著者

椿原 美治 飯田 喜俊 湯浅 繁一 河島 利広 中西 功 横川 朋子 友渕 基

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.24, no.10, pp.1127-1136, 1982-10-25 (Released:2010-07-05)

参考文献数

30

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Borah, et al, demonstrated that HD is a severe catabolic stress to N-metabolism. EAA loss during HD has been speculated as a stress. In order to study this mechanism, AMIYU® (contained 8 EAA and His. 7% solution, Morishita Pharm. Co. Ltd., ) was infused into venous line throughout 5 hrs. HD with the speed of 40 ml/hr. (study A) and during the last 1 hr. of 5 hrs. HD with the speed of 200 ml/hr. (study B) . The time courses of urea generation rate (Gu.), aminogram and N-balance were compared among control, study A and study B-HD. There were no significant changes in EAA level during control HD suggesting that EAA loss was replacedd by protein catabolism. Gu. (mg/min) during 4 hrs, after control HD (20.1±1.2) was significantly higher than predialysis value (4.7±0.1), indicating the catabolic stress due to HD. Gu. after study A-HD (17.3±1.3) was significantly lower than that after control HD. But Gu. after study B-HD (23.0±0.9) was significantly higher than that after control. HD. This shows that the high dose of EAA administered during the last 1 hr. of HD is not lost into dialysate but is degradated to urea about a half because the last 1 hr, in 5 hrs. HD may be already the catabolic phase. N-balance was -3.6±0.8 (g/day) on control HD day and improved by EAA supplementation throughout HD (-2, 1±0.8). Plasma total. EAA and nonEAA levels significantly increased during 4 hrs. after control HD, suggesting that amino acids were supplied through protein degradation. But in study A, plasma total nonEAA level significantly decreased during HD, indicating that protein catabolism was suppressed by EAA supplementation throughut HD. From these results, HD itself is shown to be the strong catabolic stress to N-metabolism. The rapid decrease in plasma EA.A level due to EAA loss during HD would be one of this factor. The low dose administration of EAA throughout HD is considered to be not only replace the EAA loss, but also suppress this catabolic stress.

著者

中島 英明 宮崎 睦雄 今井 信行 横川 朋子 山本 茂生

出版者

社団法人 日本腎臓学会

雑誌

日本腎臓学会誌 (ISSN:03852385)

巻号頁・発行日

vol.43, no.4, pp.351-356, 2001-05-25 (Released:2010-07-05)

参考文献数

11

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A 63-year-old man was referred to our hospital for rapid deterioration of his renal function. He had worked as a metal founder for more than 40 years, and had been diagnosed as having silicosis. Laboratory data on admission showed severe anemia, thrombocytopenia, and end-stage renal failure (BUN 88.8 mg/ dl, serum creatinine 9.0mg/dl). Myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) was also detected in his sera. On the next day after admission, he complained of sudden dyspnea and hemoptysis. Mechanical ventilation with pure oxygen was insufficient to improve hypoxia without concomitant use of percutaneous cardio-pulmonary support (POPS) and continuous hemofiltration (CHF). We diagnosed his condition as MPO-ANCA-associated rapidly progressive glomerulonephritis with diffuse alveolar hemorrhage. Treat ment with plasmapheresis, pulse methylprednisolone and pulse cyclophosphamide effectively improved his hemoptysis as well as chest X-ray findings and blood gas analysis. However on his later clinical course, he was complicated with superimposed complex infection and passed away. Autopsy findings showed crescentic glomerulonephritis in the kidneys and silica nodules in the lungs. Recently it has been postulated that some relationship exists between ANCA-associated (especially MPO-ANCA-associated) glomerulonephritis and silica exposure. The reported cases of glomerulonephritisin the patients with silica exposure showed a rapidly progressive clinical course and pauci-immune necrotizing crescentic glomerulonephritis in their histology. Gregorini et al, reported that 12 of 37 (32%) male patients with RPGN had either silicosis or significant silica exposure, and 7 of 8 patients examined were ANCA-positive (6 of 7 were MPO-ANCA-positive). Therefore silica seems to cause glomerulonephritis by disrupting the immune response. Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, at least 3 cases out of which had suffered from silicosis in the past (30%) . These results indicate that silicosis should be considered a relevant pathogen of MPO-ANCA-associated glomerulonephritis beyond the race.