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Notch\u20101 and \u20102 receptors are crucially involved in nephron development and contribute to inflammatory kidney diseases. We specifically determined the participation of receptor Notch\u20103 following tubulointerstitial injury and in inflammatory responses. Here we show by heat map analyses that Notch\u20103 transcripts are up\u2010regulated in human kidney diseases. A similar response was corroborated with kidney cells following TGF\u2010\u03b2 exposure <jats:italic>in vitro<\/jats:italic>. The murine unilateral ureteral obstruction (UUO) model mirrors hallmarks of tubulointerstitial injury and damage. A subset of tubular and interstitial cells demonstrated up\u2010regulated Notch\u20103 receptor expression in diseased animals. We hypothesized a relevance of Notch\u20103 receptors for the chemotactic response. To address this question, animals with genetic ablation of receptor Notch\u20103 were analysed following UUO. As a result, we found that Notch\u20103\u2010deficient animals are protected from tubular injury and cell loss with significantly reduced interstitial collagen deposition. Monocytic cell infiltration was significantly reduced and retarded, likely due to abrogated chemokine synthesis. A cell model was set up that mimics enhanced receptor Notch\u20103 expression and activation. Here a pro\u2010mitogenic response was seen with activated signalling in tubular cells and fibroblasts. In conclusion, Notch\u20103 receptor fulfils non\u2010redundant roles in the inflamed kidney that may not be replaced by other Notch receptor family members. Thus, specific blockade of this receptor may be suitable as therapeutic option to delay progression of kidney disease. Copyright \u00a9 2012 Pathological Society of Great Britain and Ireland. 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