Growing epidemiological data demonstrate that acute kidney injury (AKI) is associated with long-term cardiovascular morbidity and mortality. Here, the authors present a 1-year study of cardiorenal outcomes following bilateral ischemia-reperfusion injury in male mice. These data suggest that AKI causes long-term dysfunction in the cardiac metabolome, which is associated with diastolic dysfunction and hypertension. Mice treated with the histone deacetylase inhibitor, ITF2357, had preservation of cardiac function and remained normotensive throughout the study. ITF2357 did not protect against the development of kidney fibrosis after AKI.
Keywords: AKI, acute kidney injury; ATP, adenosine triphosphate; BUN, blood urea nitrogen; HDACi, histone deacetylase inhibitor; MAP, mean arterial pressure; PSR, picrosirius red; SCr, serum creatinine; acute kidney injury; cardiorenal syndrome; diastolic dysfunction; histone deacetylase inhibition; systemic sequelae of kidney disease; tGFR, transcutaneous glomerular filtration rate.
© 2021 The Authors.