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Ischemic acute kidney injury (iAKI) is a common event in organ transplantation and may occur during severe surgery. To gain mechanistic insights into ischemia-induced alterations at the level of proximal tubule cells we set up an in vitro model of ischemia and reperfusion using the rat proximal tubule cell line NRK-52E. In this particular model we simultaneously applied acidosis, hypoxia and aglycemia together for 2h, using low volume buffer systems and a hypoxia chamber. Thereafter reperfusion was mimicked by subsequently culturing the cells for up to 48h under standard conditions. In order to validate the system we investigated whether effects that take place in existing in vivo models of ischemia and reperfusion can be observed. Namely, induction of necrosis, apoptosis and of ischemia reperfusion induced protein (IRIP), dedifferentiation (alphaSMA), inflammation (MCP-1), inducible NO-synthase (iNOS), release of PGE(2) and basolateral uptake of organic anions. In fact, all parameters developed as described for the in vivo situation during reperfusion after ischemia. Taken altogether we have established an in vitro model of proximal tubule cell reperfusion damage after ischemia, showing typical changes described in vivo. Additionally, our model system is suitable for isolated application of the typical insults associated with ischemia (e.g. acidosis alone, hypoxia alone, aglycemia alone), in order to obtain more insight into the mechanistic events that lead to reperfusion damage in the kidney on the cellular level.

Implementation of an in vitro Model System for Investigation of Reperfusion Damage after Renal Ischemia