Macrophage colony stimulating factor (MCSF) is a cytokine secreted by many types of cells, such as monocytes/macrophages, bone marrow stroma cells, endothelial cells and lymphocytes. It was previously reported that MCSF decreases serum total cholesterol, and that in animal experiments MCSF has an antiarteriosclerotic action. However, there are few reports on the relationship between lipid metabolism or arteriosclerosis and MCSF in hemodialysis patients. We investigated the relationships between serum MCSF and serum lipid or aortic calcification index (ACI) in 30 hemodialysis patients. Serum levels of MCSF in hemodialysis patients varied from 1.1 to 3.1ng/ml, 2.0±0.3 on average. MCSF levels were significantly higher in hemodialysis patients than in healthy volunteers (1.6±0.4 on average). A positive correlation was observed between serum MCSF level and ACI (r=0.48, p<0.01). Serum MCSF levels were negatively correlated with total cholesterol (TC) (r=-0.44, p=0.015) and high density lipoprotein-cholesterol (HDL-C) (r=-0.66, p<0.01). From our findings, it appears likely that MCSF decreases serum cholesterol and that MCSF plays a role in the mechanism of arteriosclerosis formation in hemodialysis patients.

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It has recently been shown that hepatitis C virus (HCV) infection is closely associated with mixed type cryoglobulinemia. It is also known that HCV infection is rampant among chronic hemodialysis patients. We studied 531 renal failure patients on chronic hemodialysis including 170 with positive HCV antibodies for cryoglobulinemia, and the frequency of cryoglobulinemia was compared with control groups consisting of 242 chronic hepatitis C patients without renal failure, and 183 healthy adults. Cryoglobulinemia was present in 30.6% of dialysis patients with HCV infection, 10.8% of dialysis patients without HCV infection, 29.8% of patients with chronic hepatitis C, and 0% of healthy adults. Among 30 new renal failure patients who had started on dialysis within the past 6 months, 4 were positive for HCV antibodies, and one (25%) had cryoglobulinemia; of the 26 HCV-negative patients, 4 (15%) were cryoglobulinemic. Cryocrit values among dialysis patients were much lower than those of the control and other reports. Patients with cryoglobulinemia were generally younger than negative patients. There was no correlation between cryoglobulinemia and past blood transfusion or length of dialysis. Thus, it seems that renal failure patients with HCV infection develop cryoglobulinemia less commonly compared with nondialysis patients, and that they develop cryoglobulinemia at relatively younger ages. There was no indication that the presence of cryoglobulin in serum adversely affects the liver nor increases the serum virus load in the HCV-infected dialysis patients. Patients with renal failure may be less capable of producing cryoglobulin than healthy individuals.

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We report two patients with C1-inhibitor deficiency on hemodialysis therapy who experienced frequent occlusion of their blood access. One patient, a 44-year-old woman with hereditary angioedema, has been on hemodialysis for lupus nephritis. The other patient, a 54-year-old man, was started on hemodialysis therapy for diabetic nephropathy. There were no signs of angbedema or complement abnormalities in other members of his family, so his angioedema seemed to be attributable to the acquired form of C1-inhibitor deficiency. We examined the influence of angioedema attacks on the complement, coagulation, fibrinolysis and kinin systems. The predialysis levels of thrombin-antithrombin III (TAT), plasmin-α2 plasmin inhibitor complex (PIC), and fibrinogen of 29 patients on hemodialysis therapy without vascular complications were almost all within the normal range. TAT, PIC and bradykinin levels of both patients were increased during the attacks that led to occlution of blood access. In 1 patient, though the levels increased during attacks, blood access complications did not follow. These findings suggest that the coagulation and kinin systems were affected during the attacks of angioedema, leading to acute occlusion of blood access.

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We investigated the clinical characteristics of hypoparathyroidism in inpatients on chronic hemodialysis. The subjects were 45 patients without parathyroidectomy at Kyoritsu Jyuzen Hospital, including 20 men and 25 women, aged 70±10 years (mean±standard deviation) (range; 45-85). The duration of hemodialysis was 40±44 months (range; 2-225), and the admission period was 17±15 months (range; 1-52). Twenty patients were in bed for over 50% of the day. The patients were divided into 3 groups according to the serum level of intact-PTH; 1) an absolute hypoparathyroidism (A-Hypo) group (<60pg/ml, n=32), 2) a relative hypoparathyroidism (R-Hypo) group (60-160pg/ml, n=12), and 3) a normal (Norm) group (160-360pg/ml, n=1). Forty-four patients (97.8%) had hypoparathyroidism. When the serum intact-PTH level was compared with the type of original renal disease, diabetic nephropathy showed the lowest level followed by chronic glomerulonephritis, renal sclerosis and others. Although there were no differences in age, gender, original renal disease and duration of hemodialysis between the A-Hypo and R-Hypo groups, serum Ca was higher (p<0.01), while serum Al and ALP (p<0.05) were lower in the A-Hypo group than in the R-Hypo group. There was no difference in the total bone mineral density measured by DXA, the dose of active vitamin D and the dose of calcium carbonate. Bone metabolic markers showed low levels in all the patients with hypoparathyroidism, but the A-Hypo group demonstrated lower levels than the R-Hypo group. However, there was no significant differences in these parameters except for serum ALP. We studied the relationship between the clinical profiles and the occurrence of A-Hypo or R-Hypo. A poor performance status was significantly related to A-Hypo by Fisher's exact test (p=0.039). The patients with poor perfomance status tended to become immobile and immobilized patients can easily develop hypercalcemia. Hypercalcemia then leads to hypoparathyroidism because it suppresses PTH secretion. However, the occurrence of hypoparathyroidism in inpatients on chronic hemodialysis is a new and important problem.

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The pharmacokinetics of sparfloxacin (SPFX) were investigated in continuous ambulatory peritoneal dialysis (CAPD) patients. Doses of 200mg of SPFX were orally administered to 8 CAPD patients after breakfast, and the time-courses of the drug concentration in the plasma, dialysate and urine were monitored by high-performance liquid chromatography. The pharmacokonetic parameters obtained in this study were as follows: Cmax, Tmax, T_1/2 and AUC O-∞ were 1.24μg/ml, 5.5hr, 34.0hr and 46.4μg·hr/ml, respectively. The Cmax and Tmax of CAPD patients were not significantly different from those of normal volunteers. However, the T_1/2 and AUC O-∞ of the patients, especially who were elderly or had heart disease, were markedly prolonged or increased compared to those of normal volunteers. The recovery rate in dialysate was only 1% within the first 24hr, while the urinary recovery rate in 3 patients was also only 1% within the first 48hr, suggesting that peritoneal and urinary loss for this drug were minimal.
In conclusion, although effective and safe concentrations of the drugs were obtained when 200mg of SPFX was orally administered to CAPD patients, its excretion was significantly prolonged. Therefore, drug monitoring is recommended for safe and effective treatment, if administered for a long period.

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We evaluated uremic symptoms and clinical parameters in end-stage renal disease patients started on dialysis therapy at the Yamanashi Medical University Hospital over 5 years from 1992 to 1996. The primary diseases of these patients were diabetic nephropathy (DN) (n=44), chronic glomerulonephritis (n=27), polycystic kidney (n=2) and other chronic renal diseases (n=6). The patients with DN were compared to these with nondiabetic end-stage renal disease (NDESRD). The criteria for instituting dialysis therapy, recommended by an ad hoc committee sponsered by Japanese Ministry of Health and Welfare, were used for this study. Serum levels of urea nitrogen were significantly lower in patients with DN than NDESRD. The symptoms of fluid overload and neuropathy were more frequently observed in DN. The proportion of patients whose serum levels of creatinine were under 8mg/dl was higher in DN. All the diabetic patients had met the recommended criteria. On the basis of these results, clinicians should decide to start dialysis therapy for the patients with DN mainly by evaluating clinical findings.

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We developed a software application for the management of patient information using a commercially available database software, 4th Dimension Server manufactured by ACI Company. To share patient information with other clients, we adopted an intra-hospital Local Area Network (LAN) system, which consists of Macintosh machines as client personal computers and an Ethernet system for connecting with guest client computers.
To handle the application easily, we elected to use a visualized menu-driven method as the selection of operation menu, which was shown as menu bars on the screen. In addition, we used a pop-up menu more frequently to save labor in inputting patient information.
Our application has many functions: 1) hemodialysis (HD) schedule management system, 2) patient information management system, 3) automatic output of various printed matters such as lists of patients' treatment schedules and dialysis record sheets with intradialysis administration of drugs, 4) automatic preparation of patients' referral letters, 5) statistic analysis function of our patients' data, especially for the annual registration to the Japanese Society for Dialysis Therapy, and 6) inventory management system in our clinics.
In conclusion, we easily accomplished the centralization of patients' information and data using the intra-hospital LAN system and could develop a software application at a low price by modification of a commercially available database software. Our application proved to be easy to operate and to maintain.

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We report a case of atrioventricular and intraventricular conduction disturbance induced by antiarrhythmic agent in a patient with chronic hemodialysis after CABG. A 57-year-old man, who had undergone hemodialysis 3 times per week, suffered from unstable angina pectoris. An emergent aortocoronary bypass grafting was done and he recovered without any perioperative complications, excepting for frequent ventricular premature contractions. We administered 150mg of pilsicainide hydrochloride per day because of resistance to prior treatments with mexilletine and disopyramide, and arrhythma disappeared immediately. Five days later, he suddenly developed conduction disturbance on ECG, being attributable to pilsicainide hydrochloride. Direct hemoperfusion in association with hemodialysis was applied. It took 14 days for normalization of conduction disturbance, when the drug concentration in plasma decreased from 4.74μg/ml to 0.38μg/ml. The average removal rates of the drug by direct hemoperfusion and hemodialysis were 13.7% and 23.9%, respectively, and the clearances at 120 minutes were 37.6ml/min and 84.1ml/min, respectively. The removed amount of the drug by direct hemoper-fusion and hemodialysis might be the amount in the circulatory blood. The simultaneous blood purification technique with hemodialysis and perfusion was useful for removal of the drug.

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