Ischemia/Reperfusion of Unilateral Kidney Exaggerates Aging-Induced Damage to the Heart and Contralateral Kidney

<b><i>Aims:</i></b> We aimed to determine the impact of aging on ischemic acute kidney injury, especially in terms of the pathological mechanisms of kidney and heart crosstalk. <b><i>Method: </i></b>The effects of 45 min of unilateral ischemic reperfusion (IR) of the renal artery on the contralateral kidney and heart were histologically assessed in 7- and 40-week-old SD rats after 7 days. <b><i>Results:</i></b> Glomerular sclerosis, interstitial fibrosis and numbers of ED1 cells were significantly increased in the contralateral kidneys of the 40-, but not the 7-week-old rats. The numbers of ED1 cells in the heart significantly and similarly increased in both groups, but reactive fibrosis after IR was significant only in the 40-week-old rats. The exaggerated profibrotic response induced by aging seemed to be closely associated with the increased number of ED1 cells in the affected area. <b><i>Conclusion:</i></b> Aging could play a major role in exaggerating the pathological processes of inflammation to fibrosis in remote organs including the heart and the nonischemic kidney after IR stimulation of the unilateral kidney.