Vukićević T, et al. - Researchers performed in vitro and in vivo analyses to evaluate the impact of fluconazole on aquaporin-2 (AQP2) localization, as well as they determined the influences of the drug on AQP2 phosphorylation and RhoA (a small GTPase, which under resting conditions, maintains F-actin to block AQP2-bearing vesicles from reaching the plasma membrane). They also investigated how water flow across epithelia of isolated mouse collecting ducts and urine output in mice treated with tolvaptan (a VR2 blocker that causes a nephrogenic diabetes insipidus–like excessive loss of hypotonic urine) were influenced by fluconazole. They found that collecting duct AQP2 plasma membrane localization was promoted by fluconazole in the absence of arginine-vasopressin (AVP). This indicates its possible usefulness in treating forms of diabetes insipidus (eg, X-linked nephrogenic diabetes insipidus) in which an inappropriate response of kidney to AVP is seen.