Calcium supplementation after parathyroidectomy in dialysis and renal transplant patients

Abstract

BackgroundData on the risk factors and clinical course of hungry bone syndrome are lacking in dialysis and renal transplant patients who undergo parathyroidectomy. In this study, we aimed to assess the risks and clinical course of hungry bone syndrome and calcium repletion after parathyroidectomy in dialysis and renal transplant patients.MethodsWe performed a retrospective review of parathyroidectomies performed at The Nebraska Medical Center.ResultsWe identified 41 patients, ie, 30 (73%) dialysis and eleven (27%) renal transplant patients. Dialysis patients had a significantly higher pre-surgery intact parathyroid hormone (iPTH, P<0.001) and a larger iPTH drop after surgery (P<0.001) than transplant recipients. Post-surgery hypocalcemia in dialysis patients was severe and required aggressive and prolonged calcium replacement (11 g) versus a very mild hypocalcemia requiring only brief and minimal replacement (0.5 g) in transplant recipients (P<0.001). Hypophosphatemia was not detected in the dialysis group. Phosphorus did not increase immediately after surgery in transplant recipients. The hospital stay was significantly longer in dialysis patients (8.2 days) compared with transplant recipients (3.2 days, P<0.001).ConclusionThe clinical course of hungry bone syndrome is more severe in dialysis patients than in renal transplant recipients. Young age, elevated alkaline phosphatase, elevated pre-surgery iPTH, and a large decrease in post-surgical iPTH are risk factors for severe hungry bone syndrome in dialysis patients.

Management of serum calcium reductions among patients on hemodialysis following cinacalcet initiation

“…This reduction of calcium levels related to cinacalcet-induced decreases in PTH is similar to observed PTH and calcium reductions that comprise the "hungry bone syndrome" observed after parathyroidectomy in patients with severe SHPT. [21][22][23] Severity of SHPT and associated bone disease, as assessed by the degree of alkaline phosphatase elevation, has been shown to be predictive of the development of hungry bone syndrome and the need for calcium supplementation after parathyroidectomy. 24,25 Shigematsu et al 26 evaluated changes in markers of bone resorption and bone formation after cinacalcet initiation and noted that bone resorption markers decreased swiftly, while bone formation markers actually increased acutely and only decreased later in the course of treatment.…”

Surgical management of secondary hyperparathyroidism in chronic kidney disease—a consensus report of the European Society of Endocrine Surgeons

“…Post-PTX hypocalcaemia is precipitated by several factors: increased deposition of calcium in bone (hungry bone syndrome), uncoupling of bone formation and resorption [96], failure of the parathyroid remnant (if any), and sometimes coexistent hypomagnesaemia [97,98]. Young age (<36 years), low preoperative calcium levels (<10 md/dl), elevated alkaline phosphatase (>1.92 mmol/l) and elevated presurgery PTH (>150 pmol/l), and subperiosteal bone resorption were recognized as preoperative risk factors [95,99,100] (EL 3-4).…”

Transient Hypocalcemia in a Dialysis Patient With Paget’s disease and Presumed Renal Cell Carcinoma

“…In both Paget’s disease and secondary hyperparathyroidism (SHPT), rapid turnover of bone may produce an excess of unmineralized osteoid. 20 , 21 We therefore contemplated a scenario, similar to the post-parathyroidectomy hungry-bone syndrome, 22 in which calcium flux from the skeleton had fallen while mineralization of osteoid continued unabated. We speculated that radiation-induced damage to bone or to the parathyroid glands had created the hypothetical disequilibrium.…”