Markedly increased adiponectin has been consistently reported in patients with both chronic kidney disease (CKD) and end-stage renal disease (ESRD), and this upregulation of circulating adiponectin has been deemed a compensatory mechanism to relieve further renal injury and subsequent unbound form adiponectin in excess may have been filtered through loosened and defective glomerular filtration barrier and excreted in the urine [17,18]. This evidence concerns the gene ADIPOQ and chronic kidney disease.