Atsushi Yamauchi

Publications (36)67.44 Total impact

• Article: Age and prediction of remission and relapse of proteinuria and corticosteroid-related adverse events in adult-onset minimal-change disease: a retrospective cohort study.

  Maki Shinzawa, Ryohei Yamamoto, Yasuyuki Nagasawa, Susumu Oseto, Daisuke Mori, Kodo Tomida, Terumasa Hayashi, Masaaki Izumi, Megumu Fukunaga, Atsushi Yamauchi, Yoshiharu Tsubakihara, Hiromi Rakugi, Yoshitaka Isaka
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  ABSTRACT: BACKGROUND: In adult-onset minimal-change disease (MCD) the predictors of remission and relapse of proteinuria and corticosteroid-related adverse events remain unknown. METHODS: The multicenter retrospective cohort study, the STudy of Outcomes and Practice patterns of Minimal-Change Disease (STOP-MCD), included 142 adult-onset MCD patients in 5 nephrology centers in Japan. Primary outcomes were first remission of proteinuria defined by urinary protein (UP) <0.3 g/day, UP/creatinine ratio (UPCR) <0.3, and/or negative/trace by dipstick test and first relapse of proteinuria defined by UP ≥1.0 g/day, UPCR ≥1.0, and/or dipstick test ≥1+ followed by immunosuppressive therapy. Secondary outcomes were corticosteroid-related adverse events. RESULTS: During the median 3.6 (interquartile range, 2.0-6.9) years of the entire observational period, 136 (95.8 %) and 79 (58.1 %) patients developed at least 1 remission and 1 recurrence within a median of 15 (10-34) days and 0.90 (0.55-1.57) years, respectively. Compared with younger patients aged 15-29 years at kidney biopsy, elderly patients aged ≥60 years developed remission significantly later [hazard ratio 0.53 (95 % confidence interval 0.32-0.88)], while older patients aged ≥45 years were at a significantly lower risk of relapse [45-59 years, 0.46 (0.22-0.96); 60-83 years, 0.39 (0.21-0.74)]. However, older patients were significantly more vulnerable to severe infection, diabetes, and cataract as compared with younger patients. CONCLUSION: Younger patients had a higher risk of relapse while older patients had a lower risk of relapse but a higher risk of corticosteroid-related adverse events.
  Clinical and Experimental Nephrology 03/2013; · 1.37 Impact Factor
• Article: [A case of drug-induced granulomatous interstitial nephritis during the long course of Crohn's disease].

  Seiji Itano, Ikue Nagayama, Yoshito Yamaguchi, Daisuke Mori, Natsuko Imakita, Masanobu Takeji, Atsushi Yamauchi
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  ABSTRACT: A 33-year-old man was diagnosed with Crohn's disease in 2001, and treated with mesalazine and ranitidine. Administration of infliximab was started in 2007 and led to a decrease in the activity of the Crohn's disease. He was referred to our department in the summer of 2011 following rapid progression of renal insufficiency, with serum creatinine levels increasing from 1.5 mg/dL to 4.3 mg/dL within 2 months. On admission, laboratory findings showed signs of inflammation, anemia, proteinuria, and hematuria. Renal biopsy results indicated the diagnosis of granulomatous interstitial nephritis. Neither clinical manifestations nor laboratory findings were suggestive of infectious disease, sarcoidosis, Wegener's granulomatosis or tubulointerstitial nephritis and uveitis. Mesalazine and ranitidine were discontinued in view of reports of drug-induced granulomatous interstitial nephritis. Levels of C-reactive protein immediately decreased, but renal function remained unimproved. Treatment with steroid pulse therapy was then initiated, followed by oral prednisolone at 40 mg/day, and his serum creatinine recovered to 2.3 mg/dL. Mesalazine and/or ranitidine appear to have been responsible for the granulomatous interstitial nephritis. In cases of Crohn's disease showing rapid deterioration of renal function, drug-induced renal disease should be considered, even if the drugs have been taken without apparent problems for a long duration.
  Nippon Jinzo Gakkai shi 01/2013; 55(2):167-71.
• Article: [Clinical characteristics of adult-onset minimal change nephrotic syndrome in our hospital].

  Daisuke Mori, Maki Shinzawa, Tomoko Namba, Yoshito Yamaguchi, Seiji Itano, Natsuko Imakita, Jun Matsuda, Hisako Murata, Masanobu Takeji, Ryohei Yamamoto, Yoshitaka Isaka, Atsushi Yamauchi
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  ABSTRACT: Few findings are available regarding adult-onset minimal change nephrotic syndrome (MCNS) with respect to the disease course and complications, such as acute kidney injury (AKI). We therefore performed a retrospective review to characterize the clinical presentations, steroid responsiveness and complications of adult-onset MCNS patients in our hospital. We retrospectively reviewed 40 cases of idiopathic adult-onset MCNS who had been investigated and treated at a single center. Patients between 18 and 50 years of age (Younger group) at the time of biopsy were compared with those older than 50 years (Older group) with regard to demographic data, clinical features and treatment outcome. Baseline characteristics of the 40 patients were: median age, 42 years (interquartile range: 28-63 years); male, 70%; mean (+/- standard deviation) systolic and diastolic blood pressures, 125 +/- 17 mmHg and 78 +/- 12 mmHg, respectively; estimated glomerular filtration rate (eGFR), 74 mL/min/1.73 m2 (range: 64-94 mL/min/1.73 m2); serum albumin, 1.8 +/- 0.3 g/dL; and urinary protein, 7.8 g/day (range: 3.9-10.4 g/day). All except for one patient received steroid pulse therapy. Time to complete response (CR) was 12 days (range: 8-21 days). Time to CR was significantly longer in the Older group (p = 0.011). The Late-responder group (time to CR > 2 weeks)was significantly older (p < 0.01), with a low eGFR (p < 0.001) and a higher prevalence of interstitial fibrosis in renal biopsy before the initiation of corticosteroid therapy (p < 0.05), compared with the Early-responder group. AKI was observed in 14 patients. Patients with an episode of AKI were significantly older (p = 0.005), with a lower eGFR (p < 0.002) and a higher prevalence of cellular casts (p < 0.05). At the follow-up, 19 patients (51%) had experienced relapses. The relapse rate was significantly lower in the Older group than in the Younger group (p < 0.05). The present study revealed that older patients had a longer period to CR and a higher risk of AKI at follow-up.
  Nippon Jinzo Gakkai shi 01/2012; 54(7):1023-30.
• Article: The effects of blood pressure control levels on the renoprotection of type 2 diabetic patients without overt proteinuria.

  Takashi Uzu, Yasuo Kida, Atsushi Yamauchi, Shinji Kume, Keiji Isshiki, Shin-Ichi Araki, Daisuke Koya, Masakazu Haneda, Atsunori Kashiwagi, Hiroshi Maegawa, Ryuichi Kikkawa
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  ABSTRACT: There is little evidence regarding the target blood pressure level in patients with type 2 diabetes mellitus without overt proteinuria. We followed 608 Japanese patients with type 2 diabetes without apparent cardiovascular disease and overt proteinuria who underwent cerebral magnetic resonance imaging for a mean of 7.5 years. The patients were categorized according to their mean systolic blood pressure during the follow-up period (strict: <130 mm Hg, moderate: ≥130 and <140 mm Hg, poor: ≥ 140 mm Hg). The risks for the primary composite outcome of death or end-stage renal disease were not different among the three groups. The renal risk of the doubling of serum creatinine for the poor group was significantly higher than those in other groups. In addition, among the patients without silent cerebral infarction (SCI), the renal risk was significantly lower in the strict group than in the moderate group. Further, in both the SCI and non-SCI groups, strict blood pressure control slowed the progression of albuminuria. In nonproteinuric diabetic patients without SCI, strict blood pressure control was associated with improved renal outcomes. There may be different effects of intensive blood pressure control on the renoprotection of diabetic patients according to their complications.
  Journal of the American Society of Hypertension (JASH) 12/2011; 6(2):124-31.
• Article: Gene polymorphisms contributing to hypertension in immunoglobulin A nephropathy.

  Maki Shinzawa, Ryohei Yamamoto, Yasuyuki Nagasawa, Tatsuya Shoji, Yoshitsugu Obi, Tomoko Namba, Harumi Kitamura, Tetsuya Kaneko, Noriyuki Okada, Hirotsugu Iwatani, Atsushi Yamauchi, Yoshiharu Tsubakihara, Enyu Imai, Yoshitaka Isaka, Hiromi Rakugi
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  ABSTRACT: Hypertension, which is affected by genetic and environmental factors, is one of the major risk factors for chronic kidney disease. Identification of the genetic factor contributing to hypertension in patients with chronic kidney disease may potentially refine a therapeutic strategy. In the present multicenter cross-sectional study, 240 patients were eligible (aged 15-50 years with urinary protein ≥0.25 g/day) out of 429 patients who were diagnosed as having immunoglobulin (Ig) A nephropathy (IgAN) by renal biopsy between 1990 and 2005 and enrolled in our previous study, PREDICT-IgAN. The outcome was hypertension defined as ≥140 and/or ≥90 mmHg of systolic and diastolic blood pressure and/or use of antihypertensives at renal biopsy. We assessed associations between hypertension and 28 polymorphisms with the frequency of minor genotype ≥10% among 100 atherosclerosis-related polymorphisms using the Chi-squared test in dominant and recessive models. We identified polymorphisms associated with hypertension in multivariate logistic regression models. Baseline characteristics: hypertension 36.3%. Among 28 polymorphisms, the Chi-squared test revealed that CD14 (-159CC vs CT/TT, P = 0.03) and ACE (DD vs DI/II, P = 0.03) were significantly associated with hypertension after Bonferroni correction. Multivariate logistic regression models revealed that CD14 -159CC [vs CT/TT, odds ratio (OR) 3.58 (95% confidence interval (CI) 1.66-7.63)] and ACE DD [vs DI/II, OR 4.41 (95% CI 1.80-10.8), P = 0.001] were independently associated with hypertension. CD14 C-159T and ACE I/D contributed to hypertension in patients with IgAN.
  Clinical and Experimental Nephrology 11/2011; 16(2):250-8. · 1.37 Impact Factor
• Article: A candidate gene approach to genetic contributors to the development of IgA nephropathy.

  Ryohei Yamamoto, Yasuyuki Nagasawa, Tatsuya Shoji, Naoto Katakami, Kentaro Ohtoshi, Rieko Hayaishi-Okano, Yoshimitsu Yamasaki, Atsushi Yamauchi, Yoshiharu Tsubakihara, Enyu Imai, Hiromi Rakugi, Yoshitaka Isaka
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  ABSTRACT: Genetic factors contributing to the development of IgA nephropathy remain to be elucidated. The present multicenter cross-sectional case-control study measured genotype frequencies of 65 atherosclerotic disease-related gene polymorphisms in 230 Japanese patients with IgA nephropathy and 262 apparently healthy volunteers with estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m(2) and negative or trace proteinuria and hematuria by dipstick test [non-chronic kidney disease (CKD) participants]. Clinical characteristics at kidney biopsy of patients with IgA nephropathy and those at the study recruitment of non-CKD participants were included as covariates in multivariate logistic regression models. Among 31 gene polymorphisms with ≥5% of minor genotype in non-CKD participants, methionine synthase MTR A2756G (D919G) was significantly associated with IgA nephropathy using χ(2) test even after controlling for family-wise error rate by the method of Bonferroni (P = 0.044). A multivariate nonconditional logistic regression model identified MTR A2756G as a significant contributor of IgA nephropathy [2756AG and GG versus AA, odds ratio 0.42 (95% confidence interval 0.25-0.69) and 0.21 (95% confidence interval 0.06-0.68), P(trend) < 0.001]. After each patient with IgA nephropathy was randomly matched to a non-CKD participant on age (±5 years), gender, mean arterial pressure (±5 mmHg) and eGFR (±5 mL/min/1.73 m(2)), a multivariate conditional logistic regression model also verified their significant association [odds ratio 0.42 (95% confidence interval 0.18-1.00) and odds ratio 0.09 (95% confidence interval 0.01-0.73), P(trend) = 0.004]. MTR A2756G was not associated with slope of eGFR (mL/min/1.73 m(2)/year) in 230 patients with IgA nephropathy. MTR A2756G was associated with the development, but not progression, of IgA nephropathy.
  Nephrology Dialysis Transplantation 07/2011; 27(3):1020-30. · 3.40 Impact Factor
• Article: A case of MPO-ANCA-positive polyarteritis nodosa complicated by exudative otitis media, mononeuritis multiplex, and acute renal failure.

  Takeshi Yamamoto, Jun Matsuda, Hiroyuki Kadoya, Daisuke Mori, Daisuke Ito, Tomoko Namba, Masanobu Takeji, Megumu Fukunaga, Atsushi Yamauchi
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  ABSTRACT: In December 2008, a 69-year-old Japanese woman was admitted to the Department of Otorhinolaryngology because of hearing impairment due to bilateral exudative otitis media, and was discharged without complete recovery despite conventional treatment. Two weeks later, she was readmitted for worsened deafness, numbness, gait disturbance, and general fatigue. She was referred to our department for general investigation. On admission, laboratory examination revealed severe inflammatory signs and active nephritic urinary sediments. Cranial computed tomography (CT) revealed progressive exudative otitis media and sinusitis. Initially, Wegener's granulomatosis was suspected. Nasal cavity biopsy, however, showed no granuloma formation or vasculitis. Serology revealed high titer of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA), suggestive of microscopic polyangitis (MPA). However, contrast CT identified stenosis of a celiac artery, and renal biopsy showed tubulointerstitial changes with minor glomerular abnormalities. Therefore, polyarteritis nodosa (PAN) was suspected and treatment with intravenous methylprednisolone was initiated. However, a lacunar infarct developed followed by cerebral hemorrhage, and the patient died 19 days after readmission. Autopsy revealed fibrinoid necrosis, neutrophilic infiltration, and giant cell reaction in small to medium-sized arteries in multiple organs. These findings led to diagnosis of systemic vasculitis anatomically compatible with PAN. This was a rare case of a patient with MPO-ANCA-positive PAN who may have developed bilateral exudative otitis media and hearing loss as the initial manifestation of PAN.
  Clinical and Experimental Nephrology 05/2011; 15(5):754-60. · 1.37 Impact Factor
• Article: [Case of mixed connective tissue disease complicated with sarcoidosis and central diabetes insipidus].

  Jun Matsuda, Daisuke Ito, Daisuke Mori, Hiroyuki Kadoya, Hisako Murata, Masanobu Takeji, Atsushi Yamauchi
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  ABSTRACT: In 2003, a 64-year-old woman was diagnosed with mixed connective tissue disease and treated with oral prednisolone (30 mg/day). The prednisolone dose was gradually decreased, and a dose of 5 mg/day had been maintained since 2004. In 2009, she gradually developed vision loss, malaise, anorexia, and throat pain due to hydrodipsia. She was noted to have iritis and vitreous opacity by an ophthalmologist, and was referred for further evaluation. Fine rales were audible throughout the entire lung field, and chest CT showed diffuse small nodules that were more prominent on the upper and middle lobes, and swelling of the mediastinal and hilar lymph nodes. Transbronchial lung biopsy showed many epithelioid granulomas with multinuclear giant cells, compatible with sarcoidosis. Polyuria was identified as a cause of hydrodipsia and a diagnosis of partial central diabetes insipidus was made. High-dose prednisolone (40 mg/day) together with intranasal administration of desmopressin resulted in improvement of all of her clinical symptoms. MCTD followed by sarcoidosis is rare. Furthermore, this is the first reported case of MCTD complicated by sarcoidosis and central diabetes insipidus.
  Nippon Jinzo Gakkai shi 01/2011; 53(7):1041-5.
• Article: Azelnidipine-induced chyloperitoneum in a patient with microscopic polyangiitis.

  Takeshi Yamamoto, Jun Matsuda, Hiroyuki Kadoya, Tomoko Namba, Masanobu Takeji, Atsushi Yamauchi
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  ABSTRACT: A 76-year-old man developed fever and appetite loss, and then was referred to our hospital because of rapidly progressive renal insufficiency; his serum creatinine increased from 1.2 to 5.9 mg/dl within 1 month. On admission, his blood pressure was 166/92 mmHg, and laboratory findings showed signs of inflammation, anemia, proteinuria, and hematuria. Chest computed tomography (CT) suggested interstitial pneumonia, while a renal biopsy revealed that small arteries and arterioles were affected, and there was pauci-immune glomerulonephritis with cellular and fibrocellular crescents. In addition, an increased myeloperoxidase antineutrophil cytoplasmic antibody titer confirmed microscopic polyangiitis. Treatment with oral prednisolone was initiated and seemed to successfully resolve the vasculitis activity. On the 11th day of admission, a calcium channel blocker, azelnidipine, was added to treat hypertension. Two days later, the patient developed abdominal distension, and abdominal CT showed massive ascites. The ascitic fluid was a milky white transudate with a normal leukocyte count. Neither clinical manifestations nor laboratory findings suggestive of liver cirrhosis, malignancy, infectious peritonitis, or bowel perforation were observed. On the 18th day of admission, azelnidipine was discontinued in view of reports of calcium channel blocker-induced chyloperitoneum in patients undergoing peritoneal dialysis. Immediately, the abdominal distension disappeared, and the ascites appeared to decrease. Azelnidipine appears to have been responsible for the chyloperitoneum. Since a few cases of secondary vasculitis developing chyloperitoneum have been previously reported, vasculitis may have played a role in the development of chyloperitoneum.
  Clinical and Experimental Nephrology 10/2010; 14(5):496-500. · 1.37 Impact Factor
• Article: Cigarette smoking and progression of IgA nephropathy.

  Ryohei Yamamoto, Yasuyuki Nagasawa, Tatsuya Shoji, Hirotsugu Iwatani, Takayuki Hamano, Noritaka Kawada, Kazunori Inoue, Takuya Uehata, Tetsuya Kaneko, Noriyuki Okada, Toshiki Moriyama, Masaru Horio, Atsushi Yamauchi, Yoshiharu Tsubakihara, Enyu Imai, Hiromi Rakugi, Yoshitaka Isaka
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  ABSTRACT: Multiple community-based cohort studies of mainly middle-aged and elderly populations have shown that cigarette smoking is a risk factor for chronic kidney disease. However, little information is available about an effect of cigarette smoking on progression of primary kidney diseases, including immunoglobulin A (IgA) nephropathy. Retrospective cohort study. 971 of 1,001 patients with a diagnosis of IgA nephropathy in 3 major nephrology centers in Osaka, Japan, between 1992 and 2005 who enrolled in the Study of Outcome and Practice Pattern of IgA Nephropathy (STOP-IgAN). Smoking status and number of cigarettes smoked at the time of diagnosis using kidney biopsy. Dose-dependent associations between cigarette smoking and outcomes were assessed in multivariate Cox proportional hazards models. Significantly different clinical characteristics between non-/past and current smokers were controlled for using propensity score-based adjustment, stratification, and matching. 50% increase in serum creatinine level as primary outcome. A composite outcome of a 100% increase in serum creatinine level or end-stage renal disease (ESRD) and ESRD alone as secondary outcomes. During the median 5.8 years (interquartile range, 2.6-10.2) of the observational period, 117 participants progressed to a 50% increase in serum creatinine level and 47 advanced to ESRD. Multivariate Cox proportional hazards models identified current smokers (HR, 2.03 [95% CI, 1.33-3.10] for primary outcome) and number of cigarettes at kidney biopsy (HR, 1.21 [95% CI, 1.06-1.39] per 10 cigarettes per day) as significant predictors of outcomes. Propensity score-based models confirmed these results. Tests for interaction showed that the association of current smoking with adverse outcomes was stronger in those with lower compared with higher estimated glomerular filtration rates. Baseline smoking status was not verified using biochemical tests. Smoking status during the observational period was unavailable. Cigarette smoking, in a dose-dependent manner, was identified as a key prognostic factor in IgA nephropathy. Smoking cessation should be encouraged as part of the treatment for IgA nephropathy.
  American Journal of Kidney Diseases 08/2010; 56(2):313-24. · 5.43 Impact Factor
• Article: Successful treatment of HCV-related cryoglobulinemic glomerulonephritis with double-filtration plasmapheresis and interferon combination therapy.

  Tomoko Namba, Rie Shiba, Takeshi Yamamoto, Yasuhiro Hirai, Takuma Moriwaki, Jun Matsuda, Hiroyuki Kadoya, Masanobu Takeji, Yukinori Yamada, Harumasa Yoshihara, Atsushi Yamauchi
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  ABSTRACT: A 67-year-old, hepatitis C virus (HCV)-positive woman was admitted to our hospital because of proteinuria and leg edema. Laboratory examination showed decreased serum albumin and complement activity and positive cryoglobulin. The HCV RNA genotype was 1b with high viral load. Kidney biopsy showed membranoproliferative glomerulonephritis (MPGN) with capillary deposition of C3, IgM, and IgG, indicating HCV-associated glomerulonephritis. In addition to interferon (IFN) therapy, double-filtration plasmapheresis (DFPP) was performed to reduce HCV RNA blood levels in the early stage of IFN therapy. This treatment greatly reduced the viral load and induced clinical remission of MPGN, suggesting that DFPP plus IFN combination therapy may represent a potentially effective modality for refractory-type HCV-associated glomerulonephritis.
  Clinical and Experimental Nephrology 05/2010; 14(4):372-6. · 1.37 Impact Factor
• Article: Cerebral microvascular disease predicts renal failure in type 2 diabetes.

  Takashi Uzu, Yasuo Kida, Nobuo Shirahashi, Tamaki Harada, Atsushi Yamauchi, Makoto Nomura, Keiji Isshiki, Shin-Ichi Araki, Toshiro Sugimoto, Daisuke Koya, Masakazu Haneda, Atsunori Kashiwagi, Ryuichi Kikkawa
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  ABSTRACT: Abnormalities in small renal vessels may increase the risk of developing impaired renal function, but methods to assess these vessels are extremely limited. We hypothesized that the presence of small vessel disease in the brain, which manifests as silent cerebral infarction (SCI), may predict the progression of kidney disease in patients with type 2 diabetes. We recruited 608 patients with type 2 diabetes without apparent cerebrovascular or cardiovascular disease or overt nephropathy and followed them for a mean of 7.5 years. At baseline, 177 of 608 patients had SCI, diagnosed by cerebral magnetic resonance imaging. The risk for the primary outcome of ESRD or death was significantly higher for patients with SCI than for patients without SCI [hazard ratio, 2.44; 95% confidence interval (CI) 1.36 to 4.38]. The risk for the secondary renal end point of any dialysis or doubling of the serum creatinine concentration was also significantly higher for patients with SCI (hazard ratio, 4.79; 95% CI 2.72 to 8.46). The estimated GFR declined more in patients with SCI than in those without SCI; however, the presence of SCI did not increase the risk for progression of albuminuria. In conclusion, independent of microalbuminuria, cerebral microvascular disease predicted renal morbidity among patients with type 2 diabetes.
  Journal of the American Society of Nephrology 03/2010; 21(3):520-6. · 9.66 Impact Factor
• Article: [Adult case of severe Henoch-Schönlein purpura associated with steroid-resistant nephrotic syndrome successfully treated with intravenous cyclophosphamide].

  Tomoko Namba, Takeshi Yamamoto, Jun Matsuda, Hiroyuki Kadoya, Masanobu Takeji, Atsushi Yamauchi
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  ABSTRACT: Henoch-Schönlein purpura (HSP) is a systemic disorder characterized by small vessel vasculitis with the deposition of IgA immune complexes. Renal involvement is the major cause of morbidity and mortality in patients with HSP. We report here a 37-year-old female patient with HSP nephritis (HSPN) associated with steroid-resistant nephrotic syndrome and renal dysfunction despite conventional therapy. The patient was successfully treated with intravenous cyclophosphamide following treatment with intravenous pulse methylprednisolone and oral prednisolone. The combination therapy resulted in a significant decrease in proteinuria, together with improvement of renal function. The patient finally reached a stage of clinical remission.
  Nippon Jinzo Gakkai shi 01/2010; 52(1):66-72.
• Article: [Clinical characteristics of five elderly patients with severe hypokalemia induced by glycyrrhizin derivatives].

  Takeshi Yamamoto, Masaki Hatanaka, Jun Matsuda, Hiroyuki Kadoya, Atsushi Takahashi, Tomoko Namba, Masanobu Takeji, Atsushi Yamauchi
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  ABSTRACT: Although hypokalemia is a common clinical problem, symptoms generally do not become manifest unless the serum potassium (K) falls rapidly. We encountered five cases with symptomatic severe hypokalemia (K<2.0 mEq/L) hospitalized for the past 15 months at our hospital. We examined the clinical characteristics and treatment of these patients. All five patients were women, and their mean age was 77.8 (73-82)years. They suffered from hypertension. Mean K level at admission was 1.66 (1.4-1.9) mEq/L and HCO3(-) was 48.3 (33.6-56.1) mmol/L. Plasma aldosterone level was low and plasma rennin activity was suppressed. All patients developed progressive muscle weakness with elevated creatinine phosphokinase. Three of the patients had received Chinese medicine which contained licorice, one received glycyrrhizin and the other one had received both. We diagnosed these cases as pseudoaldosteronism induced by glycyrrhizin. With discontinuation of the drugs and intravenous as well as oral K supplementation, serum K were normalized and clinical symptoms improved within 12 days. For one patient who developed cardiac dysfunction, concentrated K solution (230 mEq/L) was infused into the central vein. These findings show that glycyrrhizin ingestion should be kept in mind as a cause of an extreme degree of an hypokalemia, especially in elderly patients.
  Nippon Jinzo Gakkai shi 01/2010; 52(1):80-5.
• Article: [Case of AL amyloidosis associated with a remarkable histological progress in a short period].

  Hiroyuki Kadoya, Tomoko Namba, Jun Matsuda, Takeshi Yamamoto, Masanori Takeji, Atsushi Yamauchi
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  ABSTRACT: AL amyloidosis is the most common form of systemic amyloidosis. Although kidney biopsy often is the method by which the disease is identified, small amounts of amyloid in kidney biopsy specimens may be missed on routine examination unless specifically investigated. We present here a previously healthy 60-year-oldmissed on routine examination unless specifically investigated. We present here a previously healthy 60-year-old man who developed nephrotic syndrome. His first renal biopsy showed minimal change nephrotic syndromeman who developed nephrotic syndrome. His first renal biopsy showed minimal change nephrotic syndromesuggesteda subtle depost ommon formsystemicamyloidfibrilhediminationof an early lesion of renal amyloido-s (MCNS). Proteinuria remained refractory to immunosuppressive treatments. Six months later, a repeat renal biopsy clearly showed AL amyloidosis. Re-examination of the first biopsy in the light of the final diagnosis again suggested a subtle deposition of amyloid fibrils. The discrimination of an early lesion of renal amyloidosis with MCNS may often be difficult. It is necessary to maintain a high level of alertness for amyloidosis especially in aged patients with nephrotic syndrome and to consider a repeat biopsy in steroid-resistant cases.
  Nippon Jinzo Gakkai shi 01/2010; 52(5):590-4.
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  Article: A candidate gene approach to genetic prognostic factors of IgA nephropathy--a result of Polymorphism REsearch to DIstinguish genetic factors Contributing To progression of IgA Nephropathy (PREDICT-IgAN).

  Ryohei Yamamoto, Yasuyuki Nagasawa, Tatsuya Shoji, Kazunori Inoue, Takuya Uehata, Tetsuya Kaneko, Tomonori Okada, Atsushi Yamauchi, Yoshiharu Tsubakihara, Enyu Imai, Yoshitaka Isaka, Hiromi Rakugi
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  ABSTRACT: Renal prognosis of IgA nephropathy (IgAN) is affected by environmental and genetic factors. Other studies demonstrated that some atherosclerotic disease-related genes were significantly associated with renal prognosis. The Polymorphism REsearch to DIstinguish genetic factors Contributing To progression of IgAN (PREDICT-IgAN) was a multicentre retrospective observational study to investigate associations between progression of IgAN (a 50% increase of serum creatinine level and slope of eGFR) and a hundred atherosclerotic disease-related gene polymorphisms, mainly single nucleotide polymorphisms (SNPs) in 320 IgAN patients who had more than a normal range of urinary protein (> or =0.25 g/day) at diagnosis. During 8.3 +/- 4.2 years of a follow-up period, 83 patients (25.9%) developed progression. In log-rank tests, glycoprotein Ia GPIa C807T and G873A and intercellular adhesion molecule-1 ICAM-1 A1548G (K469E) were found to be significantly associated with progression even after adjustment for multiple comparisons by the method of Bonferroni (adjusted P = 0.0174, 0.0176 and 0.0430, respectively). In a multivariate Cox proportional-hazards model, GPIa 807TT (873CC) [versus 807TT, adjusted hazard ratio 2.05 (95% confidence interval 1.13-3.71)] and ICAM-1 1548GG [versus 1548AA, 2.55 (1.40-4.65)] were identified as independent genetic predictors of progression, along with conventional clinical prognostic factors such as eGFR, urinary protein and use of antihypertensives at diagnosis. PREDICT-IgAN distinguished GPIa C807T/ G873A and ICAM-1 A1548G from multiple athero- sclerotic disease-related gene polymorphisms by their predictive indicator for progression of IgAN.
  Nephrology Dialysis Transplantation 05/2009; 24(12):3686-94. · 3.40 Impact Factor
• Article: Probucol inhibits intercellular adhesion molecule‐1 expression on cultured rat mesangial cells

  Toshihiro SUGIURA, Akira WADA, Atsushi YAMAUCHI, Masaru HORIO, Enyu IMAI, Masatsugu HORI
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  ABSTRACT: Interleukin-1 (IL-1) has been reported to participate in the progression of glomerulonephritis by, in part, up-regulating intercellular adhesion molecule-1 (ICAM-1) expression in experimental glomerulonephritis. In the present study, we examined whether probucol, an antihyperlipidemic agent, inhibited IL-1-induced inflammatory processes in mesangial cells in culture. Northern blot analysis demonstrated that 200 U/mL IL-1 up-regulated ICAM-1 messenger RNA (mRNA) expression with its peak at 4-6 h after stimulation. Ten μg/mL lipopolysaccharide (LPS), a stimulant to release IL-1 from mesangial cells, induced ICAM-1 mRNA expression by five-fold within 6 h and 10 μg/mL probucol notably reduced this induction. Immunoblotting also confirmed that LPS increased ICAM-1 protein by two-fold within 24 h and probucol inhibited this increase. IL-1 receptor antagonist (IL-1ra; 1–100 ng/mL) suppressed LPS-induced ICAM-1 mRNA expression in a dose-dependent manner and 100 ng/mL IL-1ra completely inhibited ICAM-1 induction, indicating that LPS increased ICAM-1 expression through the action of secreted IL-1. Interleukin-1 activity in culture media, measured by thymocyte proliferation assay, was significantly enhanced by LPS and inhibited by probucol. However, neither LPS nor probucol substantially affected IL-1 mRNA expression, suggesting that the IL-1 activity might be regulated at post-translational level. These results suggest that probucol may act as an anti-inflammatory drug by suppressing IL-1 activity from mesangial cells in the progression of glomerulonephritis.
  Nephrology 06/2008; 4(1‐2):75 - 80. · 1.31 Impact Factor
• Article: [Case of scleroderma with rapid progressive glomerulonephritis associated with both MPO-ANCA and anti-GBM antibodies].

  Tomoko Namba, Masaki Hatanaka, Atsushi Takahashi, Masanobu Takeji, Ken Takahara, Takashi Uzu, Atsushi Yamauchi
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  ABSTRACT: A 66-year-old male with scleroderma developed rapidly progressive glomerulonephritis (RPGN). Renal pathology revealed crescentic glomerulonephritis with interstitial inflammation and fibrosis. Immunofluorescent micrography showed linear deposition of IgG along the glomerular capillary wall. Both anti-glomerular basement membrane antibody (anti-GBM Ab), and myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) were detected by an enzyme-linked immunosorbent assay (ELISA). These findings were compatible with ANCA-related vasculitis and anti-GBM Ab nephritis. Laboratory findings showed rapid elevation of the serum creatinine level (5.9 mg/dL), and a high titer of MPO-ANCA (530 EU) and anti-GBM Ab (21 EU). He was started on methylprednisolone pulse therapy and temporary hemodialysis. Since the immunosuppressive therapy lowered both antibody titers steadily and improved renal function, hemodialysis was discontinued 4 weeks after the therapy. It has been reported that some scleroderma patients developed rapid progressive glomerulonephritis due to ANCA-associated vasculitis in addition to the typical scleroderma renal crisis. There have been few reports of a scleroderma patient associated with RPGN, in whom both MPO-ANCA and anti GBM antibodies were detected.
  Nippon Jinzo Gakkai shi 02/2008; 50(1):64-8.
• Article: Treatment of diffuse alveolar hemorrhage with plasmapheresis plus steroids in patients with MPO-ANCA associated vasculitis

  Ken Takahara, Tomoko Namba, Atsushi Takahashi, Masaki Hatanaka, Takeshi Yamamoto, Masanobu Takeji, Atsushi Yamauchi
  Nihon Toseki Igakkai Zasshi 01/2008; 41(6):371-376.
• Article: New therapeutic strategies of molecular intervention in glomerulonephritis

  Enyu IMAI, Yoshitaka ISAKA, Yoshitaka AKAGI, Yutaka ANDO, Makoto ARAI, Tetsuya KANEKO, Masaru TAKENAKA, Toshiki MORIYAMA, Atsushi YAMAUCHI, Masaru HORIO, Akio ANDO, Yoshimasa ORITA, Naohiko UEDA
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  ABSTRACT: Recent progress of genetic engineering allows us to create animal models expressing the new genetic phenotype and also indicates a sure future for clinical use of gene therapy. We applied HVJ-liposome method for manipulation of transforming growth factor (TGF)-β gene expression in anti-Thy-1 experimental glomerulonephritis. Either the glomerular introduction of TGF-β antisense oligodeoxynucleotides or transfection of gene for decorin, a natural inhibitor of TGF-β, into the skeletal muscle could suppress the extracellular matrix (ECM) expansion in glomerulonephritis. Thus, these results may suggest the potential of gene therapy as a novel treatment for fibrotic diseases caused by TGF-β.
  Nephrology 04/2007; 3(s2):s755 - s757. · 1.31 Impact Factor