis session, an arteriovenous fistula was surgically created to provide permanent access to the blood stream. Several minutes after the intravenous infusion of unfractionated heparin during surgery, the patient developed chest pain and became tachypenic. Thereafter, diagnostic computed tomography demonstrated the presence of thrombus, which had formed around the catheter for hemodialysis and also a right kidney infarction. However, there were no signs of any pulmonary embolism, and the presence of platelet-activating antibodies that recognize the complexes of platelet factor 4 and heparin was serologically confirmed. We therefore discontinued heparin and initiated the administration of argatroban followed by the normalization of the depleted platelet count, and the patient's respiratory symptoms finally subsided. We attributed the sustained respiratory symptoms observed in our patient to a pseudopulmonary embolism that might have resulted from a microembolism of pulmonary capillaries. We must therefore always bear in mind that the development of respiratory symptoms may be associated with the onset of HIT in patients treated with heparin. In our patient, the role that PV may have played in the clinical course of HIT remains to be elucidated. However, the identification of PV among patients with end stage renal failure may facilitate the diagnosis of thrombotic disorders including HIT, since the combination of HIT and PV is not so exceptionally rare in clinical settings.

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We report a 61-year-old man on chronic hemodialysis for 10 years who developed pheochromocytoma of the urinary bladder and left renal cell carcinoma. He was admitted with no complaint. Abdominal computed tomography scans demonstrated left renal tumor and bladder tumor. He was admitted for further examination. Contrast-enhanced computed tomography scan showed solid, posterior renal cell carcinoma. Pelvic magnetic resonance imaging demonstrated invasive tumor on the right side of the urinary bladder. Two surgical procedures were then simultaneously carried out to achieve partial cystectomy and radical nephrectomy under general anesthesia. Pathological examination confirmed two distinct primary tumors. The renal tumor was confirmed to be clear cell carcinoma. The bladder tumor was confirmed to be pheochromocytoma of the urinary bladder. In patients on hemodialysis, determinations by urinary examination are impossible because such individuals are usually anuric. Pheochromocytoma of the urinary bladder in hemodialysis patients is very rare. Only 5 cases have been reported previously. We recommend that hemodialysis patients undergo scheduled abdominal CT scans and urine cytology because of the high risk of urinary tract malignancy.

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