In vivo models of acute kidney injury

Acute kidney injury (AKI), a serious clinical outcome of renal hypoxic, toxic or septic insults, has a profound impact on patients’ morbidity and mortality and increases medical expenses. The pathogenesis of human AKI is compound and only partially understood and data regarding human AKI morphology are sparse. Thus, our understanding of this disorder depends, to a large extent, on animal studies. Various AKI animal model types are used for the elucidation of the pathogenesis of AKI and for testing the efficacy of therapeutic interventions. Simple and reproducible models are mostly produced by severe single insults and display a rather extensive structural damage. By contrast, low-intensity combined insults, probably better representing clinically relevant AKI setups, are associated with more subtle and sublethal structural changes, alas at the price of low consistency and reproducibility. Thus, different models may have diverse mechanisms of injury and renal repair, an issue to be considered while testing drug efficacy in experimental AKI.Researchers are also encouraged to extend experimental end points, beyond simple parameters of glomerular filtration. Fine morphology can be obtained by optimizing renal fixation techniques and evaluation methods. New renal imaging technologies and measures of spatial and temporal mapping of hypoxia, adaptive cellular responses and cell injury are now available. Together with novel urine biomarkers these new tools provide a wider range of renal functional and structural assessment and may improve our perspectives regarding the AKI pathogenesis and prevention.