All issues
Volume 49, Issue 4
Displaying 1-11 of 11 articles from this issue
- |<
- <
- 1
- >
- >|
-
Role of the kidney in mineral metabolismMasafumi FUKAGAWA, Tadao AKIZAWA2007 Volume 49 Issue 4 Pages 404-405
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (358K) -
The kidney and mineral endocrine systemKenichi MIYAMOTO, Hiroko SEGAWA2007 Volume 49 Issue 4 Pages 406-411
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (2741K) -
Regulatory system of bone metabolism and kidneyJunichiro KAZAMA2007 Volume 49 Issue 4 Pages 412-415
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (625K) -
Ectopic calcification in CKD patientsKayo SHINOHARA, Tetsuo SHOUJI, Yoshiki NISHIZAWA2007 Volume 49 Issue 4 Pages 416-421
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (829K) -
Bone and mineral metabolism in renal tubular dysfunctionHiroyuki TANAKA2007 Volume 49 Issue 4 Pages 422-426
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (618K) -
Mineral and bone disorders with progression of CKDTakayuki HAMANO2007 Volume 49 Issue 4 Pages 427-432
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (555K) -
Conception and the control of CKD-MBDIchiro OOKIDO, Keitaro YOKOYAMA2007 Volume 49 Issue 4 Pages 433-437
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSDownload PDF (2602K) -
Histological investigation of renal pathological changes in MPO-ANCA-related nephritis using repeat renal biopsiesMasami KOMEDA, Yutaka YAMAGUCHI, Izumi YAMAMOTO, Makoto OGURA, Yasunor ...2007 Volume 49 Issue 4 Pages 438-445
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSWe compared the histological changes before and after treatment in 14 cases of myeloperoxidase antineutrophil cytoplasmic autoantibodies (MPO-ANCA)-related nephritis in whom we were able to perform two renal biopsies.
The results show that the clinical findings and acute glomerular and tubulointerstitial injuries decreased, while chronic glomerular injuries increased. No changes were seen in minor glomerular abnormalities (MGAs) or chronic tubulointerstitial injuries between the first and second biopsies. In the vascular system, no treatment-related aggravation of arteriosclerosis occurred and it was found that fibrinoid necrosis disappeared with treatment.
Finally, in MPO-ANCA-related nephritis, the care given between the first and second biopsies caused acute glomerular injuries to become chronic glomerular injuries, but no changes were detected in the MGA. We believe that the changes in acute tubulointerstitial injuries reflected an improvement in renal function, since the acute tubulointerstitial injuries obviously improved in response to PSL, contributing to the improved renal function. In other words, MPO-ANCA-related nephritis is a condition that involves “acute glomerulonephritis+acute tubulointerstitial nephritis+angiitis, ” and it is thought that the characteristics of each are independent. We believe that the renal function improved as the acute tubulointerstitial nephritis improved, while the acute glomerular injuries developed into chronic glomerular injuries.View full abstractDownload PDF (6057K) -
Yoko ITOH, Yuko TSURUMI, Toshihiro KIMURA, Yasuyo TAKESHITA, Yasuo TOK ...2007 Volume 49 Issue 4 Pages 446-451
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSWe report a case of theophylline-induced hypercalcemia. The patient, a 51-year-old women, had been administered theophylline for about five years because of bronchial asthma. She was referred to us in March 2003 for the treatment of renal failure and hypercalcemia (15.2mg/dL), which had been increasing since 2001. Clinical and laboratory findings were not consistent with any endocrinopathy. We suspected drug-induced hypercalcemia. Three months after discontinuation of theophylline therapy, the hypercalcemia was completely cured. When admitted to our hospital, the patient was diagnosed as also having Hashimoto's disease. Hyperthyroidism might enhance the effect of theophylline on parathyroid hormone action. Therefore, theophylline induced hypercalcemia even though she was taking the therapeutic level. Moreover, her calcium excretion did not increase despite hypercalcemia. We concluded that her hypercalcemia was induced by theophylline and hyperthyroidism, and that hypocalciuria might have enhanced these conditions.View full abstractDownload PDF (411K) -
Yoshikuni NAGAYAMA, Shigeki IWASAKI, Hiroyuki YAMAGUCHI, Ashio YOSHIMU ...2007 Volume 49 Issue 4 Pages 452-458
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSA 29-year-old man was admitted to our hospital because of high fever and dyspnea. About two months before this admission the patient was diagnosed as Henoch-Schönlein purpura nephritis who was treated with 40mg/day of prednisolone (PSL). When the dose of PSL was decreased to 32.5mg/day, his temperature was 40°C, the pulse was 120 beats per minute and the blood pressure was 71/36mmHg. In the peripheral blood study, the white blood cell count was 23, 800/μL and C-reactive protein was 6.1mg/dL. He was diagnosed as bilateral lower lung pneumonia by chest-computed tomography findings, non-segmental and high-density consolidation of the bilateral lower lungs. Streptococcus pneumoniae was detected from blood culture. Therefore it was concluded that sepsis was caused by severe pneumonia. Thereafter infective endocarditis was diagnosed from the findings of vegetation of both the tricuspid and mitral valves detected by ultrasonic cardiography.
Infective endocarditis resulted from septicemia caused by Streptococcus pneumoniae. The infection-related endocarditis was completely healed by early treatment including an adequate quantity of penicillin G with high sensitivity.
There have been few case reports of infective endocarditis in patients with nephritis under steroid therapy. Steroid therapy is widely used in patients with various types of nephritis including IgA nephropathy and focal segmental glomerular sclerosis in addition to Henoch-Shönlein purpura. Infective endocarditis should be recognized as a complication of steroid treatment of these patients.View full abstractDownload PDF (6558K) -
Akiko ICHIKAWA, Azusa HASHIMOTO, Ari SHIMIZU, Junnichi SHIZUKU, Yasuto ...2007 Volume 49 Issue 4 Pages 459-463
Published: May 25, 2007
Released on J-STAGE: May 18, 2010
JOURNAL FREE ACCESSA 62-year-old woman was referred to our hospital because of acute renal and liver dysfunction. Prior to admission, she had already been started on hemodyalysis filtration (HDF). She showed facial edema and lumbar pain caused by an L1 compressive fracture.
Laboratory examinations revealed hypercalcemia (13.2mg/dL), hyperammonemia (297μg/dL) and her serum creatinine, blood urea nitrogen and total bilirubin levels were 3.9mg/dL, 37.4mg/dL and 3.2mg/dL, respectively. Among the components of immunoglobulin, IgA was increased, while IgG and IgM were decreased. Serum immunoelectrophoresis revealed the presence of the IgA-kappa type of M component. Punched out lesions were noted on her head radiography. Severe plasmacytosis (60-70% of total cells) were observed by a bone marrow aspiration test, indicating the diagnosis of multiple myeloma.
Steroid pulse therapy was started with dexamethasone (40mg/day, 3days), and plasma exchange was performed 8 times with continuous HDF. These treatments failed to control hemodynamics and she died of disseminated intravascular coagulation (DIC). Autopsy demonstrated amyloid-like depositions in perisinusoidal space in the liver. In the kidney, there were nodular lesions in the glomeruli, and depositions in the basement membrane of the uriniferous tubuli. Congo red staining of these organs for amyloid yielded negative results. Immunohistochemical staining gave positive results for IgA and kappa. Electron microscopy revealed granular electron deposits in the glomeruli and tubular basement membrane as well. Taken altogether, the diagnosis of the patient could be light chain deposition disease (LCDD).View full abstractDownload PDF (3092K)
- |<
- <
- 1
- >
- >|