Hypercalcemia and secondary hyperparathyroidism can lead to vascular calcifications, further impairing renal perfusion and contributing to a decline in kidney function.[3] In our patient, despite regular hemodialysis and medical management, persistently elevated parathyroid hormone (PTH) levels exacerbated bone turnover and calcium-phosphorus imbalance, complicating the overall management. The gene discussed is PTH; the disease is secondary hyperparathyroidism.