Impairment in renal function leads to decreased phosphate clearance, resulting in increased FGF23 levels which impair 1-alpha-hydroxylase activity. This leads to decreased activation of 25-hydroxyvitamin D. As a result, calcium absorption is decreased, leading to a compensatory secondary hyperparathyroidism. As renal function deteriorates, parathyroid hormone (PTH) action diminishes due to increasing PTH resistance further exacerbating the secondary hyperparathyroidism to maintain serum calcium. Hyperparathyroidism may cause renal osteodystrophy and increase the risk for tertiary hyperparathyroidism. Management of calcium disorders in renal failure involves normalizing serum phosphate levels, preventing vitamin D deficiency, normalizing serum calcium levels as well as keeping PTH levels within a range appropriate for the level of renal function. Treatment may include nonaluminum-containing phosphate binders such as sevelamer and calcium; activated vitamin D analogs such as calcitriol, doxercalciferol, and paricalcitol; as well as calcimimetic agents such as cinacalcet and etelcalcetide. Close monitoring and working with the patient’s nephrologists, to avoid hypercalcemia and adynamic bone disease is paramount. Bone-specific alkaline phosphatase, which is reflective of PTH action on the bone, may be useful in individualizing the PTH target range. Hypercalcemia developing as part of tertiary hyperparathyroidism may be managed medically, by limiting calcium and activated vitamin D intake, using cinacalcet, or surgery, with parathyroid debulking. These patients are at high risk for hungry bone syndrome.