Since phosphorus retention in hemodialysis (HD) patients is known to be an important factor in the development of secondary hyperparathyroidism and renal osteodystrophy, phosphate binders have been needed for the control of serum phosphate levels (P). However, the calcium-containing phosphate binders that have been used widely can cause a rise in serum calcium levels and cause secondary hypoparathyroidism. We have recently experienced decreases in P after the administration of niceritrol (NT), a prodrug of nicotinic acid, for the treatment of low HDL-cholesteremia (HDL-C) in HD patients. The aim of the present study was to assess the mechanism of the P-lowering effect of NT in comparison with nicomol (NC), another prodrug of nicotinic acid. NT (750 mg/day) or NC (600 mg/day) was given orally to 10 or 14HD patients respectively. Blood samples were collected before the first dialysis of each week for the determination of serum urea nitrogen (UN), Cr, Ca, P, total cholesterol (TC), triglyceride (TG) and HDL-C. Serum nicotinic acid concentration (NAC) by gas chromatograph mass-spectrometry method was determined before, 4 weeks and 8 weeks after the administration of these drugs. After NT administration, P was decreased from 6.2±0.4 mg/dl to 5.1 ±0.4 mg/dl (1st week, p 0.001, Mean ±SE) and 4.5±0.3 mg/dl (2nd weeks, p<0.001) with no change in UN, Cr or Ca levels ; these significant decreases in P lasted for 8 weeks. NAC increased significantly after NT administration from 25.5±1.3 ng/ml to 549.8± 102.2 ng/ml (4 weeks, p < 0.01) and 431.7±51.4 ng/ml (8 weeks, p < 0.01). HDL-C also increased (33.6±4.0 mg/dl vs 42.7±4.6 mg/dl, p<0.05), but TC and TG did not change. In contrast, no significant changes were observed in P, NAC and HDL-C after NC administration. These discrepancies could be ascribed to the differencies in serum NAC levels. These data suggest that NT could be useful for the control of P in HD patients. However further studies are needed to confirm the mechanism of the P-lowering effect of NT.

抄録全体を表示

Hyperhomocysteinemia has been recognized as one of the risk factors for atherosclerosis and premature vascular disease. Patients on dialysis and end-stage renal disease also manifest high plasma concentrations of homocysteine. We performed this study to evaluate the effects of folic acid supplementa tion on hyperhomocysteinemia in CAPD patients. Twenty-three CAPD patients (8 males, 15 females, 49.1±14.2-years-old) dialyzed for 22.7±19.2 months participated in the study. Daily 5-mg doses of folic acid supplementation for 4 weeks significantly reduced plasma concentrations of total homocysteine (p < 0.01) and serine (p < 0.001) . This observation suggests that the reduction of plasma concentrations of total homocysteine results from activation of homocysteine remethylation to methionine. On the other hand, folic acid supplementation also revealed significant correlations between changes in serum concentrations of both dihomo-γ-linolenic acid and arachidonic acid and changes in plasma concentrations of total homocysteine (r = -0.517, p<0.05, r = -0.451, p<0.05, respectively) . In addition, serum concentrations of both dihomo-γ-linolenic acid and arachidonic acid in 11 CAPD patients with hyperhomocysteinemia (≥ 35 micromol/litter) were significantly lower than those of 12 CAPD patients with normohomocys teinemia ( < 35 micromol/litter) (p < 0.05, p < 0.05, respectively). Serum concentrations of both dihomo-γ-linolenic acid and arachidonic acid in CAPD patients with hyperhomocysteinemia increased significantly (p<0.01, p<0.05, respectively) and reached similar levels of CAPD patients with normohomocys teinemia, while plasma concentrations of total homocysteine decreased after folic acid supplementation. These findings suggest that correction of hyperhomocysteinemia in patients on dialysis produces an increase in unsaturated fatt acids.

抄録全体を表示

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40°C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission : his serum glutamic oxaloacetic transaminase was 3, 203 IU/ml, serum glutamic pyruvic transaminase was 3, 825IU/ml, lactic dehydogenase was 2, 840IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19 day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody, HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. How-ever, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.

抄録全体を表示

A 41-year-old woman took an overdose of sedatives on the, and remained a sleep in the straight sitting position until she was woken up on the 15th. The next day she consulted our hospital complaining of pain and swelling of her right leg. X-ray examination with contrast medium revealed obstruction of the deep vein of her right leg by a thrombus. On, her serum urea nitrogen was 75.9 mg/dl and creatinine was 5.4 mg/dl accompanied by oliguria. The myoglobin value was 27, 000ng/ml in serum and 88, 000 ng/ml in urine. She was diagnosed as acute renal failure caused by rhabdomyolysis and hemodialysis therapy was started. She was released from hemodialysis on the . The swelling of her right leg disappeared at the end of February. However, her right foot was affected paralysis of the fibular nerve. Electromyogram of her right anterotibial muscle and the test of conduction velocity of right tibial nerve revealed that the neurological disturbance of her right leg was caused by thrombosis of the deep vein. Generally speaking, the swelling of the extremities resulting from rhabdomyolysis caused by crush syndrome is due to a massive shift of body-fluid into the crushed muscles. We believe that when the extremities are compressed (and/or crushed) for a long time, venous thrombosis of the extremities occurs due to compression, there by causing swelling of the compressed extremities, as in this case.

抄録全体を表示

We report a case of recurrent nephrotic syndrome with transient blindness after taking cyclosporin A (CsA). Renal biopsy showed minimal change of nephrotic syndrome and the patient was treated with predonisolone (PSL) and cyclophosphamide leading to remission of nephrotis. CsA was given to the patient. Because of recurrence of nephrotic syndrome after tapering off PSL to 5 mg a day, 12 days after taking CsA, the patient complained of sudden onset of left eye blindness lasting for 30 minutes. When the patient visited our hospital, the disturbed vision had recovered already and there were no abnormal neurological findings, such as tremors and seisures. Funduscopic examination revealed no evidence of abnormalities and brain computerized axial tomography was unremarkable. From these findings, we predicted that constriction of an artery and temporarily formed thromboembolization in an eyeground artery had caused the sudden vision distur bance. Even though there is a high incidence of thrombotic complications in cases of nephrotic syndrome, we believe that vascular constriction and formation of thrombi in the eyeground artery of the case were mediated by the pathogistic effects of CsA. Because actions in association with CsA may produce constriction of small arteries, there by decreasing blood flow, initiating coagulopathy and causing endothelial cell damage, all these effects may lead to the formation of thrombo-embolic complications. In addition, when using CsA for the treatment of nephrotic syndrome, anti-platelets and/or anti-coagulant medicines should be concomitantly prescribed to avoid the thrombo-embolic complications.

抄録全体を表示