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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. Kratak sadržaj Smanjenje koncentracije NO i/ili nedovoljna raspolo`ivost ovog molekula kod pacijenata sa bubre`nim bolestima mo`e biti razlog pove}anja krvnog pritiska, kardiovaskularnih bolesti (KVS) i progresije bubre`nog o{te}enja. Metilarginini nastaju u procesu proteolize posttranslaciono metilisanih argininskih rezidua u proteinima. Asimetri~ni dimetilarginin (ADMA) je kompetitivni inhibitor azot oksid sintaze (NOS). Najva`nija uloga bubrega u eliminaciji ADMA podrazumeva procese urinarne ekskrecije i razgradnju pod uticajem dimetilarginin dimetilaminohidrolaze (DDAH). Na aktivnost DDAH uti~u oksidativni stres i inflamacija. ADMA nije samo uremijski toksin ve} i zna~ajan marker endotelne disfunkcije i ateroskleroze, kao i nezavisni prediktor mortaliteta i kardiovaskularnih bolesti kod pacijenata sa HBI. Osnovni uzroci koji dovode do akumulacije ADMA su pove}ana metilacija proteina, njihov pove}an metabolizam, smanjena aktivnost DDAH i smanjena urinarna ekskrecija. Klirens simetri~nog dimetilarginina (SDMA) u plazmi zavisi samo od renalne funkcije (pozitivna korelacija sa kreatininom) i njena akumulacija predstavlja nespecifi~ni indikator uremijskih toksina. Redukovana koli~ina NO pra}ena akumulacijom ADMA, udru`ena sa inflamacijom mo`e biti va`an patogeni faktor endotelne disfunkcije kod bubre`nih pacijenata. Porast koncentracije ADMA mo`e biti veza izme|u KVS i HBI.

Dimethylarginine – biomarkers in progression of kidney disease / Dimetilarginini – biomarkeri u progresiji bubrežnih oboljenja