Epoetin-alpha (α-group) and epoetin-beta (β-group) were administered to regular hemodialysis (RHD) patients. With regard to initial effect in improving anemia, the difference in increase in hematocrit between 13 α-group patients and 12 β-group patients was not significant, nor was there a significant difference in maintenance dose between 37 α-group patients and 19 β-group patients. These studies suggest that epoetin-alpha is equal to epoetin beta in therapeutic efficacy. rEPO was administered to 20 RHD patients for 104 weeks. The mean±SD hematocrit increased from 20.6±1.8 to 27.9±3.2%. Phosphate, blood urea nitrogen, creatinine and potassium did not increase significantly, uric acid was the only exception. The dose of aluminum agents and cation exchange resins, however, did require supplementation. In addition, the dialyzers of two patients had to be exchanged for a larger models because of the increase in blood urea nitrogen. These facts suggest an increase in a variety of parameters. AntiHTLV-1-positive and antiHCV-positive RHD patients were treated with rEPO. The difference in maintenance dose between the positive and negative patients was not significant. This suggests that HTLV-1 and HCV virus infection do not have any influence on the effect of treatment.

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Secondary hyperparathyroidism is a frequent complication in long-term dialysis patients. Measurement of serum parathyroid hormone (PTH) and calcium (Ca) levels is important in assessing the severity of secondary hyperparathyroidism. An immunochemiluminometric assay (Chemilumi-PTH, Ciba Corning Co.) system has become available for intact PTH assay.
Seventy six hemodialysis patients had intact PTH levels of 145.4±228.9pg/ml (M±1SD), significantly higher (p<0.01) than in healthy subjects (n=31, 28.4±10.6). An attempt was made to treat severe secondary hyperparathyroidism by markedly suppressing elevated PTH levels in the blood by administering active vitamin D₃ or by parathyroidectomy.
Treatment of secondary hyperparathyroidism with active vitamin D₃ or parathyroidectomy was evaluated by measuring intact PTH using the Chemilumi-PTH immunoassay.
The results suggest that the Chemilumi-intact PTH assay is useful in assessing secondary hyperparathysoidism in dialysis patients.

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Dialysis hypotension is mainly caused by reduction of plasma volume (PV), that is due to weight loss by ultrafiltration and water shift by osmolar change. Reduction of PV results in both decrease of venous return and cardiac output.
Secretion of hANP is regulated by atrial tension and its half life is within several minutes. We measured hANP to assess whether it could be an indicator of vascular stability in various modes of blood purification.
In this study pre and post serum concentration of hANP with 10l substitution fluid with no removal of body weight were evaluated in six combination of Na (135, 165mEq/l), HCO₃- (35, 60mEq/l) and glucose (0, 250mg/dl). As the methods with body weight reduction, single ultrafiltration (UF), bicarbonate hemodialysis (BiHD) with Na 135 or 145mEq/l, and acetate hemodialysis (AcHD) with Na 135 or 145mEq/l were performed. Fluid removal was 2% of pre-body wight in the first one hour. In HF without body weight reduction, %hANP changed significantly with different Na and glucose concentration. Change with HCO₃- was not significant. Na and glucose work as osmolar active solute to preserve PV. In single UF, BiHD and AcHD, %hANP changed significantly with different Na and buffers (BiHD vs AcHD). With body weight reduction, %hANP were as follows: BiHD (Na 145)>UF>BiHD (Na 135)=AcHD (Na145)>AcHD (Na135). Our date supports preveous reports on vascular stability. hANP could be useful marker to select or develop blood purification with superior vascular stability.

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A significant correlation between the increase of serum erythropoietin levels and the decrease of hematocrit (Ht) was observed in kidney transplant recipients.
Before hemodialysis was restavted, seven patients with chronic rejection (CR) and anemia were treated with recombinant human erythropoietin (r-HuEPO). This was given as an intravenous bolus twice weekly in increasing doses within the range of 30-120IU/kg. Six patients showed increases in hemoglobin concentrations with the simultaneous administration of iron, but one patient did not respond to the rEPO treatment. Examination of this patient's bone marrow revealed purered cell aplasia due to azathioprine.
During treatment, no patients had episodes of hypertension, liver dysfunction or deterioration of renal function. rEPO had no effect on lymphocyte, white blood cell or platelet counts during the treatment with rEPO. With the increase of hematocrit, exercise performance and activity levels improved and all the patients felt better.

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We measured famotidine concentrations in plasma and cerebrospinal fluid (CSF) in two hemodialyzed female patients (75 and 67 years) who developed mental confusion after the administration of this H₂-receptor antagonist at intravenous (i. v.) doses of 40 and 10mg/day, respectively. All measurements were made during convalescent periods following drainage operation for subdural hematoma. We also measured CSF famotidine concentrations in a male patient (3 years) with normal renal function who was diagnosed as having tuberculous meningitis and given famotidine at an i. v. dose of 40mg/day. The CSF concentrations of famotidine measured in the two mentally confused patients were 160 and 249ng/ml and concomitantly measured plasma famotidine concentrations were 419 and 396ng/ml, respectively. Mental status returned to normal in both cases after cessation of the famotidine therapy. In contrast, the CSF famotidine concentrations of the patient with normal renal function were 10 and 12ng/ml on two separate occasions. These results suggest that famotidine may accumulate in the brain to a level causing mental confusion in patients whose clinical courses are complicated not only by an impaired blood brain barrier but also by severe renal insufficiency. Mental status deterioration may be averted if an appropriate reduction of famotidine dosage is undertaken.

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We report a rare case of a patient who developed syndrome malin (SM) during maintenance hemodialysis.
A 42-year-old man, for whom maintenance hemodialysis was being been performed for diabetic nephropathy, was admitted to the hospital because of high fever, nystagums, tremor and hallucinations. On the blood examination, the GOT was 459IU/l, LDH 1, 669IU/l, CPK 529IU/l, aldolase 13.3mU/ml, myoglobin 3, 200ng/ml, and an arterial blood gas examination revealed severe hypoxemia (PO₂ 27.1mmHg, PCO₂ 42.8mmHg). At that time he had been prescribed metoclopramide hydrocloride (30mg/day) orally, which is often used for the control of nausea, for five months. The symptoms of hyperthermia, autonomic instability, extrapyramidal signs and altered consciousness were consistent with a diagnosis of syndrome malin.
Accordingly we withdrew the metoclopramide and performed extraemoialysis therapy. The symptoms then rapidly improved and the patient made a rapid recovery.

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