Hyper And Hypocalcemia

Approximately 10% of transplant recipients develop hyperkalemia. The hyperkalemia is due to persistent hyperparathyroidism. Secondary hyperparathy-roidism is improved following successful kidney transplant due to restoration to normal levels of the active form of vitamin D [1,25 (OH2 D3] and the reversal of hyperphosphatemia. In most cases, mild hyperkalemia resolves slowly over 6-12 months as the parathyroid glands involute. Severe or persistent hyperkalemia may require parathyroidectomy. The indications for parathyroidectomy: 1) Acute, severe hyperkalemia (calcium level > 14 mg/dl) elevation of the PTH levels and evidence of continuing or worsening bone disease of hyperparathyroidism (ostitis fibrosa cystica) and proximal myopathy. Phospage supplementation is usually all that is needed to keep plasma calcium and phosphate at acceptable levels while the parathyroid glands involute.

Patients who have undergone parathyroidectomy prior to transplantation may develop severe hypocalcemia posttransplant. This is caused by 1) PTH deficiency, 2) temporary deficiency of the active form of vitamin D [1,25 (OH) 2 VitD3] immediately following transplantation before new kidney begins to function and converts the inactive 25 (OH VitD3 to the active form, 3) calcium loss in the urine by the newly functioning kidney, and 4) steroid-induced reduction in intestinal calcium symptomatic.

Treatment of severe symptomatic hypocalcemia see Table 17.4. Treatment for asymptomatic hypocalcemia is the addition of oral calcium supplements as calcium carbonate to provide 1 gm of elemental calcium t.i.d. each day and 1,25 (OH)2 D3 in a starting dose of 0.25 mg p.o. each day.

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