The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Volume 17, Issue 9
Displaying 1-4 of 4 articles from this issue
  • Kosei Kuhara
    1975 Volume 17 Issue 9 Pages 803-809
    Published: September 30, 1975
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    Gastrointestinal bleeding is a recognized complication of renal failure, traditionally being asso-ciated with peptic ulceration. Nevertheless, the pathogenesis of the so-called “uremic gastropathy ” is not clear. Recently, it is generally agreed that the kidney is a major site of gastrin degradation. In view of these facts, I attempted to clarify the pathogenetic significance of hypergastrinemia asso-ciated with chronic renal failure. Fasting serum-gastrin and gastric acid secretion were examined in 16 patients with chronic renal failure and 7 normal controls. The mean fastingserum-gastrin was 147 pg/ml in the chronic renal faillure and 78 pg/ml in the controls. The mean basal acid output was 3.4 mEq/hr in the chronic renal failure and 2.2 mEq/hr in the controls. The mean stimulated peak acid output was remarkably higher in the renal failure group (121 mEq/L) than in the control group (81 mEq/L). (p<0.05). The examination of the stomach and the duodenum was done radiologically and endoscopically. There was no patient with ulcer, but the majority of patient3 had severe gastric mucosal abnormalities. Fiberscopic gastric biopsy was done in 3 patients, and all specimens showed marked morphological changes of rnucosal & submucosal hemorrhages, hyperemia and cellular infiltrations. It is as yet unable to decide, whether the uremic damage of the gastric mucosa is brought about by hypergastrinemia. But this study supports the hypothesis that the hypergastrinemia is very impor-tant in the pathogenesis of the so-called “ uremic gastropathy. ”
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  • Hidekata Shimada
    1975 Volume 17 Issue 9 Pages 811-821
    Published: September 30, 1975
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    If, by means of few simple formulae, we can determined the period and conditions of dialysis necessary for reducing the creatine (or BUN) concentration to arbitrary degree, it would be helpful for bettering dialystic treatment. Many factors have direct or indirect influences on dialystic results. Kinds of a dialyzer and dialy-sate flow rate being constant, the most influential factors on the required dialysis time are the quantity of body fluid and blood flow rate of patients. If we choose the time unit shown by follow, it was found experimentaly that is a definite regula-rity between the half life of decreasing creatinine (or BUN) concnetration degree and the blood flow rate. Dialysis Time Unit (D)=circulating blood volume (ml)/blood flow rate (ml/min)The unit per time period "D" is expressed by the minute unit of the time required for consumately passing through the dialyzer of same quantity of the circulating blood volume. If the conditions of dialyzer and blood flow rate are constant, about of all cases, the decreasing rate of creatinine (or BUN) concentration degree is constant in the time period " D ". With the period " D ", I have devised several formulae and graph of the formulae, the time required for necessary dialysis easelys determined.
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  • Tomihisa Funyu, Shigenobu Kudou, Kazumi Ohno, Kazuo Nigawara, Hiroshi ...
    1975 Volume 17 Issue 9 Pages 823-836
    Published: September 30, 1975
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Metabolism of adrenocortical hormone in patients with chronic impaired renal function was investigated in this study. Urinary 17-OHCS (total, free and fractions-com. F, comp. E, THF, THE) we(re measured by use of thin layer in these 12 patients, including 6 patients who were made to artificial dialysis. Three patients of them were studied on load with ACTH-Z 20 units/day for 3 days intramuscularly and 9 patients were studied on administration of cortisol (1 mg/kg of body weight) intra-venously. Moreover, blood free 11-OHCS was determined in 3 patients with treatment of artificial dialysis. Following results were obtained. 1) The excretion volume of urinary total 17-OHCS remained low coincidently with decrease in creatinine clearance on control, on load with ACTH-Z and on administration of cortisol. 2) In above mentioned patients, the rate of urinary free 17-OHCS to total 17-OHCS exhibited various values which may be influenced with glomerular and tubular lesion, being compared with certain values of normal control. 3) The fractions of urinary 17-OHCS showed small pattern similar to normal control. 4) The excretion pattern of urinary 17-OHCS fractions shifted to cortisol pathway from cortisone pathway on load with ACTH-Z as normal control. 5) In the group with non-hyper BUN, the changes of the excretion volume of urinary 17-OHCS was seemed to be similar to normal control in every 2 hours measurement on administration of cortisol, while in the group with hyper BUN, the changes was not observed. 6) In the patients with artificial dialysis free 11-OHCS remained within normal range but showed abnormal in diurnary variation.
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  • Takeshi Sakiyama, Hiromi Suzuki, Osamu Nishiya, Noriko Mashiko, Yumio ...
    1975 Volume 17 Issue 9 Pages 837-847
    Published: September 30, 1975
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    A two-year-old boy with nephrotic syndrome took the fatal clinical course due to the wide spread cerebral thrombosis, associted with the hypercoagulopathy. The thrombosis in nephrotic syndrome have been sometimes noted in the patients with hypoalubminemia, hypercholesterolemia, and massive proteinuria. However, few cases with cerebral thrombosis has been reported. In our patient, the hypercoagulopathy was exacervated by the steroid therapy and by suffering from the infections of mumps and varicella. The immunoelectrophoretic study of the scrum protein in the patient revealed the transient in-crement of the monoclonal IgM (k type) twice after these viral infection. The appearance of the monoclonal protein in serum suggested that the cellular immunity was deficient in the patient. It was identified by the clinical immunological examinations such as negative delayed hypersentivity, reduced PHA responce, and decreased MIF. At autopsy, the thymus was grossly hypoplastic, which revealed that Hassall's corpuscles were rudimental, and numbers of lymphocytes were decreased. The brain showed the multiple thrombosis with subarachnoidal hemorrhage. But no thrombosis was found in other organs. Histological exami-nation in the kidney showed membranoproliferative and lobular glomerulonephritis. There was evidence of Rio and fibrinogen deposition within the glomeruli by immunofluorescent microscopy. On electron microscopy, there was subendothelial deposit in the glomeruli. Based upon the findings in the present case, we propose that some case of nephrotic syndrome might be associated with the cellular immunodeficiency.
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