The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Volume 28, Issue 6
Displaying 1-14 of 14 articles from this issue
  • MASAKI KOBAYASHI, AKIO KOYAMA, HIROMI INAGE, HIDEKO NAKAMURA, HIROSHI ...
    1986 Volume 28 Issue 6 Pages 699-705
    Published: 1986
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    In order to investigate the effect of antigenic charge on the glomerular localization of immune complexes (IC), we used the system of chronic serum sickness nephritis in rabbits. Chemically modified cationic BSA was used as an antigen. Rabbits were immunizedd with 4 mg of cationic BSA containing Freund's complete adjuvantd After 2 weeks, 500μg of cationic BSA, were daily injected intravenously for 6 weeks and l week later, renal biopsy and bleeding were performed (1st biopsy). After 1 week, furthermore, these rabbits were injected daily 5 mg of cationic BSA for 1 week and 1 week later, renal biopsy and bleeding were performed (2nd biopsy) Renal specimen at 1st biopsy showed no significant finding of glomerular capillary walls, but at 2nd biopsy it revealed typical membranous glomerulonephritis. The prowperties of antibody to cationic BSA showed low precipitating and low avidity at bothh biopsies. Antigen to antibody ratio was in antibody excess state at 1st biopsy, but in antigen excess state at 2nd biopsy. From the above results, we speculated that: 1) Chemically modified cationization alters the immunogenicity of BSA, thereby producing low precipitating and low avidity antibody even in prolonged immunization. 2) Membranous glomerulonephritis induced in this system may result from small sized circulating IC depositions in antigen excess state.
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  • -Significance of urinary protein analysis-
    TAKASHI YAMAMOTO
    1986 Volume 28 Issue 6 Pages 707-720
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    β2-microglobulin, lysozyme, transferrin and IgG were measured in unconcentrated 24-hr urine and serum from 12 healthy subjects and 134 patients with various renal diseases of glomerular or tubular type. The selectivity of proteinuria (glomerular and/or tubular) was defined as the slope of regression line relating the log of renal clearance of proteins relative to that of transferrin to the log of their molecular weight. The range of 24-hr urinary excretion in healthy subjects were 11-98μg/m2/day (Md. 40μg/m2/day) for β2-microglobulin, 880-5, 000 ng/m2/day (Md. 2, 400 ng/m2/day) for lysozyme, 73-630 μg/m2/ day (Md. 240 pg/m2/day) for transferrin and 130-700 pg/m2/day (Md. 310 μg/m2/day) for IgG. The presence of glomerular damages were suggested in patients with heavy proteinuria (Ig/m2/day or over). The selectivity patterns were revealed a persistent presence of glomerular damages in patients of membrano-prolif erative glomerulonephritis, crescentic glomerulonephritis and Henoch-Schönlein purpura nephritis in spite of the decrease of urinary excretion of protein. The selectivity pattern (glomerular or tubular) was correlated with morphological findings and useful to diagnose the location of renal damage.
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  • KENJI SODA, MASANORI SUGAWARA, SHIGEAKI NISHIMURA, JUNKO KOHMOTO, TOSH ...
    1986 Volume 28 Issue 6 Pages 721-728
    Published: 1986
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    This study was performed to clarify the clinical features and the histopathological findings in IgA nephropathy with nephrotic syndrome. The results were as follows: 1) The nephrotic syndrome was observed in nine (4.8%) out of 187 patients with IgA nephropathy. 2) They were classified into 2 groups: (1) minor glomerular abnormalities (Minor group) = 3 cases, (2) diffuse mesangial glomerulonephritis (DPGN group) =6 cases 3) All of Minor group were normotensive and had no hematuria. All of DPGN group were associated with hematuria and two cases had hypertesion. Serum IgA was elevated in all of Minor group and three in six cases of DPGN group. 4) In immunofluorescence study, C3 was present weakly (less than 1+) in Minor group but strongly (more than 2+) in DPGN group. We thought that degree of C3 deposition was related to that of histological change. IgG was present only in one out of 9 cases. The frequency of IgG deposits was lower than that of IgA nephropathy without nephrotic syndrome. 5) All of Minor group were good responders to corticosteroid pulse therapy and came into complete remission. In contrast, DPGN group (especially more than moderate change) had poor prognosis and fell into hemodyalysis relatively soon. 6) In conclusion, our results showed that the nephrotic syndrom associated with minor glomerular abnormalities in IgA nephropathy was similar to lipoid nephrosis and different from DPGN group in the response to steroid therapy and the clinical course.
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  • -Sequential change of mesangial IgA deposits found one hour post transplantation kidney biopsies-
    SATOSHI SUGIYAMA, TOMIO YAMAMOTO, MIKITO TSUYUKI, SHINICHI OHSHIMA
    1986 Volume 28 Issue 6 Pages 729-737
    Published: 1986
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    We experienced six cases whose one hour post-transplantation kidney biopsies showed mesangial IgA deposits. They were all living related transplantation recipients. The purposes of this study are; first, to evaluate whether the IgA deposits found in one hour biopsy specimens belong to the donors or it develop following transplantation, second, to assess the fate of the IgA deposits; and thirdly, to know if it happens the recurrence or de novo IgA nephropathy. We examined the biopsy specimens which were taken before and after the recirculation to the transplanted kidney in two cases. The findings of immunofluorescence method and electron micrographs in these two specimens were quite similar. This made sure that the IgA deposits seen in one hour biopsies were pathological findings of the donors who did not have abnormal urinalysis at donation. This suggests the families of the recipients may have subclinical IgA nephropathy. The fate of the mesangial IgA deposits are variable. It seems that the mesangial IgA deposits are fading gradually in at least two cases who do not have abnormal urinalysis following successful renal transplantation. But the deposits did not fade out completely up to 12 months. In three cases who develop abnormal urinalysis, the intensity of the IgA deposits became more dominant than one hour biopsy and biopsies that were taken during normal urinalysis following transplantation. We cannot make clear whether these manifestations show recurrence of IgA nephropathy or de novo nephritis because the original renal diseases before renal transplantation are not confirmed. However, their histories are compatible with those of renal failure secondary to IgA nephropathy. We concluded that probably in half of these patients the posttransplant renal changes are the recurrence of IgA nephropathy.
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  • KEIHACHIRO KUZUHARA, HITOSHI KANIU, HIROYUKI TSUJI, KEIICHI FURUKAWA, ...
    1986 Volume 28 Issue 6 Pages 739-747
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    Myo-inositol is a precursor and component of phosphoinositides which is involved in propagation and generation of action potentials as the nerve function. The first stage of catabolism of serum myo-inositol is performed by an oxidase in the renal cortex. During renal insufficiency, the activities of the oxidase decrease to cause retention of myo-inositol in the blood. Experimental rats of hypermyoinositolemia showed delayed MCV in the sciatic nerve. In this study, serum free myo-inositol (S, fm-I) and serum creatinine (S-Cr) levels as well as peripheral nerve conduction velocity (NCV) were measured prior to dialysis in the patients for whom dialysis therapy has recently been instituted or who have been on dialysis for no less than 10-years. As a result, S. fm-I level was clearly high in those with abnormal NCV compared with those with normal NCV in both groups of patients. In the patients for whom dialysis was recently instituted, there was clealy an inverse correlation between S. fm-I and all of NCV measured in both upper and lower extremities. Based on the above, it will not be unreasonable to consider myo-inositol as a metabolic factor in uremic neuropathy and a uremic toxin.
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  • TADASHI ASAMI, KINYA HASHIMOTO, KAORU SAKAI
    1986 Volume 28 Issue 6 Pages 749-761
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    The roles of proliferated glomerular mesangial cells in the regulation of glomerualar filtration rate and urinary sodium excretion are now in debate. Using 246 children aged 6 to 18 years with chance proteiuria and/or hematuria and biopsy-proved chronic glomrulonephritis (GN), we studied the relations between the severity of mesangial cell proliferations and the changes of fractional urinary sodium (Na), potassium (K), and chloride (Cl) excretions in response to standing and walking from sustained recumbencey. Greater decreases of urinary Na, K, and Cl excretions were found to be induced immediately after standing and walking in moderate to severe mesangial proliferative UN including membranoproliferative GN than in minimal change GN. Urinary Na/K rations were also decreased, but they were not relevant to the severity of mesangial cell proliferations, which suggested no significant role of aldosterone in the observed simultaneous decreases of urinary Na, K, and Cl excretions. These results suggest that the proliferated mesangial cells regulate and decrease simultaneously fractional urinary Na, K, and Cl excretions in response to positional changes from recumbence to standing and walking, presumably, by the contractile activity of mesangial cells and aldosterone seems to play no significant role in these processes. These non-invasive renal function tests may give an aid to estimate the presence and severity of glomerular mesangial cell proliferations in children with chance proteiuria and/or hematuria.
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  • WATARU SAKAMOTO
    1986 Volume 28 Issue 6 Pages 763-775
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    We have carried out simultaneous measurement of cardiac output, regional blood flows and intrarenal blood flow distribution, using microsphere technige in the glycerol-induced acute renal failure in the water-drinking (water group), 0.9% NaCl-drinking for 4 weeks (saline group), 0.1% captopril-drinking (captopril group) rats. In all groups, cardiac output, renal blood flow and the other regional blood flows significcantly decreased 4 hours after glycerol injection. Intrarenal blood flow redistribution from outer cortex to inner cortex was occured. At 10 hours after glycerol injection, cardiac output, renal blood flow and liver blood flow returned to almost the control values only in the saline group, but still remained significantly lower in the other groups. Intrarenal blood flow redistibution toward inner cortex was still persisted in the all groups. Not only acute renal failure but also hepatic disorder were evident, as indicated by significantly elevated mean BUN and GPT values in the water and the captopril groups. However the protection of not only acute renal failure but also hepatic disorder was recognized in the saline group. The above results suggest that the systemic hemodynamics changes relate to the development of acute renal failure and that the rapid recovery not only renal blood flow but also liver blood flow would be important to prevent the development of acute renal failure.
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  • YUTAKA KASAI, KEISHI ABE, KAORU YOSHINAGA, SHUNICHI SASO
    1986 Volume 28 Issue 6 Pages 777-788
    Published: 1986
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    The purpose of the present study is to assess the effect of arachidonic acid (AA) and renal perfusion perssure on renal prostaglandin (PG) metabolism. The rat isolated blood-free perfused kidney was used. This system has been proven to be a useful tool for studying the renal hormonal metabolism. In the present study, two different perfusion pressures were employed. We assumed the low perfusion pressure (LPP) as an ischemic state of the kidney expecting the increase in prostacyclin production and the high perfusion pressure (HPP) as a physiological state of the kidney. In high perfusion pressure experiments, AA stimulated the perfusate PGE2, PGF secretions biphasically but perfusate 6-keto-PGF secretion monophasically. In LPP experiments, perfusate 6-keto-PGF1a increased 6-folds higher than that of HPP experiments. There was no difference in perfusate 6-keto-PGF between with AA and without AA experiments in LPP experiments. In HPP experiments, urinary PGE2, PGF and thromboxane B2 (TxB2) excretions were stimulated by AA but urinary 6-keto-PGF excretion was not stimulated by AA. From these results, the following conclusions were obtained. (a) The prostaglandin metabolisms were different between HPP and LPP experiments. (b) The rat isolated blood-free perfused kidney was able to produce TxB2 and excrete it. (c) 6-keto-PGF showed the different releasing pattern from that of PGE2, PGF and TxB2 suggesting different metabolic site and/or releasing mechanism.
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  • MASAYA TANNO, KEISHI ABE, MINORU YASUJIMA, KEN OMATA, YUTAKA KASAI, MA ...
    1986 Volume 28 Issue 6 Pages 789-797
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    To assess the role of sodium metabolism and renin-angiotensin-aldosterone system in the regulation of the synthesis orr activation of renal kallikrein, we studied chronic effect of sodium loading with 1% NaCl and angiotensin II infusion (900μg/kg/day) on urinary active and inactive kallikrein excretion in rats. Angiotensin II infusion was done under normal sodium diet and sodium loading. Urinary inactive kallikrein was evaluated as the kallikrein activated by trypsin (200μg/ml urine). Chronic loading of sodium increased urine volume, urinary sodium excretion, and urinary total, active and inactive kallikrein without the change in the ratio of active to total kallikrein, whereas it decreased plasma angiotensin II and aldosterone concentration. Chronic infusion of angiotensin II on regular diets increased urinary total, active and inactive kallikrein excretion without the change in the ratio of active to total kallikrein, urine volume, and urinary sodium excretion. Additionally it elevated systolic blood pressure, plasma angiotensin II and aldosterone levels. On the contrary, chronic infusion of angiotensin II on sodium loading with 1% NaCl did not induce any changes in urinary total, active, and inactive kallikrein, the ratio of active to total kallikrein, urine volume, and urinary sodium excretion, whereas it increased slightly plasma angiotensin II and aldosterone concentration. These results indicate that chronic sodium loading and angiotensin II infusion might stimulate the synthesis of renal kallikrein. In addition, it is suggested that volume status may play some role in the regulation or the synthesis of renal kallikrein.
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  • MASANOBU HONDA, RYOKO TAKAYAMA, NOBORU FUKUDA, MASAYA MINATO, MASASHI ...
    1986 Volume 28 Issue 6 Pages 799-806
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    In the present study, the effects of calcium antagonist [Nicardipine hydrochloride (NH)] on the prostaglandin [prostaglandin E2 (PGE2), and 6-keto-prostaglandin F (6-keto-PGF)] and thromboxane B2 levels in the blood and urine were examined in 6 patients with essential hypertension following intravenous infusion of NH for 120 minutes. At the same time, the plasma reamn activity (PRA), plasma aldosterone concentration. (PAC), and plasma and urinary electrolyte levels were also determined. During NH administration, the blood pressure was significantly decreased (p<0.05) with an increased pulse rate (p<0.05). PRA was significantly increased after NH loading (p<0.05) but PAC showed no change. The plasma PGE2 and 6-keto-PGF levels tended to increase slightly, while the blood thromboxane B2 level showed a decreasing tendency, The 6-keto-PGF to thromboxane B2 ratio was significantly increased after NH loading as compared to the preloading ratio (p<0.05), and then returned to the preloading value at about 30 minutes after discontinuation of NH loading. On the other hand, concerning the urinary excretions of PGE2, 6-keto-PGF and thromboxane B2, PGE2 and 6-keto-PGF tended to decrease after NH loading. In particular, the decrease in PGE2 was statistically significant (p<0.05). No change occurred in the urinary excretion of thromboxane B2. The above findings indicate that NH increased the plasma 6-keto-PGF to thromboxane B2 ratio but decreased the urinary excretion of prostaglandins. In addition, the possible involvement of an enhanced 6-keto-PGF/thromboxane B2 ratio in part of the hypotensive mechanism of NH is suggested.
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  • HARUTOSHI KOIDE
    1986 Volume 28 Issue 6 Pages 807-813
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    Red blood cell (RBC) membrane permeability and its interaction with Ca-antagonists in spontaneously hypertensive rats (SHR) were examined and compared with those of their normotensive control Wistar-Kyoto (WKY). Oral administration of nifedipine or diltiazem in SHR resulted in marked fall of blood pressure and vasodilating action of Caantagonists seemed to reduce the hypertonic state of SHR's vessels, so interaction of the drugs with cell membrane was considered to play critical role. On the other hand, incubation of RBC with 131I-orthoiodohippurate (OIH) showed increased membrane permeability of the RBC of SHR. Inhibition of Band 3 protein, which is responsible for the anion transport of RBC membrane, with its specific inhibitors showed that free diffusion through RBC membrane is more feasible in SHR (p<0.005), because OIH enters RBC partially through carrier (Band 3 protein) -mediated anion transport system as organic anion and partially by free diffusion. OIH has a halogen binding to aromatic ring, so it is considered to be lipophilic and easy to pass through cell membrane by diffusion. Nifedipine increased permeability of RBC membrane more in SHR than in WKY (p<0.02), but diltiazem had no effect on it. It seemed likely that as nifedipine is very insoluble in water, it interacts with cell surface but diltiazem does not do so. The difference of the reaction to nifedipine between SHR's RBC and WKY's also suggests that SHR's cell membrane differs from that of WKY.
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  • HIDEAKI YAMAZAKI, MANABU YOSHIMURA, SEHCHI KANBARA, RYOSAKU TAKASHINA, ...
    1986 Volume 28 Issue 6 Pages 815-820
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    To investigate the role of adrenal catecholamines (CAs) on the synthesis of renal CAs, renal contents of CAs, turnover of norepinephrine (NEp), urinary excretion of electrolytes and blood pressure were estimated after medullectomy (MEX) or adrenalectomy (ADX) a In the MEX-rats, renal content of NEp and NEp turnover of the kidney were significantly enhanced as compared with sham-operated rats. However, blood pressure, , heart rate, urinary excrection of electrolytes, plasma renin activity (PRA) and plasma aldosterone concentration were not different from the sham-operated rats. On the contrary, in the ADX-rats, increased content of renal NEp and enhanced turnover of NEp were observed in addition to a decrease of blood pressure, an enhanced urinary excretion of sodium, reduced urinary excretion of potassium and an increased level of PRA, as compared with the sham-operated rats. Although increased content of renal NEp and enhanced turnover of renal NEp were observed in both MEX and ADX rats, the ADX-rats showed reduction of blood pressure and a impaired urinary excretion of electrolytes which were probably due to insufficiency of adrenocortical steroid hormones. Therefore, the removal of adrenal medullary CAs induced to enhance the renal content of NEp and NEp turnover of kidney. Renal dopamine was not influenced by the removal of adrenal CA. From these results, it is suggested that the NEp synthesis of kidney was enhanced compensatively against the lack of adrenal CA for maintenance of blood pressure and electrolyte handlings of the kidney.
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  • JUNKO KOUMOTO, KENJI SODA, TOSHIO OGURA, YASUAKI MINO, TERUHIKO HATTOR ...
    1986 Volume 28 Issue 6 Pages 821-828
    Published: 1986
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    We assessed renal hematomas following percutaneous renal biopsy by using ultrasonography in 50 patients, and in 38 patients of them, computerized tomography was also used. The incidence of perirenal hematomas was 22/38(58%) checked by CT and 29/50(58%) by US. Posterior pararenal hematomas, which located outside Gerota's Fascia, were found 3/38 by CT, but only one of them was found by US. Intrarenal hematomas, with the volume of 0.5 ml to 3.5 ml, were found in 5/38 by CT, but they could not be demonstrated by US. The volume of perirenal hematomas measured by CT ranged from 2.9 ml to 367 ml, and these were statistically correlated with the products of three dimensions measured by US. There was no difference between Tru-Cut disposable needles and Vim-Silverman needles in the frequency of perirenal hematomas, but the frequency of Intrarenal hematomas was higher in using Silverman needles. A correlation was found between the fever following renal biopsy and the size of hematomas, but not between flank pain or decrease in hematocrit and the size of hematomas.
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  • AKIKATSU NAKASHIMA, TATSUHIKO TOYAMA, KOJI OKUDA, HIROSHI KURODA
    1986 Volume 28 Issue 6 Pages 829-835
    Published: 1986
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
    We presented two cases of chronic renal failure on maintenance hemodialysis, presenting macro CK (creatine kinase). The first case, 53 year-old, male, patient, has showed 500-1500IU/l of serum CK level since, which was within normal range at the start of HD therapy in. He complained of no myalgic pain or muscle atrophies. On the electrophoresis of CK isoenzyme in the serum of this patient, so called "extrabands" were detected in a broad of MM and between MM and MB bands. These components has been proved to be heat stable by heating at 56°C for 5 min. Enzyme-immunofixation electrophoresis revealed that the heavy chain of CK-linked immunoglobulin was of class α. The light chain type was identified as both κ and λ. The another case, 41 year-old, male, patient, showed macro CK linked to IgA, κ, λ during the course of maintenance hemodialysis. There were no signs suggesting the presence of malignancies in these cases. Several papers described that serum level of CK frequently increased in the patients on maintenance hemodialysis and there was a significant correlation between the serum CK level and pre-dialysis BUN level, macro CK, however, has never been detected in the patients on maintenance hemodialysis. Macro CK has been noticed in patients with some malignancies, but we could not detect any malignancies in our two cases. Therefore, some immune dyscrasia might be involved in the production of macro CK in chronic renal failure.
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