日本腎臓学会誌
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
45 巻, 7 号
選択された号の論文の8件中1~8を表示しています
  • 森田 俊
    2003 年 45 巻 7 号 p. 667-672
    発行日: 2003/10/25
    公開日: 2011/03/01
    ジャーナル フリー
  • 柳澤 尚紀
    2003 年 45 巻 7 号 p. 673-680
    発行日: 2003/10/25
    公開日: 2010/07/05
    ジャーナル フリー
    We have already reported that serum levels of soluble Fas (sFas) and Fas-positive mononuclear cells increased concomitantly with deterioration in renal function and the increases were statistically significant. Moreover, the severity of renal anemia in renal failure patients was significantly correlated with serum levels of sFas. Therefore, we investigated whether or not Fas and Fas ligand (Fast) influenced the production of erythropoietin (EPO). Hep G2 cells, an EPO productive human hepatocellular carcinoma cell line, were cultured in MEM medium with 10 % of FCS containing 1, 10 or 100 ng/ml of sFas, or sFasL. The EPO concentrations of the supernatants were measured by the ELISA method, Annexin Vpositive cells were calculated by flow cytometry, H3 leucin uptake was measured by a liquid scintillation counter, an MTT assay was performed using the light absorption method, fragmented nuclei were stained by the TUNEL method and DNA laddering was observed by agarose gel electrophoresis. Their characteristics evaluated at 0, 24, 48 and 72 hrs. Both EPO production and H3 leucin uptake were suppressed in culture with sFas or sFasL, dose-dependently and declines in MTT activities accompanied these changes at 24 hrs. In addition, nuclear fragmentation and DNA laddering were found to be stimulated in culture with sFas or sFasL at 48 hrs. These data suggest that sFas induced apoptosis and had a cytotoxic effect on Hep G2 cells. In conclusion, hyper-sFas-emia observed in chronic renal failure may regulate the production of EPO, which indicates that sFas acts as a uremic toxin.
  • 塚田 三佐緒, 本田 一穂, 新田 孝作, 湯村 和子, 二瓶 宏
    2003 年 45 巻 7 号 p. 681-688
    発行日: 2003/10/25
    公開日: 2011/03/01
    ジャーナル フリー
    The frequency of incidental mesangial IgA deposition and its clinicopathological features were investigated in patients with minimal change nephrotic syndrome (MCNS) . Mesangial IgA deposition was present in 15/63 patients (23.8 %), and co-deposition of IgA and C3 was present in 10/63 patients (15.9 %). The serum IgA concentration was significantly higher in IgA (+) patients than in IgA (-) patients (341±79 mg/dl vs. 252±99 mg/dl, p=0.034) . The urinary red blood cell count tended to be higher in IgA (+) patients than in IgA (-) patients (12.8±24.9 vs. 5.0±7.9 counts/HPF, p=0.58) . Histologically, no significant differences were observed between IgA (+) and IgA (-) patients. After steroid treatment, 14 patients with mesangial IgA deposition showed complete remission and one patient had persistent proteinuria . The microhematuria also disappeared after steroid treatment in 13/15 patients (86 .7 %), although it reappeared in 6/13 patients (46 %) during reduction of steroid administration. The present study indicated that the incidental mesangial IgA deposition was frequently observed in MCNS patients (23 .8 %) . The phenomenon of mesangial IgA deposition was related to the higher concentration of serum IgA . However, no influence of mesangial IgA doposition in MCNS patients was found on the post treatment amount of proteinuria, renal function and clinical outcome of MCNS.
  • 松本 博, 岡田 知也, 長岡 由女, 外丸 良, 岩澤 秀明, 和田 憲和, 中尾 俊之
    2003 年 45 巻 7 号 p. 689-694
    発行日: 2003/10/25
    公開日: 2011/03/01
    ジャーナル フリー
    The therapeutic approach to patients with membranous lupus nephropathy (MLN) remains controversial. We have attempted combination therapy for MLN. Five patients with MLN (WHO class Va and Vb) and nephrotic syndrome were treated with 1 g methylprednisolone intravenously for 3 consecutive days followed by daily prednisolone at the dose of 30.40 mg plus cyclosporine at the dose of 100-200 mg and angiotensin receptor blocker (40 mg of valsartan). Initial dosage prednisolone was given for 1 month, and then tapered gradually in terms of dosage and interval. These patients were followed up for a minimum of 12 months. Complete remission was obtained in 4 patients after a mean of 7.3±2.1 months, and partial remission was obtained in the remaining patient. Daily prednisolone dosage significantly decreased from a baseline mean of 0.69±0.11 mg/kg to a mean of 0.10±0.02 mg/kg at the last follow-up. Lupus activity, as measured by SLE disease activity index, significantly decreased in all patients. Serum creatinine level and blood pressure remained stable. It was concluded that quadritherapy, including intravenous methyl prednisolone, prednisolone, cyclosporine, and angiotensin receptor blocker, was beneficial in inducing remission of nephrotic syndrome, reducing lupus activity, and sparing prednisolone dosage with an acceptably low risk for side effects.
  • 神谷 有香子, 市原  淳弘, 山下 智子, 高瀬 敦, 林 松彦, 猿田 享男
    2003 年 45 巻 7 号 p. 695-700
    発行日: 2003/10/25
    公開日: 2011/03/01
    ジャーナル フリー
    Primary renal artery dissection is a rare condition that causes renal infarction and renovascular hypertension. We describe a case of a 48-year-old man who was admitted for left renal infarction due to a primary dissecting aneurysm of renal artery. He was diagnosed by a contrast enhanced abdominal CT scan and a renal angiography demonstrating a dissection at the branch of the left renal artery. He was treated with conservative medical management, including anticoagulation therapy. Forty-five primary renal artery dissections in 38 patients from previous reports were analyzed. Based on this analysis, many cases of primary renal artery dissection were male and had a high blood pressure. Primary renal artery dissection occurred at the right side (12 cases), left side (19), and bilaterally (7) . The renal arterial branches were rarely involved in primary renal artery dissection. Assays of peripheral blood renin activity were performed in 15 patients, and all cases had a high value. Therefore, the present case is thought to be unique because he was a normotensive patient with normal plasma renin activity and the renal arterial branch was only dissected.
  • 西本 愛, 原口 総一郎, 岸 知哉, 藤崎 大整, 池田  裕次, 酒見 隆信, 山元 博
    2003 年 45 巻 7 号 p. 701-705
    発行日: 2003/10/25
    公開日: 2010/07/05
    ジャーナル フリー
    Although many cardiovascular complications have been described in systemic lupus erythematosus (SLE), aortic involvement is rare. We report here a 51-year-old woman who suffered from SLE and died of a rupture of abdominal aortic aneurysm. She was diagnosed as having SLE in 1981, and administered prednisolone. She was admitted to our hospital for the treatment of nephrotic syndrome and hypocom plementaemia in December, 1996. Kidney biopsy revealed lupus nephritis (type IV of WHO classification). Methylprednisolone and cyclophosphamide pulse therapies were started, which resulted in an incomplete remission of nephrotic syndrome. After discharge, her clinical course was uneventful, and the dose of prednisolone was tapered. On April 22, 2001, she developed sudden abdominal pain and was admitted to a nearby hospital. Abdominal CT showed calcification of the aorta and an abdominal aortic aneurysm of 6.3×8 cm. She died of a rupture of abdominal aneurysm on the first hospital day. We think that prolonged prednisolone therapy might play a major role in accelerating atherosclerosis, which could result in aortic aneurysmal enlargement in this patient. Considerable attention should be paid to patients with SLE who are given prednisolone to detect and prevent vascular complications such as aneurysm.
  • 伊藤 和子, 田中 元子, 松下 和孝, 冨永 芳博
    2003 年 45 巻 7 号 p. 706-712
    発行日: 2003/10/25
    公開日: 2010/07/05
    ジャーナル フリー
    We report here a dialysis patient with secondary hyperparathyroidism who had a history of parathyr oidectomy for primary hyperparathyroidism 27 years previously. The patient was a 48-year-old male. In 1974, he was diagnosed as having primary hyperparathyroidism and an adenoma was completely resected in the Department of Urology, Osaka University Hospital. In 1997, he started hemodialysis for chronicrenal failure by diabetic nephropathy. Since his intact-PTH was high, we started intravenous vitamin-D pulse therapy, but intact-PTH did not decrease. We could not detect any parathyroid glands by ultrasonography and 201TIC1- 99mTc04- scintigraphy around the thyroid gland. Finally, chest-CT and 99mTc-MIBI scintigraphy revealed a ectopic parathyroid gland in the mediastine, and the ectopic parathyroid gland was successfully resected in July, 2001. In order to distinguish whether the resected ectopic parathyroid gland was due to primary adenoma or secondary hyperplasia, we used an immunohistochemical technique to examine the expression of PRADI/cyclin Dl, Ki67, and p27 and sequence analysis of the MENI gene. As a result, the labeling index(LI)of PRAD1/cyclin Dl was 4, LI of Ki67 was 36, and LI of p27 was 257. Moreover, germline-mutation and somatic-mutation of MEN 1 gene was not detected. These findings suggested that the resected parathyroid gland was a nodular hyperplasia of secondary hyperparathyroidism. In conclusion, immunohistochemical findings of parathyroid tissue and sequence analysis of MENI gene could be useful for the differential diagnosis of primary adenoma and secondary hyperplasia.
  • 2003 年 45 巻 7 号 p. 713-729
    発行日: 2003/10/25
    公開日: 2010/07/05
    ジャーナル フリー
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