Asymmetric Dimethylarginine (ADMA) in Pediatric Renal Diseases: From Pathophysiological Phenomenon to Clinical Biomarker and Beyond

Figures

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  Figure 2. Person correlation and linear regression analyses between plasma ADMA level and (A) plasma creatinine level and (B) estimated glomerular filtration rate (eGFR) in 216 CKD stage 1–4 children and adolescents. This figure was constructed with data reported in part elsewhere [63,64,72,73].

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  Figure 1. Simplified schema of synthesis, transport, and elimination of ADMA in the kidney. The enzymes in protein arginine methyltransferases (PRMTs) family methylate protein-bound L-Arginine residues (purple cycle) to generate protein-bound ADMA (red circle) and SDMA (yellow circle). Upon proteolysis, free ADMA is released and moved out of the cells via cationic amino acid transporter (CAT). In the kidneys, ADMA can be removed via urinary excretion or enzymatic degradation. Dimethylarginine dimethylaminohydrolase-1 (DDAH-1) and -2 (DDAH-2) can catalyze ADMA to generate L-Citrulline and dimethylamine (DMA). In addition, ADMA can be metabolized by alanine-glyoxylate aminotransferase 2 (AGXT2). In the kidney, ADMA can inhibit nitric oxide (NO) synthase to inhibit NO production.