Experimental models have shown maladaptive repair or disordered regeneration or both, due to renin-angiotensin activation, tubular G2/M arrest, inflammation, epigenetic changes, and mitochondrial dysfunction among others, culminating in vascular drop-out and resulting in glomerulosclerosis and interstitial fibrosis with tubular atrophy, each of which contributes to progressive renal dysfunction by perpetuating injury and hampering repair [9,22]. Here, REN is linked to glomerulosclerosis.