The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Volume 22, Issue 4
Displaying 1-10 of 10 articles from this issue
  • Masashi Sato, Tsuyoshi Yamagishi, Hiroshi Hirano, Hisao Fueki, Masaaki ...
    1980 Volume 22 Issue 4 Pages 343-355
    Published: 1980
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    A study of complement receptor (GCR) was performed in the human renal glomerulus in normal and various pathologic situations. Frozen section of 4μ thickness were incubated with two kinds of the indicator cells, namely sheep erythrocyte coated with IgM antibody and C3 (EAC3b) and fluorescein-labeled bacteria coated with C3 (FBC), in order to determine the activity of GCR. Numerous EAC3bs adhered specifically to the glomeruli under the light microscope. On the other hand, the sections were incubated with FBC and tetramethyl rhodamine isothiocyanate (TRITC)-labeled anti-human GBM antibody. The double-stained specimens under the immunof luorescent microscope (IF) showed that FBCs were bound to the external (or epithelial) side of GBM. Furthermore, frozen sections of 12μ thickness were incubated with EAC3b and FBC, and were observed under the scanning electron microscopes It was noted that the indicator cells adhered to the surface of glomerular epithelial cells. The C3 deposits under IF and the C3 receptor activity for binding of EAC3b were examined inn the glomeruli of sixty-six biopsy specimens from various renal diseases The loss or reduction of GCR activity was detected in twelve cases (acute glomerulonephritis 3, lupus nephritis 4, membranous nephropathy 3, membranoproliferative glomerulonephri.tis 2), of which eleven cases revealed subepithelial C3 deposits. However, the restoration of GCR activity did not occure removal of C3 deposits by acid treatment. The GCR activity was noticed even after incubation with fresh serum and urine of patients with various renal diseases. In conclusion, the GCR is located on the epithelial cells of the glomerulus and its activity is closely related subepithelial C3 deposits. It seems that the GCR may play an important role in trapping and deposition of immune complexes containing complement in immunologically mediated renall diseases.
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  • Part II. The role of anti-GBM antibody in the Pathogenesis of Human Glomerulonephritis
    Masashi SATO
    1980 Volume 22 Issue 4 Pages 357-376
    Published: 1980
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    Circulating anti-GBM antibodies were examined in various forms of human glomerulonephritis(GN) by passive hemagglutination test using prepared human soluble GBM antigen. Also, these assay system were fundamentaly checked up. Their clinical diagnosis were acute GN in 13, rapidly progressive GN in 1, chronic GN in 36, membranous nephropathy in 15, IgA-IgG nephropathy in 9, membranoproliferative GN (MPGN) in 4, lipoid nephrosis in 6, purpura nephritis in 2 and acute renal failure in 2. The relationship between circulating anti-GBM antibodies and the clincal diagnosis, the renal histological findings, the renal immunofluorescent findings, the streptcoccal infection and the clinical findings were investigated. The pathogenetic role as well as the methods of detection and the significance of circulating anti-GBM antibodies in human GN were discussed. 1. This method used here is excellent than the methods of immunofluorescence and Ouhterloney on the aspect of specificity and sensitivity. 2. Circulating anti-GBM antibodies were found in high titer in patients with 5 of acute GN, 1 of rapidly progressive GN, 4 of chron GN and 1 of MPGN. 3. High titer of circulating anti-GBM antibodies were found in proliferative GN, but 1 of MPGN and sclerosing GN had also high titer. The grade of proliferation were more severe in the patients with linear deposits of IgG on the GBM associated with one of complement. 4. Positive circulating anti-GBM antibodies were found in patients with linear deposits of IgG on the GBM, but 3 patients with mixed patte.zn had also high titer. 5. The group with elevated ASLO titers contained significantly more number of patients with positive circulating anti-GBM antibodies than one with normal ASLO titers. 6. The clinical course of poststreptcoccal GN with positive circulating auti-GBM antibodies cont-inued for more bug period compared with one with negative circualting anti-GBM antibodies. 7. The patients with positiva ciroilating anti-GBM antibodies were divided into four group :·typical onset of acute or rapidly progressive poststreptcoccal GN.μtypical anti-GBM antibody induced GN from unknown onset without streptcoccal infection.·evolution of immune complex GN into anti-GBM antibody GN.·immune complex GN only with positive circulating anti-GBM antibodies.
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  • Motoaki Sano, Haruo Suzuki, Shizuo Tojo, Ryuichi Kitagawa, Ryuichi Kit ...
    1980 Volume 22 Issue 4 Pages 377-384
    Published: 1980
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    A case (52yrs, female) of idiopathic tetroperitoneal fibrosis that developed rapidly progressive glomerulonephritis in the course of the disease was reported. Autopsy showed disseminated vasculitis of small arteries in various organs (esophagus, trachea, heart, liver, spleen and adrenal gland) and extracapillary proliferative-crescentic-glomerulonephritis with focal segmental necrotizing glomerulitis in addition to idiopathic retroperitoneal fibrosis. By an analysis of the clinical course, these lesions of the vessels and kidney were assumed to have been developed on the basis of hypersensitivity angiitis induced by contrast medium (Iodine). The possibility that vasculitis bore an etiologic relationship to idiopathic retroperitoneal fibrosis was discussed.
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  • Keihachiro Kuzuhara, Tsunamasa Inou, Eiko Wada, Toru Tsumita
    1980 Volume 22 Issue 4 Pages 385-392
    Published: 1980
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    It is known that a decrease in sciatic nerve motor-nerve conduction velocity is occured in rat with experimental hypermyoinositolemia. We found raised blood myo-inositol lvels in uremic patients. It suggests that blood myo-inositol is one of uremic toxins. However, the relationship between the blood myo-inositol levels and reral function was not known. In this study, we have measured the serum free myo-inositol levels in healthy donors, uremic patients under chronic hemodialysrs and renal transplants using a 200 cm column of 5% Ucon on Gaschromatography. Average of serum free myo-inositol levels in 12 healthy donors was 0.46±0.03 mg/dl (mean±S.E). Those of pre- and post- dialysis levels of 21 uremic patints under chronic hemodialysis were 11.19 ± 0.72 mg/dl and 3.77 ± 0.33 mg/dl respectively. The level of serun free myo-inositol was remarkably drawn by hemodialysis. We found that a change of serum free myo-inositol levels in postoperative course of some renall transplants showed just like parallel change of serum creatinine levels of them. Furthermore, the serum free myo-inositol levels were more linealy related to the serum creatinine levels than to the serum urea nitrogen. On the other hand, it seems that the recognition of the relation in high or low serum free myoinositol levels may show some new concepts of unknown diseases excepting renal dysfunction from these results. In some renal transplants, we measured the urine free myo-inositol and serum free myo-inositol, too. We found that there were some relations between the myo-inositol levels and the acute rejections. We observed in four acute rejections of three renall transplants that the urine free myo-inositol contents and the myo-inositol clearance were elevated in a few days prior to the acute rejections. It seems that the measurement of the urine free myo-inositol in post-operative renal transplants is a new methode of predictable and rapid diagnosis of the acute rejection.
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  • H. Inage, A. Koyama, M. Narita, S. Tojo, K. Iesato, I. Takei, Y. Wakas ...
    1980 Volume 22 Issue 4 Pages 393-399
    Published: 1980
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    In our population of 99 patients with SLE, 5 patients have developed avasculsr bone necrosis(AN).And in 230 patients with nephrotic syndrome wthout SLE, one has developed AN. All patients with AN received corticosteroids prior to the onset of AN, however, patterns of corticosteroid therapy have no relationship to the development of AN. There is significant higher incidence of developing AN in the patients with SLE (5%) as compared with the patients with nephrotic syndrome (0.44%), although patterns of corticosteroid therapy in those two control groups are similar. These findings suggest that SLE has certain etiologic factors to develop AN. Among the possible etiologic factors in SLE, vasculitis has been the mose considerable, and the hypercoagulability has been thought to be aggravated by the adminietration of corticosteroids. However, in our cases with SLE, signs of vasculopathy are less remarkable in those with AN than in those without AN, furtherr more one case with SLE who had received anticoagulant agents prior to the onset of AN has also developed AN.The pathogenesis of AN is to be discussed more further.
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  • Shunsuke Kawaguchi, Kenji Maeda, Shuichi Tsutsui, Kaizo Kobayashi
    1980 Volume 22 Issue 4 Pages 401-412
    Published: 1980
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    We investigated redox balance in chronic renal failure patients by ascorbate-cyanide test and by measuring G-6-PDIH activity of red blood cells and serum lipoperoxide. The patient's reducing power is impaired slightly or is latent before the institution of hemodialysis but aggravates and becomes manifestive with hemodialysis therapy. The influence of exogenous oxidant (free chlorine in tap water) is remarkable in dialyzed patients and the reducing power decreases furthermore. As the concentrations of serum vitamin E and A which are antioxidants are dependent on carrier protein concentrations in blood, their concentrations in tissue are unclear. Globin conformation should be investigated to clarify the cause of impaired reducing power of red blood cells in chronic renal faiiure.
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  • Ichiro Nakamura
    1980 Volume 22 Issue 4 Pages 413-427
    Published: 1980
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    To clarify the abnormalities of calcium metabolism in chronic renal failure patients maintained on hemodialysis, the calcium-related hormones and acid-base balance were measured in 46 patients before and during hemodialysis with a dialysate containing 7mg/dl of calcium. Before dialysis, the mean percentage of plasma ionized-calcium to plasma total calcium was high from acidosis, though both were within normal limits. The plasma inorganic phosphate level which was mostly high, correlated with the plasma parathyroid hormone (PTH) level. The plasma PTH and plasma human calcitonin levels were mostly high, but they did not correlate with the ionized-calcium level. A positive correlation was noted between plasma 25-hydroxycholecalciferol and plasma totalcalcium levels. Metabolic acidosis was observed in 24 patients, metabolic acidosis with respiratory compensation in 21, and respiratory acidosis in one. During hemodialysis, plasma PTH level decreased in 21 patients, but the overall mean did not. The mean levels of plasma albumin and arterial pH were elevated, At the completion of hemodialysis, 9 patients had respiratory alkalosis due to hyperventilation ; the plasma ionized-calcium level did not increase as a whole, but was markedly high in 3 patients. On the other hand, the mean plasma total calcium level, which increased significantly during hemodialysis, was remarkably high at the completion in 13 patients. The changes during hemodialysis in the plasma total calcium and plasma albumin levels correlated. These findings suggest that 7 mg/dl of calcium is not enough to prevent PTH hypersecretion in chronic renal failure. However, a dialysate containing more calcium may cause dangerous hypercalcemia. Therefore to prevent hypocalcemia and secondary hyperparathyroidism, adequate hemodialysis, and oral intake of aluminium hydroxide to correct hyper-phosphatemia and of activated vitamin D3 to increase intestinal calcium absorption are necessary.
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  • Hiroshi Takada
    1980 Volume 22 Issue 4 Pages 429-441
    Published: 1980
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    In order to obtain direct informations on the mechanisms of transepithelial urate transport in the rat kidney, renal clearance study, tissue analysis study and methods of tracer (2-14C-urate) microinjection into tubular lumen and peritubular capillary were performed. Futhermore, thin layer chromatogm raphic analysis were performed to clarify whether or not 2-14C-urate injected was metabolized. Results obtained from these studies are summerized as follows. 1) Fractional excretion rate of filtered urate was below 1.0 under hydropenic state, indicating net tubular reabsorption of urate. 2) Reabsorption of urate was found to occur primarily in the proximal comvoluted tubule, partly in the Henle's loop, and negligibly both in the distal tubule and collecting tubule. 3) The lack of conversion of radioactive urate to allantoin in the tubular lumen after microinjection indicated that the obtained values of reabsorptive fluxes were neither overestimated nor underes-timated. 4) Unidirectional secretary flux of 2-14C urate from the peritubular capillary into tubular lumen was also found, although the secretion sites along the nephron was not clarified. 5) Mannitol diuresis resulted inn an increment in fractional excretion rate of filtered orate inn accordance with decrement in the unidirectional reabsorptive flux of 2-14C-urate across the proximal tubule and Henle's loop.
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  • Shigeko Hara
    1980 Volume 22 Issue 4 Pages 443-463
    Published: 1980
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    1. A new type of primary glomerulonephritis was experienced. Light microscopic and immuno fluorescence findings of renal biopsy were similar to those in cases of IgA-IgG nephritis, but exact observation revealed changes in glomerular capillary loops. Furthermore, electron microscopic findings were indistinguishable from those of membran.oproliferative glomerulonephritis (MPGN) type. 2. 17 cases demonstrating the pathological findings outlined above have been among 118 cases of primary glomerulonephritis. Among 17 cases, serial renal biopsy was performed in three cases. The Second renal biopsy findings of these three cases revealed evidently changes in glomerular capillary loops. 3. All 17 cases had persistent proteinuria and microscopic hematuria, with over 1g/day proteinuria and moderate microscopic hematuria in about 60% of the cases.Renal function was almost normal at first biopsies. Three cases, serial renal biopsy were performed, showed nephrotic syndrome, hypertension and moderate or severe impairment of renal function after a few years from the first renal biopsy. High IgA and IgM serum values were detected. The compiement was normal in 16 cases and low in one cases, leading to the presumption that the complement in the latter was activated by the classical pathway. 4. The clinical features and pathological findings of renal biopsy were such that these cases could not be diagnosed as either IgA-IgG nephritis or MPGN, i. e., these 17 cases lay somewhere between IgA-IgG nephritis and MPGN. Therefore, taking into consideration pathological findings regarding the glomerular capillary loops, this "new" primary glomerulonephritis was defined as IgA predominant atypical MPGN.
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  • Kazutoshi Kanazawa
    1980 Volume 22 Issue 4 Pages 465-475
    Published: 1980
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Immunological study in IgA Nephropathy, characterized by the finding of IgA, predominantly inn the mesangium, was performed in 46 patients without evidence of systemic diseases. The following results were obtained, 1. It was supported that by immunofluorescent study, the activation of complement in IgA Neph ropathy was induced mainly by the alternative pathway. 2. In immunoserological study, no any characteristic findings were found in IgA Nephropathy. 3. It was considered that further studies are necessary to clarify the relationship between IgA and the mechanism of mesangium in IgA Nephropathy.
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