The pathogenesis of hyperparathyroidism in renal failure is multifactorial and is associated with elevated fibroblast growth factor 23 (FGF23), reduced 1α,25(OH)2D levels, hyperphosphatemia, hypocalcemia, and reduction of vitamin D receptors (VDR) and calcium-sensing receptors (CaSR) in the parathyroid gland [14,15]. Here, CASR is linked to acute kidney injury.