**1. Introduction**

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Kidney transplantation is the preferred therapy for most patients with end-stage renal disease. The demand for kidney grafts however far exceeds the supply of available organs. As a result, transplant teams increasingly use organs from extended criteria donors, of older age or with significant comorbidity. This use of extended criteria organs is not without consequences.

Older donor age is strongly related to impaired kidney graft function and graft failure because older kidneys are limited in their capacity to tolerate injury [1]. Aging is associated with renal structural changes en functional decline. Older kidneys lose renal parenchyma and trough this have a decreased renal plasma flow and tubular dysfunction. The mechanisms required for tissue repair after damage become less reliable, resulting in a decrease in repair capacity. This functional decline in the potential to repair and regenerate is often considered a hallmark of the aging phenotype [2] [3].

Another major component of the aging phenotype is replicative or cellular senescence, which is defined as permanent, irreversible growth arrest. In this chapter we draw the parallel between the aging kidney in the transplantation setting and cellular senescence.
