This is in partly due to the mechanisms previously described and is further exacerbated by pharmacological interventions aimed at slowing CKD progression, specifically, renin-angiotensin aldosterone system inhibitors (RAASi) including angiotensin-converting enzyme inhibitors (ACEi), angiotensin-receptor blockers (ARBs) and non-steroidal/steroidal mineralocorticoid receptor antagonists (ns-MRAs/MRAs) [12]. This evidence concerns the gene NR3C2 and chronic kidney disease.