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- 저자 : ( Yasuhiko Tomino ) (검색결과 3 건)
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Diagnosis and treatment of patients with IgA nephropathy in Japan
( Yasuhiko Tomino ) 대한신장학회 2016 Kidney Research and Clinical Practice Vol.35 No.4
Chronic kidney disease (CKD) is a worldwide public health problem that affects millions of people from all racial and ethnic groups. Although CKD is not one specific disease, it is a comprehensive syndrome that includes IgA nephropathy. As reported by the Japanese Society of Nephrology, 13.0 million people have CKD. In Japan, major causes of end-stage kidney disease are type 2 diabetic nephropathy, chronic glomerulonephritis, especially IgA nephropathy, hypertensive nephrosclerosis, and polycystic kidney disease. IgA nephropathy is characterized by polymeric IgA1 with aberrant galactosylation (galactose-deficient IgA1) increased in the blood and deposited in the glomerular mesangial areas, as well as partially in the capillary walls. The tonsils are important as one of the responsible regions in this disease. The clarification of the mechanism of galactose-deficient IgA1 production will pave the way for the development of novel therapies. The results of future research are eagerly awaited. At present, the most important therapeutic goals in patients with IgA nephropathy are the control of hypertension, the decrease of urinary protein excretion, and the inhibition of progression to end-stage kidney disease. Several investigators have reported that renin-eangiotensin-ealdosterone system inhibitors reduce levels of urinary protein excretion and preserve renal function in patients with IgA nephropathy. In Japan, tonsillectomy and steroid pulse therapy are more effective for patients with IgA nephropathy. Copyright ⓒ 2016. The Korean Society of Nephrology. Published by Elsevier. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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( Mochamad Yusuf ),( Mochamad Thaha ),( Nilamsari Wenny ),( Mochamad Amin ),( Dokter Pranawa ),( Yasuhiko Tomino ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: A symmetric dimethylarginine (ADMA) is a potent endogenous inhibitor of nitric oxide synthases (NOS) which could reduce nitric oxide (NO) level and causesendothelial dysfunction, vasoconstriction, elevation of blood pressure, and as a potent predictor of cardiovascular event in end-stage kidney disease (ESKD) patients as well. Experimental evidence has convincingly shown that inhibition of NOS by ADMA leads to enhanced norepinephrine release from sympathetic nerves in rats and humans, whereas sympathetic activation impairs endothelium-dependent, nitric-oxide-mediated vasodilatation in healthy humans and ESKD patients. ADMA is formed through the catalytic activity of protein arginine methyltransferases (PRMTs). Thus, type 1 PRMT (PRMT-1) catalyzes the asymmetric dimethylation of arginine residues. Moreover, there are several pathways lead to the increased ADMA level, where PRMT-1 gene polymorphism has been one of the hypothesis. Methods: A total of 56 patients (total sampling) from a private hospital were enrolled in this study. Venous blood samples were taken just before hemodialysis. ADMA was measured using an enzyme-linked immuno- sorbent assay. All samples went through processes of DNA extraction, Polymerase Chain Reaction, and Electrophoresis. Thirteen out of 56 samples (consecutive) were further undergone DNA isolation and purifi cation, labelling, precipitation and sequencing. Genotyping of the polymorphisms was performed using PCR-based SNP detection methods (Applied Bio- systems, Carlsbad, USA)Conclusions: It appears that PRMT-1 gene polymorphism may partially explain the ADMA increasement in hemodialysis patients.
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( Shuntaro Maruyama ),( Tomohito Gohda ),( Yusuke Suzuki ),( Hitoshi Suzuki ),( Yuji Sonoda ),( Saki Ichikawa ),( Zi Li ),( Maki Murakoshi ),( Satoshi Horikoshi ),( Yasuhiko Tomino ) 대한신장학회 2016 Kidney Research and Clinical Practice Vol.35 No.4
Background: IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide. Tonsillectomy plus steroid pulse therapy has been able to induce clinical remission in early-stage IgAN. However, its possible effect on systemic and local cytokines and tubular markers has not been fully investigated. Methods: We obtained serum and urine samples from 38 patients just before renal biopsy and third steroid pulse therapy. Markers of tubular damage such as N-acetyl-β- D-glucosaminidase, and kidney injury molecule-1 and inflammation such as interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 were measured by immunoassay. Results: Before renal biopsy, only urinary inflammatory markers, except MCP-1, were associated with glomerular (proteinuria) and/or tubular damage markers. Proteinuria, hematuria, and estimated glomerular filtration rate dramatically improved after therapy. In addition, levels of serum IL-6 and ICAM-1 and all urinary markers declined significantly; however, serum MCP-1 and VCAM-1 levels did not. None of the urinary markers correlated with the serum inflammatory markers. Conclusion: Tonsillectomy plus steroid pulse therapy for patients with IgAN might be useful for improving not only glomerular damage marker but also tubular damage markers through the improvement of local renal inflammation. Copyright ⓒ 2016. The Korean Society of Nephrology. Published by Elsevier. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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