Acute and chronic kidney injury have become global healthcare burdens with high morbidity and mortality rates. Early diagnosis and preventive treatment halting progress of renal insufficiency are thus needed. Keratins (K) are useful and widely used epithelial cell-specific disease biomarkers, e.g. in diagnostic pathology as tissue markers for cancer or as circulating biomarkers of neoplastic and non-neoplastic diseases. In the kidney K7, K8, K18 and K19 were previously described. We could show that these keratins are significantly and progressively upregulated in renal disease with tubular cell injury, independently of the underlying pathomechanism. We showed, that these keratins can be used as markers of tubular epithelial cell stress on tissue and in urine. The described keratins were not upregulated in an expected equimolar ratio, which hinted to possible other keratins being expressed in kidney diseases. Reanalysis of publicly available microarray data revealed K10, K14 and K17 as potentially expressed in the kidney. Expression of those three keratins was validated using RT-PCR and Western Blot.K10 was downregulated in a model of renal fibrosis, representing the first keratin in the kidney to be downregulated in response to renal injury. K14 showed a low expression in healthy kidneys and was progressively upregulated during disease similarly to the other keratins.K17 was de novo expressed during disease, independently of the underlying injury: with only single K17-positive cells in the beginning, continuously expanding to entire K17-positive tubular crosssections in advanced disease stages. In contrast to the main keratins, K17 did not colocalize with NGAL, a well-recognized marker of tubular epithelial cell injury. Thus, K17 seems to be associated with renal injury, but does not mark injured tubular epithelial cells. Further studies are needed to evaluate the nature of K17-positive cells, before it can be evaluated as a possible biomarker
