Other contributing factors include skeletal resistance to PTH, which limits the hormone’s ability to restore serum calcium levels, upregulation of the calcium-sensing receptors in both the kidneys and parathyroid glands, triggered by proinflammatory cytokines and altering the set point for calcium–PTH feedback regulation and the intracellular calcium accumulation, which occurs in patients with septic AKI [18]. This evidence concerns the gene CASR and acute kidney injury.