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Featured researches published by Fuminori Sato.


Hypertension | 2003

Interaction Between ACE and ADD1 Gene Polymorphisms in the Progression of IgA Nephropathy in Japanese Patients

Ichiei Narita; Shin Goto; Noriko Saito; Jin Song; Junya Ajiro; Fuminori Sato; Daisuke Saga; Daisuke Kondo; Kohei Akazawa; Minoru Sakatsume; Fumitake Gejyo

Abstract—An interaction effect between the angiotensin-converting enzyme insertion/deletion (ACE I/D) and &agr;-adducin (ADD1) Gly460Trp polymorphisms (G460W) on blood pressure regulation has recently been suggested, although its significance in the prognosis of renal function in IgA nephropathy (IgAN) has not been fully investigated. Therefore, we evaluated the clinical manifestations and renal prognosis in 276 Japanese patients with histologically proven IgAN with respect to their ACE I/D and ADD1 G460W polymorphisms. The prognosis of renal function was analyzed by Kaplan-Meier survival curves and multivariate Cox proportional-hazards regression models. Baseline data, including blood pressures, proteinuria, renal function, and incidence of hypertension, were similar for the different genotypes of ACE and ADD1. The individual genotypes taken alone were not associated with the progression of renal dysfunction. However, renal survival of patients with the 460WW polymorphism of ADD1 was significantly worse within the group with the II genotype of ACE (Kaplan-Meier, log rank test; &khgr;2=6.062, P =0.0138) but not for those with other ACE genotypes. In the Cox proportional-hazards regression model with adjustment for clinical risk factors, including hypertension, proteinuria, and no administration of an angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, the 460WW variant of ADD1 was a highly significant and independent risk factor only for patients with the ACE II genotype, with a hazard ratio of 3.65 (P =0.0016), but not for those with other ACE genotypes (hazard ratio=0.65, P =0.2902). These findings suggest an interaction between ACE and ADD1 polymorphisms not only on blood pressure regulation but also on the progression of renal dysfunction in patients with IgAN.


Clinical and Experimental Nephrology | 2005

Monocyte chemoattractant protein-1 A-2518G gene polymorphism and renal survival of Japanese patients with immunoglobulin A nephropathy.

Honami Mori; Yoshikatsu Kaneko; Ichiei Narita; Shin Goto; Noriko Saito; Daisuke Kondo; Fuminori Sato; Junya Ajiro; Daisuke Saga; Asa Ogawa; Minoru Sakatsume; Mitsuhiro Ueno; Kaoru Tabei; Fumitake Gejyo

BackgroundMonocyte chemoattractant protein (MCP)-1 is closely related to the pathogenesis of the progression of various chronic renal diseases, including IgA nephropathy (IgAN), through its chemoattractant effect on macrophages. However, the correlation of MCP-1 gene polymorphism with the long-term prognosis of Japanese patients with IgAN has not been clearly determined yet.MethodsWe investigated 277 Japanese patients diagnosed with IgAN based on renal biopsy to clarify the association between the progression of IgAN and MCP-1 gene polymorphism at position A-2518G, which regulates the transcription of the MCP-1 gene.ResultsThe incidence of endstage renal disease was significantly higher in patients with the AA genotype (47.1%) compared to those with the AG (24.1%) or GG (27.4%) genotype (P = 0.024). Moreover, Kaplan-Meier analysis revealed that the AA genotype significantly facilitated the progression of renal disease (log rank; P = 0.0029), and Cox proportional hazards regression model analysis showed that the AA genotype represented a 2.058-fold risk for the progression of renal disease (P = 0.026) compared to the AG/GG genotype. However, when the patients were treated with angiotensin-converting enzyme inhibitor and/or angiotensin receptor blocker, or corticosteroid, homozygosity for the -2518A allele was not associated with a higher rate of incidence of endstage renal disease. Serum MCP-1 levels were higher although not significantly so, in the patients with IgAN possessing the AA genotype.ConclusionsThe AA genotype at MCP-1 -2518 was an independent risk factor for the progression of renal disease in Japanese patients with IgAN, and was closely associated with renal survival.


Journal of Medical Genetics | 2003

Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy.

Jin Song; Ichiei Narita; Shin Goto; Noriko Saito; Kentaro Omori; Fuminori Sato; Junya Ajiro; Daisuke Saga; Daisuke Kondo; Minoru Sakatsume; Fumitake Gejyo

Immunoglobulin A nephropathy (IgAN), which is the most prevalent form of primary glomerulonephritis and one of the major causes of end stage renal disease (ESRD), has a variable clinical course.1–3 Poor prognostic factors for the progression of renal dysfunction in IgAN have been identified as high blood pressure, heavy proteinuria, and a severe histopathological appearance of the renal biopsy.4,5 In addition to these prognostic factors, it has been proposed that several genetic backgrounds are associated with a susceptibility to ESRD in patients with IgAN.6,7 The renin-angiotensin-aldosterone system is an important regulator of blood pressure and plays a central role in the development and progression of end organ damage. Polymorphisms in genes that encode components of this system have been reported to be associated with physiological risk factors for progressive renal dysfunction in IgAN. The most consistent of these is the angiotensinogen ( AGT ) gene, which is associated with essential hypertension and with an increased risk of cardiovascular diseases and renal failure.8–10 A deletion polymorphism in the angiotensin converting enzyme ( ACE ) gene influences the circulating ACE levels, and although it has little effect on blood pressure, it has been associated with an increased risk of cardiovascular diseases in some but not all studies.11–13 Aldosterone is one of the main effectors of the renin-angiotensin system14 and has classically been thought to act as a regulator for the absorption of Na and water, as well as the excretion of K in normal physiology, and as a mediator of oedema in numerous disease states. However, it is now well recognised that the actions of aldosterone are not limited to effects on ion transport in epithelial tissue, and its important role in cardiovascular disease involves non-epithelial tissues.15,16 Recently, it has been shown that …


Internal Medicine | 2017

IgG4-related hypophysitis with subtle hypopituitarism in an elderly diabetic patient: Is treatment or observation preferable?

Motoki Kawasaki; Motoyoshi Tsujino; Fuminori Sato; Maya Sakurada; Kenji Nishida; Takayasu Kise; Yuko Hijioka; Mitsugu Ishizawa; Kazuaki Enatsu; Yoshihiro Ogawa

A 70-year-old man with diabetes mellitus presented with an enlarged pituitary stalk in 2014. IgG4-related parotitis and submandibular sialoadenitis were diagnosed in 2012. He denied any symptoms related to a pituitary mass. His visual field was intact, and his hypopituitarism was subtle. The serum IgG4 level was elevated. A lip biopsy revealed strong fibrosis and hyper-infiltration of IgG4-positive plasma cells. Based on these findings, IgG4-related hypophysitis was diagnosed. The patient was carefully followed without specific intervention. His clinical condition showed no change until December 2016, suggesting a stable, natural course. Care should be taken when considering glucocorticoid therapy, especially for elderly diabetic patients, given possible side effects.


Nephrology | 2003

Association study of Japanese IgA nephropathy with microsatellite markers in 6q22–23, IGAN1

Shin Goto; Ichiei Narita; Kentaro Omori; Jin Song; Noriko Saito; Daisuke Kondo; Junya Ajiro; Fuminori Sato; Minoru Sakatsume; Akinori Miyashita; Ryozo Kuwano; Fumitake Gejyo

A heretofore undefined genetic component has been implicated in the development of IgA nephropathy (IgAN), although not generally considered a hereditary disease. Previous literatures disclosed that 3.8–14% of IgAN patients had genetic predisposition in their family. In our preliminary study, about 10% of biopsy-proven IgAN patients had a family history of haematuria and/or proteinuria. Recently, a linkage analysis of familial IgAN in Italy and US identified the disease susceptibility locus in 6q22–23, IGAN1. To address whether the disease susceptibility to IgAN are involved in this region also in Japanese patients, we conducted an association study of Japanese patients with IgAN using microsatellite markers in this region.


Kidney International | 2006

Etiology and prognostic significance of severe uremic pruritus in chronic hemodialysis patients

Ichiei Narita; Bassam Alchi; Kentaro Omori; Fuminori Sato; Junya Ajiro; Daisuke Saga; Daisuke Kondo; M. Skatsume; S. Maruyama; Kazama Jj; Kohei Akazawa; Fumitake Gejyo


Kidney International | 2005

Pretreatment serum FGF-23 levels predict the efficacy of calcitriol therapy in dialysis patients

Junichiro James Kazama; Fuminori Sato; Kentaro Omori; Hitomi Hama; Suguru Yamamoto; Hiroki Maruyama; Ichiei Narita; Fumitake Gejyo; Takeyoshi Yamashita; Seiji Fukumoto; Masafumi Fukagawa


Modern Rheumatology | 2006

SAA1 gene polymorphisms and the risk of AA amyloidosis in Japanese patients with rheumatoid arthritis.

Junya Ajiro; Ichiei Narita; Fuminori Sato; Daisuke Saga; Hisashi Hasegawa; Takeshi Kuroda; Masaaki Nakano; Fumitake Gejyo


Tissue Antigens | 2004

Transforming growth factor‐β1 gene polymorphism modifies the histological and clinical manifestations in Japanese patients with IgA nephropathy

Fuminori Sato; Ichiei Narita; Shin Goto; Daisuke Kondo; Noriko Saito; Junya Ajiro; Daisuke Saga; Asa Ogawa; M. Kadomura; F. Akiyama; Yoshikatsu Kaneko; Mitsuhiro Ueno; Minoru Sakatsume; Fumitake Gejyo


Kidney International | 2005

Bezafibrate suppresses rat antiglomerular basement membrane crescentic glomerulonephritis

Daisuke Saga; Minoru Sakatsume; Asa Ogawa; Yutaka Tsubata; Yoshikatsu Kaneko; Takeshi Kuroda; Fuminori Sato; Junya Ajiro; Daisuke Kondo; Takashi Miida; Ichiei Narita; Fumitake Gejyo

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