The “oxidative” linkage between CKD and its complications is achieved through several pathophysiological mechanisms, including mitochondrial dysfunction [144], uremic neurotoxin-induced endothelial nitric oxide synthase (eNOS) uncoupling [145], and increased nicotinamide adenine dinucleotide phosphate-oxidases (NADPH oxidases (NOX)) activity [146], myeloperoxidase (MPO) [147], but also antioxidant enzymes depletion due to dietary restriction, and/or decreased intestinal absorption [148]. Here, NOS3 is linked to chronic kidney disease.