Hypercalcemia and Hyperparathyroidism after Renal Transplantation

Dear Sir,After renal transplantation persistent hypercalcemia is seen in approximately 8.5–53% of recipients. Mostly this is due to tertiary hyperparathyroidism. After renal transplantation secondary hyperparathyroidism may regress due to normalization of stimuli (such as hyperphosphatemia) for parathyroid proliferation. Sometimes, parathormone (PTH) levels are found elevated in a few recipients. These recipients have long-term hemodialysis therapy in their medical history and renal osteodystrophy with hypercalcemia and high serum alkaline phosphatase (ALP) levels. Persistent hypercalcemia is rare. Parathyroidectomy is rarely necessary in hypercalcemic recipients. However, hypercalcemia normalizes in 5–17% of these recipients after parathyroidectomy [1, 2, 3, 4, 5].Ten of 185 (5.4%) renal recipients with normal allograft function who are being followed up in our outpatient clinic were found to have persistent hypercalcemia (>11.0 mg/dl). In this study, we examined parathyroid function in 10 recipients (group A) showing persistent hypercalcemia. In these recipients, the parameters determined were: time on hemodialysis; time from transplantation; daily doses of prednisolone and cyclosporin A used; serum calcium (normal 8.6–11 mg/dl); serum phosphate (3.6–4.5 mg/dl); ALP (70–306 IU/ml); intact PTH (RIA 12–72 pg/ml); serum creatinine (0.5–1.5); creatinine clearance; serum albumin (3.6–5.0 g/dl), and the rate of aseptic bone necrosis. We compared these recipients to 20 randomly selected normocalcemic recipients (group B). Parathyroid hyperplasia was detected with ultrasound scan and TC-MIBI nuclear scan in recipients with high PTH levels. Student’s t test and χ2 test were used for statistical analysis. Age, time on hemodialysis, time from transplantation, and immunosuppressive drug doses were not different between the 2 groups. Hypercalcemic recipients had a low mean phosphate and high mean ALP levels compared to normocalcemic recipients. High PTH levels were found only in group A. The incidence of aseptic bone necrosis was not different between 2 study groups.In 4 hypercalcemic recipients (2.1% of all recipients) higher PTH levels (>200 pg/dl) were found. Parathyroid adenomas were shown in 3 recipients on ultrasound scan. In these recipients parathyroidectomy was performed to treat persistent hypercalcemia. Calcium levels returned to normal following parathyroidectomy. Nodular hyperplasia was seen in 2 and adenoma (0.5%) in 1 patient during histopathologic examinations of the glands. We followed other cases in the outpatient clinic, since their serum calcium levels were below 12 mg/dl. Results are seen in table 1.Persistent hypercalcemia due to hyperparathyroidism is not rare in our renal allograft recipients. Their time on hemodialysis and allograft functions were not different from other recipients. Since hypercalcemia usually resolves spontaneously with time, Diethelm et al. [6]suggested that parathyroidectomy was not necessary. Parathyroidectomy is indicated on only a few cases where severe hypercalcemia complications are seen [1]. We performed parathyroidectomy in our recipients because the imaging techniques showed parathyroid adenoma in patients with higher parathyroid levels. Using active vitamin D to suppress PTH is not effective in recipients with parathyroid adenoma [1, 2, 3, 4, 7].In conclusion, hypercalcemia is not rare in renal transplant recipients. In recipients who had high serum ALP levels and hypercalcemia parathyroid hyperplasia can occur. Parathyroid adenoma was found infrequently in these recipients.