The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Volume 12, Issue 3
Displaying 1-6 of 6 articles from this issue
  • Takao Yasue, Akitsugu Ojima
    1970 Volume 12 Issue 3 Pages 323-332
    Published: 1970
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    One thousand autopsy cases were studied in regard to the clinico-pathological factors influencing renal crystalline deposition. Cases with calcium oxalate crystals (CaOX group) were 67, cases with leucine like crystals (LLC group) were 105, and cases with CaOX+LLC were 28.1. Significant factors found through 3 groups were oliguria, albuminuria, anemia, decrease of Ht, increased erythrocyte sedimentation rate, hypoalbuminemia, increased serum α2-gl, disturbances of liver function, hypocalcemia, azotemia, decreased PSP excretion, blood transfusions, supplemental fluids of large amounts, vitamins, diuretics, antibiotics, and surgical operations.2. Oliguria, albuminuria, anemia, azotemia, supplemental fluids of large amounts, diuretics, and surgical operations were found in markedly high incidences in all 3 groups. These factors seemed to be the important and common causes to/or results of/the renal tubular degeneration.3. In the CaOX group, disturbances of the renal function such as alubuminuria, abnormalities in urinary sediments, increased serum α2-gl, azotemia and decreased PSP excretion were marked, and a close relationship between CaOX deposition and renal diseases was supposed. In the LLC group, disturbances of the liver functions such as bilirubinuria, jaundice and increased GOT was significant and influence of liver diseases upon LLC deposition was considered. In the CaOX+LLC group, the findings were roughly intermediate between those in the CaOX and LLC groups. These findings perfectly coincided with pathological findings already reported by the author.4. This is the first report studied on the factors for renal CaOX and LLC depositon respectively.
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  • Akira Ono
    1970 Volume 12 Issue 3 Pages 333-364
    Published: 1970
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    Distribution in the glomerular tufts of IgG, A, M, β1C/β1A, globulin and fibriongen was immunologically investigated in 46 renal biopsy specimens. The subjects were 23 cases of chronic diffuse proliferative glomerulonephritis, 14 cases with minimal glomerular changes (6 cases of mild glomerulonephritis, 6 cases of orthostatic proteinuria and 2 cases of minimal change nephrosis), 4 cases of membranous nephropathy and 5 cases of SLE nephritis. The results obtained were as follows. (1) In membranous nephropathy and SLE nephritis IgG was the major component of the deposit, while small amount of other kinds of Ig was found occasionally. In membranous nephropathy there were cases with additional deposition of IgM. In SLE nephritis IgA and M were found in all cases as accessory components. (2) Chronic proliferative glomerulonephritis: (a) IgG was found in the glomerular deposits in 8 cases, IgA in 20 cases, IgM in 19 cases. Coexistence of IgG, A, and M was seen in 8 cases, IgA and M in 8 cases. IgA alone was deposited in 4 cases and IgM alone in 3 cases. When the cases were classifiod into G, A and M types according to the dominant Ig component, 16 cases belong to A type, 6 cases to M type and only 1 case to G type. (b) The deposits along basement membranes of glomerular tufts ware, except in one case of lobular glomerulonephritis, discontinuously distributed and variously shaped-fine granular, linear, crescent-like or lumpy. So they are different from the grenular, continous deposits observed in membranous nephropaty and in many cases of SLE nephritis and also from the deposits reported in acute post-streptococcal glomerulonephritis. (c) Definite deposition into mesangium was observed in 7 cases with glomerular changes of higher grade. Five cases belonged to A type, 1 case to G type and 1 case to M type. (d) The case of lobular glomerulonephritis described above was the only case of chronic proliferative glomerulonephritis, that showed granular deposits of G type along basement membrane and diffuse deposition of Ig of the same type into mesangium. It suggests that lobular glomerulonephritis belongs, immunohistologically, to acute glomerulonephritis, and that the deposition of A type and M type is characteristic to chronic proliferative glomerulonephritis. (e) The cases of A type had from mild to severe proteinuria and nearly good renal function. Histologically, IgA was assumed to be less active in causing mesangial cell proliferation than IgG, though it does not always assure favorable of the cases of A type. (f) Out of 6 cases of M type, 4 cases showed renal insufficiency and 2 cases were suffering from nephrotic syndrome. The former cases had long duration of the illness from 4 to 9 years, and showed, light-microscopically, widespread sclerosing changes and fibrinoid necrosis of glomerular capillaries. Histologically, mesangium infiltrated by IgM showed as mild mesangial cell proliferation as in the case of IgA. The immunological state of these patients was compared with " dysimmune " state (Okabayashi) observed'd in the end stage of prolonged sensitization with egg albumin or bovine serum globulin.(g) Judging from the amount of urinary protein, the activity to injury basement membrane was thought to be nearly the same among IgG, A and M. Relation was found between the amount of deposition of IgA along basement membrane and the grades of proteinuria.(3) In the cases with light-microscopically minimal glomerular changes, mild deposition of fine granular or linear materials was found along basement membrane in all of 6 cases of mild glomerulonephritis, in 2 of 6 cases of orthostatic proteinuria and in one of 2 cases of nephrotic syndrome. The dominant Ig was G in one case, A in 6 cases and M in one case.(4) Ths results of the present study indicate that immunohistological study, especially directed to IgG, . A and M, is essential to the clinico-pathologic study of chroic diffuse proli
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  • IV. On the enterobacterial common and O antibody response in patients and rabbits, especially on the production of 7S and 19S antibodies
    Renpei Kondo
    1970 Volume 12 Issue 3 Pages 365-382
    Published: 1970
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    In the previous papers of the study it was reported that in the patients of pyelonephritis and in animal 4experiments, the enterobacterial common antigen-antibody system behaves in a different way from that of Jthe enterobacterial O antigen-antibody system. The purpose of the present study is to classify the immunoglobulins in which the common and O antibodies are contained. For this purpose, rabbits were immunized with heated suspension of E. coli 014, ethanol soluble fraction of E. coli 055 and supernate of E. coli 0111 mixed with complete Freund's adjuvant. Experimental pyelonephritis of rabbits was produced by intravenous injection of E. coli 014 and 055 after ligation of unilateral ureter. The sera from the patients and rabbits were fractionated by gel filtration on Sephadex G-200 and the fractions were measured on the common antibody titer by hemagglutination and on the O antibody titer by hemagglutination inhibition reaction.The results were as follows. Enterobacterial common antibody was produced in 19 S globulin in every case. Enterobacterial O antibody was excessively produced in 19 S class of immunoglobulin, but evidence was obtained that small amount of O antibody was also produced in 7 S globulin in the sera obtained from the rabbits of experimental hematogenous pyelonephritis infected with E. coli 055 and the rabbits immunized with supernate of E. coli 0111 mixed with complete Freund's adjuvant. It is suggested that particular feature of enterobacterial common antigen-antibody system is due to the fact that enterobacterial common antibody is produced in 19 S fraction only.
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  • Yumiko Nishimoto
    1970 Volume 12 Issue 3 Pages 383-409
    Published: 1970
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Clinically the Phosphatase, especially Acid-Phosphatase (Acid-Pase) has not been considered important except in the prostate disease.But recently, a high level of Acid-Pase activity was observed in diseased tissues of the brain, the liver, the lung and so forth.So I considered the Acid-Pase playing an important role in the degeneration of the tissues, and I studied the Phosphatase, especially Acid-Pase in renal failure, clinically and experimentally.Material and Method ; Kidney of human patients suffering from chronic renal failure and rabbit kidneys damaged by potassium chromate were used.The human and animal materials were divided into the three parts ; cortex, medulla, and papilla.The Phosphatase activity was determined by the kind and king's method using phenylphosphate as a substrate. Further more, isoenzymes were separated by liquid chromatography, Sephadex G-75. The effects of the inhibitory action of cyanide, sodium fluoride, tartrate, and formaldehyde were observed.Results ; The Acid-Pase activity in the every part of the damaged kidneys was higher than in the normal ones. From the view-point of pH, the highest increase of activity was observed at pH 5.The kidney tissue supernatant, which was obtained by 96600 g ultracentrifugation, was divided into Enzyme I and Enzyme II components by liquid chromatography, Sephadex G-75.The activity of the Enzyme I component increased to a great extent in every part of the contracted human kidney and in the damaged rabbit kidney.It was presumed that the molecular weight (M. W.) of the Enzyme I component was more than 70, 000 and the M. W. of the Enzyme 11 component was 10, 00020, 000.The Enzyme I originated in the prostate, because its activity in the contracted human kidney and in the injured rabbit kidney was inhibited by tartrate and sodium fluoride.The Enzyme 11 originated in the erythrocyte because it was inhibited only by formaldehyde.The increase of the serum Acid-ease activity in the damaged rabbit kidney was observed at pH 4, but the Acid-ease activity in the erythrocyte did not change.The Acid-Pase activity in the human serum of patients suffering from chronic renal failure (BUN more than 100 mg/dl) did not change, but it increased in the erythrocyte and in the urine.The human urinary Acid-Pase belonged to the Enzyme I component.The erythrocyte Acid-Pase activity in the rabbit which was taken out the both kidneys increased.It is clear from these results that the increase of the Acid-Pase activity was caused by some agent from outside the kidney-possible uremic poison.It can be supposed that an unknown dialysable low-molecular factor contributes to the increase of the Acid-Pase activity, because when the serum of uremic patients was added to the rabbit kidney homogenate, the Acid-Pase activity increased. Also the Acid-Pase activity in the erythrocyte and in the urine of the uremic patients beefing treated with haemodialysis, did not change.There was a low statistical correlation between the Acid-Pase activity in the urine and urinary urea N, urinary creatine and urine protein.The Acid-Pase activity in the human erythrocyte suffering from renal failure, was directly proportional to the serum urea N level.1 For the diagnosis of kidney disease it can be concluded that the Acid-Pase activity in the kidney tissue, erythrocyte and urine increases to a great extent at the end stage of renal failure.2 It can be presumed that the Acid-Pase activity is an important factor in metabolism of the pathologi-cally diseased kidney.
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  • Ryôkô Nakamura
    1970 Volume 12 Issue 3 Pages 411-437
    Published: 1970
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    1, Peritoneal Dialysis.Twenty-eight autopsy cases, including 25 cases of chronic glomerulonephritis, one case of malignant: nephrosclerosis, 2 cases of chronic pyelonephritis were used for this study. The similar number cases without dialysis were also used as control. Histopathological findings were obtained as follows.(1). Renal contraction were remarkable in patients of chronic glomerulonephritis, especially, in long-termm dialysed ones. Nevertheless, completely-hyalinized glomeruli decreased in number, and on the contrary, in partially-hyalinized ones mesangeal cells were preserved rather well. Edema, plasma imbibition and fatty deposits were also seen in those glomeruli. Even the scarred glomeruli were mostly stained slightly red with Van-Gieson' staining and frequently violett-blue by Mallory' staining.(2). The renal arteriolar wall showed marked edema in the intima with proliferation of argentfile and collagen fibers, that resembled the one in malignant nephrosclersis without dialysis. But proliferation of elastic fibers and atrophy of media were seen prominent in malignant nephrosclerosis.(3). The basementmembrane of the tubules were splattered and irregularly thickened. There were irregularlyshaped crystals and metastatic calcification in the tubular lumen.(4). Uremic pneumonitis were found in 87.5 percent of the non-dialysed patients and in 68.7 percent of the patients dialysed less than three months. It was not seen in most cases dialysed more than four months. Few of the long-term dialysed cases showed focal organization of alveolar exsudates due to uremic pneumonitis.(5). Pleuritis and pericarditis were observed in most of the dialysed patients, pericarditis was frequently fibrinofibrous with organization, on the contrary, that of non-dialysed cases were fibrinous type. At that time, marked pericardial effusion was occationally noticed, it was bloody in few cases.(6). Angitis with fibrinoid necrosis was seen in every organ. Two cases showed gastrointestinal ulcer with angitis and died from bleeding of the ulcer. The another two cases revealed respectively angitis of cerebral arterioles associated with hemorrhage and of pancreatic interstitial arterioles.It was characteristic in dialysed patients that edema or edematous sclerosis were observed in glomeruli, interstices and intima of arterioles.As the factors to increase the peamiability of the arteriolar wall, the changes of blood-pressure, the decrease of serum albumin and non-protein-nitrogen and the changes of serum electrolyte through peritoneal dialysis were considered. Edema of the intima of arterioles was remarkably seen in the cases showing marked. decrease of serum albumin and non-protein-nitrogen and in the cases which had much dialysates in oneJ dialysis and urin volume of less than 100ml a day.
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  • Correlation between Clinical and Histologic Findings and Effects of Steroid Therapy on the Nephrotic Syndrome
    Fumitaka Suzuki
    1970 Volume 12 Issue 3 Pages 439-490
    Published: 1970
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    Various clinical findings and histologic changes were seen in patients with nephrotic syndrome. According to the light microscopic glomerular changes, (refered to the findings of the electromicroscopy and the immunofiuorescent study), 71 cases of the nephrotic syndrome resulting from glomerulonephritis were classified into 6 groups. In the group I, glomeruli showed no remarkable changes or very slight cellular proliferation. In the group II, slight and partial thickening of the basement membrane were present in almost all of the glomeruli. In the group III, most of the glomeruli showed marked, diffuse thickening of the basement membrane (Membranous glomerulonephritis). In the group IV, most of the glomeruli showed proliferation of mesangial and endothelial cell with glomerular lesions belonging to group II (Proliferative glomerulonephritis). In the ;group V, biopsy specimens showed lobulation of the glomerular tufts resulting from increased mesangial cells and partially thickend basement membrane (Lobular glomerulonephritis). In the group VI, biopsy specimens showed hyalinisation and sclerosis of the glomerular tufts with glomerular changes belonging to group II, IV, and V (Chronic sclerosing glomerulonephritis). An attempt was made to clarify the relationship between the various clinical and histologic findings and effects of steroid therapy on the patients.The results were as follows:(1) The relationship between various clinical findings and effects of steroid therapy. In the group with more increased nephritic changes in the nephrotic syndrome, effects of steroid therapy decreased, and the degrees of proteinuria, hypoproteinemia and hypercholesteremia, characteristic findings of the nephrotic syndrome, were not related to the effects of steroid therapy, but the cases with low amount of serum albumin had a tendency to show good effects of therapy. At the time of a high degree of edemaa it was often difficult to estimate the effects of steroid therapy from the value of NPN, PSP and renal clearance but in the cases with slight histologic changes these value recovered to the extent of normal value by the steroid therapy.(2) The relationship between histologic changes and clinical findings. In the group with slight histologic changes, patients were generally younger than in other groups and duration after onset was shorter on the almost cases, and the cases with hypertension and hematuria were few. The cases in the group III had a lot of urinary protein, and in the group with slight histologic changes amount of serum albumin were smaller than in other groups, but in the group with severe histologic changes amount of serum albumin had a tendency to increase. Renal function at the time of a high degree of edema did not reflect the severity of histologic changes.(3) The correlation between histologic changes and effects of steroid therapy. In the group I and II with few or slight histologic changes, all cases were more responsible to steroid. therapy but in the group III all were less responsible. In the group IV, about one half of cases were responsible to steroid therapy and others not responsible. When examined in detial, however, according to the severity of histologic changes the difference of the therapeuiic effec was seen also among the cases of this group and in the cases with severe histologie changes therapeutic effects were hardly observed. Therefore, on the determination of the effect of steroid therapy histologic findings are at the present moment a valueable procedure and at a considerably high percentage effects of steroid therapy can be estimated by the histology. Relapse was seen in all groups. However, relapse in the group I and II was improved by the therapy but in the group IV improvement after relapse was not easily obtained.(4) The glomerular histology after the steroid therapy was essentially identical to the histology observed. before the treatment.(5) The relationship between the
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