These were complex conditions with a wide range of glomerular and tubular anomalies that contributed significantly to overall renal dysfunction, reinforcing the idea that collecting duct water reabsorption was impaired due to AQP2 suppression in post-ischemic kidneys [36] and reduced expression of AQP2 expression in polyuria hypercalcemia in rats [43]. This evidence concerns the gene AQP2 and hypercalcemia disease.