Although autosomal dominant polycystic kidney disease is the most common monogenic kidney disease worldwide, its pathogenic mechanisms are incompletely understood. In this Review, Vicente Torres and colleagues propose a hypothesis in which the disruption of calcium signalling that results from mutations in PKD1 or PKD2 is perpetuated by the consequent dysregulation of cAMP and purinergic signalling, which magnifies the effect of vasopressin to further disrupt calcium signalling and activate downstream signalling pathways that cause impaired tubulogenesis, increased cell proliferation, increased fluid secretion and interstitial inflammation. http://bit.ly/1yqRBda
