Abstract: FR-PO696
Cinacalcet-Induced Permanent Hypocalcemia in a Patient with Primary Hyperparathyroidism and Normal Kidney Function
Session Information
- Electrolytes and Cancer Trainee Case Reports
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Rigual soler, Natacha, Albany Medical College, Albany, New York, United States
- Gosmanov, Aidar, Stratton VA Medical Center, Albany, New York, United States
- Gosmanova, Elvira, Stratton VA Medical Center and Albany Medical College, Albany, New York, United States
Introduction
Cinacalcet (C ) increases sensitivity of calcium (Ca) sensing receptor to extracellular Ca and suppresses parathyroid hormone (PTH) secretion. C is used in patients with primary hyperparathyroidism (PHPT) who are not surgical candidates. We report a case of irreversible hypocalcemia after 6 months of C administration in a patient with PHTP.
Case Description
A 58-year-old Caucasian male with PHPT, recurrent nephrolithiasis, osteopenia in femoral neck and normal kidney function (eGFR>90ml/min/1.73m2) underwent surgical resection of 2 parathyroid glands. Postoperatively, PTH remained elevated (iPTH 227pg/mL, normal level [30-69]) in association with albumin-corrected Ca (aCa) 10.4mg/dL [8.2-10.2], ionized Ca (iCa) 1.4mmol/L [1.15-1.35]) and hypercalciuria (24-hr urinary Ca 427mg). Due to persistent PHPT and refusal of further surgery C 30 mg daily was initiated. C resulted in resolution of hypercalcemia, normalization of Pi and iPTH fall to 139pg/dL in 4 weeks. However, 6 months later the patient presented to the hospital with newly developed widespread paresthesia and hypocalcemia (aCa 7.2mg/dL, iCa 0.96 mmol/L), hyperphosphatemia (4.6mg/dL) and suppressed PTH (7pg/dL). C was discontinued and Ca supplements were initiated leading to normalization of iCa (1.17mmol/L) and PTH (38pg/ml). However, the patient continued to have hypercalciuria and required continuous oral Ca supplementation to avoid paresthesia and maintain eucalcemia even 12 months later. Repeat DXA showed improvement in bone mineral density.
Discussion
Reversible hypocalcemia due to C was mainly reported in patients with advanced CKD and it usually responds to a reduction or discontinuation of C. The present case has several novel features. Firstly, C-induced hypocalcemia developed in a patient with normal kidney function. Secondly, because PTH has normalized after temporal C exposure, we suggest that C can induce apoplexy of PTH-overproducing parathyroid cells. Lastly, we suspect the development of a defect resembling renal PTH resistance based on the presence of persistent hypercalciuria despite normal PTH levels with resultant hypocalcemia requiring continuous Ca supplementation. Further clinical investigations are needed to understand whether in some patients cinacalcet can cause or unmask renal PTH resistance.