Multiple mechanisms may be involved in HCM-induced AKI, including a decrease of glomerular ultrafiltration coefficient [28], the induction of nephrogenic diabetes insipidus via down-regulation of aquaporin-2, disruption of countercurrent multiplier system [29, 30] and a loop diuretic-like effect [31], that participate to polyuria and volume depletion. This evidence concerns the gene AQP2 and acute kidney injury.