Asymmetric dimethylarginine is not a marker of arterial damage in children with glomerular kidney diseases

Introduction
Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, correlates with cardiovascular risk especially in patients with chronic kidney disease. The aim of our study was to establish significance of ADMA as a biomarker of arterial damage in children with glomerulopathies.

Material and methods
In 80 children with glomerulopathies (mean age, 11.33 ±4.25 years; 42 with idiopathic nephrotic syndrome [INS], 38 with IgA or Henoch-Schoenlein nephropathy [IgAN/HSN]), we analyzed serum ADMA [nmol/ml], peripheral and central blood pressure, arterial stiffness (augmentation index – AIx75HR, pulse wave velocity – PWV), common carotid artery intima media thickness (cIMT), and selected clinical and biochemical parameters.

Results
In the study group, mean ADMA concentration was 1.66 ±1.19 [nmol/ml] and did not differ between INS and IgAN/HSN patients. We found no significant correlations between concentration of ADMA, cIMT [mm]/Z-score, PWV [m/s]/Z-score, and AIx75HR [%] in the whole group and in INS and IgAN/HSN patients. In the whole group of 80 children, ADMA correlated (p < 0.05) with BMI Z-score (r = –0.24), uric acid (r = –0.23), HDL-cholesterol (r = –0.25), and central mean arterial pressure (r = –0.25), in children with INS also with total protein (r = 0.37), albumin (r = 0.36), and total cholesterol (r = –0.40, p = 0.028). In multivariate analysis, serum albumin was the strongest determinant of ADMA in the whole group ( = 0.536, 95% CI: 0.013-1.060, p = 0.045).

Conclusions
1. In children with glomerulonephritis, measurement of asymmetric dimethylarginine cannot replace well established and validated methods of assessment of subclinical arterial damage. 2. In children with glomerular kidney diseases, ADMA concentration is related primarily to serum albumin concentration.