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首页> 外文期刊>Journal of Medical Biochemistry >Dimethylarginine – biomarkers in progression of kidney disease / Dimetilarginini – biomarkeri u progresiji bubre?nih oboljenja
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Dimethylarginine – biomarkers in progression of kidney disease / Dimetilarginini – biomarkeri u progresiji bubre?nih oboljenja

机译：二甲基精氨酸-肾脏疾病进展中的生物标志物/二甲基精氨酸-肾脏疾病进展中的生物标志物

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Summary Decreased nitric oxide (NO) production and/or impaired NO bioavailability may occur in patients with the chronic kidney disease (CKD), and could contribute to elevation of blood pressure, cardiovascular disease (CVD) and progression of renal injury in these patients. Free guanidinomethylated arginine residues occur endogenously as a result of proteolysis of post-translational methylated tissue proteins. The asymmetric dimethyl arginine (ADMA) is a competitive inhibitor of the nitric oxide synthase (NOS) enzymes. The kidney has a predominant role in ADMA elimination by combining two mechanisms; urinary excretion and metabolization of ADMA The degradation of ADMA is accomplished intracellularly by the enzyme dimethylarginine dimethylaminohydrolase (DDAH). ADMA is not only a uremic toxin, but also a strong marker of the endothelial dysfunction and atherosclerosis and a stronger independent predictor of all-cause mortality and cardiovascular outcome in patients with the chronic renal failure. There are at least four mechanisms that may explain the accumulation of ADMA in CKD: increased methylation of proteins, increased protein turnover, decreased metabolism by DDAH and impaired renal excretion. A strong positive correlation between symmetric dimethyl arginine (SDMA) and creatinine suggests that SDMA might be of value as a marker of the renal function. Reduced NO elaboration secondary to accumulation of ADMA and elevated inflammation may be important pathogenic factors for endothelial dysfunction in patients with the renal disease. Elevation of ADMA may be a missing link between CVD and CKD.
机译：总结慢性肾脏病（CKD）患者可能发生一氧化氮（NO）产生减少和/或NO生物利用度降低，并可能导致这些患者的血压升高，心血管疾病（CVD）和肾损伤进展。由于翻译后甲基化组织蛋白的蛋白水解，游离的胍基甲基化的精氨酸残基是内源性发生的。不对称二甲基精氨酸（ADMA）是一氧化氮合酶（NOS）酶的竞争性抑制剂。通过结合两种机制，肾脏在消除ADMA中起主要作用。 ADMA的尿排泄和代谢通过二甲基精氨酸二甲基氨基水解酶（DDAH）在细胞内完成ADMA的降解。 ADMA不仅是尿毒症毒素，而且还是内皮功能障碍和动脉粥样硬化的有力标志物，也是慢性肾功能衰竭患者全因死亡率和心血管结局的更强独立预测因子。至少有四种机制可以解释CKD中ADMA的积累：蛋白质甲基化增加，蛋白质更新增加，DDAH代谢降低和肾排泄障碍。对称的二甲基精氨酸（SDMA）和肌酐之间有很强的正相关性，表明SDMA作为肾脏功能的标志物可能有价值。继发于ADMA积累的NO减少和炎症增加可能是肾病患者内皮功能异常的重要致病因素。 ADMA的升高可能是CVD和CKD之间缺少的环节。

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