Acute kidney injury induced by ischemia/reperfusion (IR) is a frequent 
complication in hospitalized patients. Mineralocorticoid receptor antagonism has 
shown to be helpful against renal IR consequences; however, the potential 
benefit of novel nonsteroidal mineralocorticoid receptor antagonists such as 
finerenone has to be further explored. In this study, we evaluated the efficacy 
of finerenone to prevent the acute and chronic consequences of ischemic acute 
kidney injury. For the acute study (24 hours), 18 rats were divided into sham, 
bilateral renal ischemia of 25 minutes, and rats that received 3 doses of 
finerenone at 48, 24, and 1 hour before the ischemia. For the chronic study (4 
months), 23 rats were divided into sham, rats that underwent 45 minutes of 
bilateral ischemia, and rats treated with finerenone at days 2 and 1 and 1 hour 
before IR. We found that after 24 hours of reperfusion, the untreated IR rats 
presented kidney dysfunction and tubular injury. Kidney injury molecule-1 and 
neutrophil gelatinase associated to lipolacin mRNA levels were increased. In 
contrast, the rats treated with finerenone displayed normal kidney function and 
significantly lesser tubular injury and kidney injury molecule-1 and neutrophil 
gelatinase associated to lipolacin levels. After 4 months, the IR rats developed 
chronic kidney disease, evidenced by kidney dysfunction, increased proteinuria 
and renal vascular resistance, tubular dilation, extensive tubule-interstitial 
fibrosis, and an increase in kidney transforming growth factor-β and collagen-I 
mRNA. The transition from acute kidney injury to chronic kidney disease was 
fully prevented by finerenone. Altogether, our data show that in the rat, 
finerenone is able to prevent acute kidney injury induced by IR and the chronic 
and progressive deterioration of kidney function and structure.