Using a microarray approach, we found that old kidneys displayed increased proximal tubular expression of zinc-α (2)-glycoprotein (Zag), which was previously implicated in epithelial proliferative inhibition. In this study, we demonstrated that aged mouse kidneys displayed a reduced epithelial proliferative reserve, and we investigated the hypothesis that this loss of proliferative capacity contributes to the age-dependent decline in renal repair. Despite significant progress in our understanding of the cellular and molecular aspects of AKI in recent years, 9, 10 the role of aging in this process has not been considered in most studies therefore, the identification of age-specific factors that mediate the altered response to AKI in the elderly are lacking. According to our recent meta-analysis, 8 it is estimated that patients who are older than 65 yr carry a 28% higher risk for failing to recover renal function completely after surviving an episode of AKI. 7 The age-dependent increase in the susceptibility to AKI coincides with a decline in functional renal recovery. 1 Aging is thought to increase the susceptibility to AKI 2 – 5 as a result of functional changes in the vasoregulatory reserve 4, 6 and a loss of cellular stress resistance.
The incidence of acute kidney injury (AKI) has steadily increased in recent years, and this increase is strongly associated with the advancing age of our population.
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