In patients with CKD, MA may accelerate impairment of renal function and consequently play a key role (Menon et al., 2010; Raphael et al., 2011, 2013) in the pathogenesis of some CKD complications, including insulin resistance, cardiovascular disease, decreased protein synthesis, increased protein catabolism and branched‐chain amino acid oxidation, low leptin levels, and protein‐energy wasting (PEW) (Kalantar‐Zadeh et al., 2004; Kopple et al., 2005; Rajan & Mitch, 2008; Stenvinkel et al., 2002). This evidence concerns the gene LEP and chronic kidney disease.