Abstract
l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial nitric oxide synthase (NOS). In contrast, protein-incorporated Arg residues can be methylated with subsequent proteolysis giving rise to methylarginine compounds, such as asymmetric dimethylarginine (ADMA) that competes with Arg for binding to NOS. Most ADMA is degraded by dimethylarginine dimethyaminohydrolase (DDAH), distributed widely throughout the body and regulates ADMA levels and, therefore, NO synthesis. In recent years, several studies have suggested that increased ADMA levels are a marker of atherosclerotic change, and can be used to assess cardiovascular risk, consistent with ADMA being predominantly absorbed by endothelial cells. NO is an important messenger molecule involved in numerous biological processes, and its activity is essential to understand both pathogenic and therapeutic mechanisms in kidney disease and renal transplantation. NO production is reduced in renal patients because of their elevated ADMA levels with associated reduced DDAH activity. These factors contribute to endothelial dysfunction, oxidative stress and the progression of renal damage, but there are treatments that may effectively reduce ADMA levels in patients with kidney disease. Available data on ADMA levels in controls and renal patients, both in adults and children, also are summarized in this review.
Highlights
In addition to the traditional cardiovascular risk factors, other factors associated with renal failure involved in common metabolic pathways have recently been studied in detail
Among the few studies reported to date, elevated levels of asymmetric dimethylarginine (ADMA) have been detected in children and adolescents with high blood pressure [42], and its levels have started to be investigated in children with chronic renal failure [24,88], and in children and adolescents with hypercholesterolaemia [89], diabetes [90] and phenylketonuria [91]
This study indicated that the levels of adiponectin, inflammatory and anti-atherogenic hormone are not correlated with the levels of ADMA or C reactive protein (CRP) before and after RTx, despite all the values corresponding to these variables having decreased after transplantation
Summary
In addition to the traditional cardiovascular risk factors, other factors associated with renal failure involved in common metabolic pathways have recently been studied in detail. The metabolism of amino acids tends to be impaired in patients with chronic renal failure due to abnormalities in their synthesis or excretion. One of the alterations of amino acid metabolism in patients with chronic renal failure is hyperhomocysteinaemia; this is considered to be an independent risk factor for cardiovascular disease [1] and occurs in more than 85% of patients after kidney transplant (RTx) and in those with end-stage renal failure [2]. It seems interesting to study the metabolism of arginine and associated metabolic pathways. It is useful to determine the levels of arginine and its methylated derivatives as part of the analysis of the cardiovascular risk and endothelial dysfunction of renal disease
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