The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
Volume 43, Issue 2
Displaying 1-5 of 5 articles from this issue
  • Naoki MATSUZAWA
    2001Volume 43Issue 2 Pages 55-62
    Published: February 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    We conducted a study on the long-term prognosis of maintenance hemodialysis patients with and without diabetes mellitus (144 cases).As a result, significant differences were observed in the long-term prognosis over a 15-year period between those with a serum albumin concentration of more than 3.8 g/ dl and those with a serum albumin concentration of less than 3.8 g/dl.The group with a serum albumin concentration of more than 3.8 g/dl showed a better prognosis than the group with a concentration of less than 3.8 g/dl. We investigated the levels of thiobarbituric acid-reactive substances (TBA-RS) in the erythrocyte membrane of maintenance hemodialysis patients (23 cases), pre-dialysis uremic phase patients (12 cases) and healthy controls (7 cases).TBA-RS in the erythrocyte membrane of pre- dialysis uremic phase patients was higher than that observed in the other groups.The TBA-RS in the erythrocyte membrane in the maintenance hemodialysis without diabetes mellitus group was lower than that in the pre-dialysis uremic phase group. The TBA-RS in the erythrocyte membrane in the maintenance hemodialysis without diabetesmellitus group thus indicated an inverse relationship with the serum albumin concentration, Kt/V and erythrocyte tocopherol contents.These results suggested that serum albumin protects against erythrocyte membrane lipid peroxidation, and that this function is related to hemodialysis. We thus conclude that hypoalbuminemia appears to increase the oxidative damage and acceleration of arteriosclerosis, while it also worsens the long-term prognosis of maintenance hemodialysis patients.
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  • Ryuji SUZUKI, Hiroyuki MORITA, Youichi SUGENOYA, Masahide MIZOBUCHI, W ...
    2001Volume 43Issue 2 Pages 63-68
    Published: February 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Proteinuria is commonly observed in patients with chyluria due to Bancroftian filariasis. However, whether or not hypoalbuminemia is caused by chyluria alone is still a matter of debate. This is because various forms of glomerulonephritis are complicated in such patients. Herein, we report a case we have recently encountered. A 72-year-old male was admitted to our division for further evaluation of nephrotic syndrome. He was from the Southernmost part of Japan, where Bancroftian filariasis has been epidemic, and had developed persistent chyluria over a period of nearly 50 years. There was no other past history of illness except for diabetes mellitus (DM) pointed out 3 months prior to admission. The physical and laboratory examinations on admission fulfilled the diagnostic criteria for nephrotic syndrome. Lympho-scintigraphy showed an intense tracer accumulation in both kidneys. A renal biopsy was performed. At the light microscopic level, the glomeruli looked normal. Edema of the tubulointerstitium was noted. At the electron microscopic level, effacement of podocyte foot processes was not observed. Immunofluorescent study did not show glomerular deposition of immunoglobulins and complements. He also had persistent microscopic hematuria. Automated urinary sediment analysis by real-time confocal scanning laser microscopy revealed red blood cells of the non-glomerular type. Taken together, these findings strongly indicated that hypoalbuminemia of this patient was caused by chyluria alone. In conclusion, a report of the present case provides strong evidence that hypoalbuminemia of a patient with Bancroftian filariasis could be caused by chyluria alone.
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  • Masanori MUKAI, Takanori SHIBATA, Hirokazu HONDA, Emiko FURUTA, Kozo K ...
    2001Volume 43Issue 2 Pages 69-75
    Published: February 25, 2001
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    A 37-year-old woman was admitted to our university hospital because of severe flaccid quadriplegia. Her laboratory data, lip biopsy and muscle biopsy findings were compatible with hypokalemic myopathy due to renal tubular acidosis (RTA) type I associated with primary Sjögren's syndrome. Kidney biopsy revealed chronic tubulointerstitial nephritis (TIN), consisting of focal mononuclear cell infiltration with tubulitis, interstitial fibrosis and tubular atrophy. Immunohistochemical analysis of the renal biopsy specimens showed that the infiltrating mononuclear cells were predominantly CD8+T cells, and CD68+ cells (macrophages), whereas CD4+T cells were fewer in number. Following potassium administration and alkali therapy, hypokalemia and metabolic acidosis were ameliorated and limb palsy gradually subsided. Finally, RTA improved with prednisolon and short term cyclophosphamide treatment without supplemental potassium and alkali therapy.
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  • Yasunori IWATA, Takashi WADA, Keiichi YOSHIMOTO, Norihiko SAKAI, Miho ...
    2001Volume 43Issue 2 Pages 76-81
    Published: February 25, 2001
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    We experienced a 24-year-old Japanese man, who was a hepatitis B virus carrier with nephrotic syndrome. Liver biopsy showed that he was suffering from chronic hepatitis (activity 2, fibrosis 2). Renal biopsy revealed membranous nephropathy (MN) with focal segmental glomerulosclerosis (FGS). Immuno fluorescentic findings revealed the presence of HBe antigen along the glomerular capillaries as well as HBe antigenemia in circulation. Therefore, we diagnosed this case as HB virus related membranous ne phropathy associated with FGS lesions. He was treated with interferon(IFN)alpha-2b for over a month and angiotensin converting enzyme inhibitor. These therapies reduced urinary protein excretion from 4-6 g/day to 1-2 g/day, in accordance with a decrease in the titer of HBV DNA polymerase. The second renal biopsy revealed that the histological change from MN to membranoproliferative glomerulonephritis Type III after IFN therapy. These results suggest that IFN therapy might be effective for HB virus-related MN associated with FGS.
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  • Hiroaki IO, Yukihiko TAKEDA, Kyoko OKUMURA, Naoharu SAKAMOTO, Keiko OB ...
    2001Volume 43Issue 2 Pages 82-87
    Published: February 25, 2001
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    A 76-year-old woman was admitted to our hospital complaining of tarry stool, general fatigue and marked anemia (Hb 5.2 g/dl). Gastric endoscopic findings showed longitudinal red stripes and diffuse erythematous spots, indicating dilated vascular vessels. They resembled the stripes of a watermelon at the gastric antrum. The marked anemia was caused by chronic blood loss from the abnormally dilated mucosal and submucosal capillary veins in the gastric antrum. She was diagnosed as having gastric antral vascular ectasia (GAVE) with chronic renal failure (CRF). The association of GAVE and CRF is considered to be rare according to previous reports in Japan. Endoscopic argon plasma coagulation therapy was performed three times. After therapy, capillary dilatation disappeared, and the marked anemia was greatly improved. Argon plasma coagulation therapy was found to be a safe and effective procedure for this disease. Although GAVE is essentially a benign gastric disease, endoscopic therapy should be the treatment of first choice for this disease.
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