HDL isolated from CKD patients depicts a reduced cellular cholesterol efflux capability [11,13,14,15], which is linked to a depletion of HDL-associated apoA-I, apoA-II, and phospholipids, and increased apoC-III and SAA (Figure 2), all factors that are known to modulate the cholesterol acceptor capability of HDL [103,129,130]. This evidence concerns the gene APOC3 and chronic kidney disease.