Abstract: FR-PO595
Patiromer Associated Hypercalcemia
Session Information
- Trainee Case Reports - III
October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 1902 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Ghaffar, Adil, Saint Vincent Hospital, Worcester, Massachusetts, United States
- Magoo, Hemant, Saint Vincent Hospital, Worcester, Massachusetts, United States
- Verma, Ashish, Saint Vincent Hospital, Worcester, Massachusetts, United States
Introduction
Patiromer calcium sorbitex is a non-absorbable cation exchange polymer approved for management of chronic hyperkalemia in patients with chronic kidney disease. We report a case of hypercalcemia in a patient with chronic kidney disease stage 5 (CKD 5) treated with patiromer.
Case Description
A 75-year-old Caucasian male had Hypertension and CKD 5 (GFR of 10 ml/min/1.73m2) secondary to biopsy proven Focal Segmental Glomerulosclerosis. He had chronic hyperkalemia despite discontinuation of RAAS inhibition. Patient was initiated on patiromer 8.4 grams daily. This has been continued for over a year now. Prior to patiromer's introduction, corrected calcium was in the 8.5 to 8.9 mg/dl range. Eight months into treatment with patiromer, calcium was between 10.5 to 11.1. iPTH was 23-29 pg/ml. 25-hydroxy vitamin D was low at 9ng/ml. TSH was normal and serum immunofixation was negative. Patient had been taking prn TUMS (calcium carbonate) otc for reflux symptoms that was discontinued upon discovery of hypercalcemia. However, hypercalcemia has persisted several months after discontinuation of TUMS.
Discussion
Patiromer binds free potassium and magnesium ions in the gut and releases calcium ions in exchange. This helps correct hyperkalemia in these patients without sodium loading, a problem with sodium polysterene sulfonate. Though 10% of the patients did develop hypomagnesemia (below 1.4mg/dL), significant hypercalcemia has not been reported in any clinical study or subsequently. The amount of calcium released from patiromer that may be systemically absorbed is modest and did not lead to significant hypercalcemia in clinical studies. However, patients with advanced CKD may be more vulnerable due to their limited ability to excrete calcium in the urine. Prolonged treatment with Patiromer may increase the risk of hypercalcemia as noted in our patient and should be monitored for, besides hypomagnesemia.