The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Volume 43, Issue 1
Displaying 1-6 of 6 articles from this issue
  • [in Japanese]
    2001 Volume 43 Issue 1 Pages 1-19
    Published: January 25, 2001
    Released on J-STAGE: July 04, 2011
    JOURNAL FREE ACCESS
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  • Yukihiko TAKEDA, Isao SHIRATO, Kayo HAYASHI, Jin-Song HE, Yasuhiko TOM ...
    2001 Volume 43 Issue 1 Pages 20-27
    Published: January 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Protein gene product 9.5 (PUP 9.5) is expressed specifically in neuroendocrine cells and considered to be one of the neuroendocrine markers. Recently, we reported that PGP 9.5 is localized in the parietal epithelial cells (PECs) of Bowman's capsules as well as in neural tissues. In the present study, immunohistochemical analysis of POP 9.5 as a specific marker of the PECs of Bowman's capsules, synaptopodin as a podocyte-specific marker, and ED -I as a specific marker of monocytes/macrophages was performed in the cellular crescents in anti-GBM antibody induced glomerulonephritis of WKY rats using serial renal sections. In the acute phase of anti-GBM antibody induced glomerulonephritis, and the expression of POP 9.5 and ED-1 was observed diffusely in proliferating cells of cellular crescents. However, in most part of cellular crescents, PGP 9.5 positive areas did not overlap with the ED-I positive areas. Synaptopodin was constantly detected along the glomerular tufts compressed by the crescents. In the chronic phase of this disease, PGP 9.5 was observed in the cells covering the surface of fibrous crescents or scattered within fibrocellular crescents. Synaptopodin was partially detected in such cells. It appears that cellular crescents are composed mainly of proliferating PECs and macrophages in rat anti-GBM antibody induced glomerulonephritis.
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  • Kaoru HAMADA
    2001 Volume 43 Issue 1 Pages 28-34
    Published: January 25, 2001
    Released on J-STAGE: March 01, 2011
    JOURNAL FREE ACCESS
    In the present study, the role of the angiotensin II type 2 receptor in the regulation of medullary blood flow in conscious Spontaneous Hypertensive Rats (SHR) was investigated. We tested the hypothesis that AT2 receptor activation may exert the opposite effects of AT 1 recptors in terms of renal hemodynamics. Mean arterial pressure (MAP), daily sodium balance, cortical blood flow (CBF), and medullary blood flow (MBF) were measured over a 10-day protocol in several groups of rats in which optical fibers for laser-Doppler Flowmetry had been implanted and which received the following drug combinations the AT1 receptor antagonist CV 11976 (CV) alone and CV plus AT2 receptor antagonist PD 123319 (PD). In the CV alone group, the renal interstitial administration of CV decreased MAP, caused sodium diuresis, and increased MBF significantly. In the CV plus PD group, the renal interstitial administration of PD prevented sustained hypotension, sodium diuresis, and increased medullary blood flow during CV administration. These data indicated that AT2 receptor activation leads to vasodilation in the renal medulla and an antihypertensive effect in SHR. AT2 receptors play an important role in the renal medullary blood flow.
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  • Junichi MINAMI, Kei ON, Hideki INADA, Hidehiko ONO, Toshihiko ISHIMITS ...
    2001 Volume 43 Issue 1 Pages 35-38
    Published: January 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    Congenital nephrogenic diabetes insipidus is a rare disorder in which the kidney is insensitive to the antidiuretic hormone, vasopressin. In most cases, a mutation in the vasopressin type 2(V2) receptor gene is the genetic cause of the disease. So far, few cases of congenital nephrogenic diabetes insipidus with hypertension have been reported. We report one male case of congenital nephrogenic diabetes insipidus accompanied by hypertension. The patient was a 24-year-old man who had suffered from polyuria and polydipsia since infancy and had been found to have hypertension at about 16 years. He was admitted to hospital in May 2000 for investigation of polyuria and hypertension with a high plasma level of renin activity of 10.4 ng/ml/hr. On physical examination, the blood pressure was 150/90 mmHg and the daily urinary output was 18.5 l. There was no change in urine volume and urine osmolality after an intramascular injection of vasopressin and water deprivation. The blood pressure and plasma renin activity were increased from 127/73 mmHg to 146/87 mmHg and from 4.9 ng/ml/hr to 6.1 ng/ml/hr, respectively, by a 4-hour dehydration test. He was found to have a C-to-T transition at nucleotide position 675 by sequencing analysis of the V2 receptor gene. After administration of hydrochlorothiazide, both the blood pressure and urine volume were reduced. Consequently, it was suggested that activation of the renin-angiotensin system by dehydration, at least in part, contributed to high blood pressure in this case.
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  • Keiko TAKAHASHI, Ashio YOSHIMURA, Yoshihiko INOUE, Naoki TAKAHASHI, Yo ...
    2001 Volume 43 Issue 1 Pages 39-43
    Published: January 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    A 81-year-old woman was admitted to our hospital because of edema and massive proteinuria on September 26, 1995. On admission, the palpebral conj uctiva were slightly anemic, and edema of the eyelids and legs was observed. Laboratory findings were as follows, urine protein (3+), occult blood (3+), WBC 2, 600/μl, Hgb 10.0 g/dl, reticulocytes 20‰, TP 5.0 g/dl, Alb 2.7 g/dl, T-Cho 376 mg/dl, TG 194 mg/dl, LDH 763 U/l, haptoglobin < 93 mg/dl, Ham's test (+), sugar water test (+), and indirect coombs (+). The erythrocytes of this patient showed a negative population consisting of double negative erythrocytes evaluated by flow cytometric two-color analysis using monoclonal antibodies specific to CD55 and CD59. From these findings, the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH) was made. The patient showed nephrotic syndrome and a renal biopsy was performed. The histological findings of renal biopsy showed focal and segmental sclerosis and adhesion of glomerular tufts. Interstitial fibrosis with atrophic tubules and lymphocyte infiltration were also observed. There was no specific staining of immunoglobulins and complement by immunofluorescence. The diagnosis of focal segmental glomerular sclerosis (FSGS) was made. There have been only three case reports of glomerular disease in patients with PNH, such as purpura nephritis, IgA nephropathy and membranous nephropathy. The complication of FSGS and PNH is very rare and there has been no report of FSGS in a case with PNH. The onset of PNH resulted from the loss of CD55 and CD59, which was critical in the onset of FSGS in the present case.
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  • Masao TOYODA, Daisuke SUZUKI, Goroh UEHARA, Tomoya UMEZONO, Terumi HOR ...
    2001 Volume 43 Issue 1 Pages 44-48
    Published: January 25, 2001
    Released on J-STAGE: July 05, 2010
    JOURNAL FREE ACCESS
    We experienced two cases of limb edema of unknown pathogenesis. No evidence was found concerning involvement of the kidneys, heart of other visceral organs. Case I was 22-year-old woman. Her white blood cell count increased to 13, 100/μl with 65.0 % eosinophils. Case 2 was a 27-year-old woman. Her white blood cell count increased to 23, 300/μl with 67.0 % eosinophils. In these cases, extensive diagnostic evaluations revealed no evidence of atopy, neoplasms, collagen vascular disease, or parasitic infestation. We diagnosed these cases as episodic angioedema with eosinophilia. In both cases, the angioedema improved gradually in parallel with a decrease in the white blood cell count. This disorder is very rare, but it is very important to consider it in differential diagnosis especially for nephrologists.
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