| Popis: |
Decreases in renal function lead to decreased phosphate clearance, resulting in FGF23 increases which impair 1-alpha-hydroxylase activity and 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. The hyperparathyroidism may cause renal osteodystrophy and increase the risk for tertiary hyperparathyroidism complicating post-renal transplant care. In addition, acid-base disturbances may lead to increased ionized calcium levels with acidemia. Management of calcium disorders in end-stage renal failure involves normalizing serum phosphate levels, preventing vitamin D deficiency, normalizing serum calcium levels and calcium-phosphate products, 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 analogues such as calcitriol, doxercalciferol, and paricalcitol; as well as calcium sensing receptor agonists such as cinacalcet. Close monitoring, 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. |
