NOS2 and chronic kidney disease: Increased aortic stiffness, altered sensitivity to vasoconstrictor agents, impaired endothelium-dependent and –independent relaxation responses, and impaired NOS-mediated relaxation are all factors that could ultimately contribute to the transmission of greater pulsatile pressures and increased risk of end organ damage (Briet et al., 2011) and as such should therefore be considered important therapeutic targets to reduce cardiovascular risk in CKD.