Although not fully understood, the cardiac consequences of AKI seem to be mediated predominantly by systemic inflammation, cardiac immune cell infiltration, activation of the renin–angiotensin–aldosterone system (RAAS), neuro-hormonal activation, oxidative stress, dysregulated calcium homeostasis, and endothelial dysfunction following AKI, all of which may induce mitochondrial dysfunction, cardiac hypertrophy, and fibrosis in the heart [12, 57–60]. The gene discussed is REN; the disease is acute kidney injury.