Kidney Week

Abstract: PO1185

Hypercalcemia and Metabolic Alkalosis Induced by the Novel Potassium Binder Patiromer: Report of Rare Event

Session Information

• Mineral Homeostasis and Acid-Base Disorders: Clinical
  November 04, 2021 | Location: On-Demand, Virtual Only
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolyte, and Acid-Base Disorders

• 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Suchow, Kathryn Joanna, Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States

Kathryn Joanna Suchow, MD

• Kanduri, Swetha Rani, Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States

Swetha Rani Kanduri,

• Velez, Juan Carlos Q., Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States

Juan Carlos Q. Velez,

Introduction

Patiromer is a calcium (Ca)-potassium (K) exchange resin approved for the treatment of hyperkalemia. Disorders of Ca or acid base balance were not reported in pre-approval clinical trials. Post-marketing, only 2 case reports of hypercalcemia associated with the use of patiromer have been recently published. We present a case of a patient with chronic kidney disease (CKD) with an unusual picture of hypercalcemia, metabolic alkalosis and hypokalemia upon intensification of patiromer dosing.

Case Description

A 56-year-old white man with CKD stage 4 (baseline creatinine 2.8 mg/dL) due to type 1 diabetes mellitus, proteinuria (1.5 g/g) and persistently high serum potassium (sK, 5.5 – 5.9 mEq/L) attributed to type 4 renal tubular acidosis was evaluated in clinic. Due to high risk of CKD progression, patiromer 8.4 g qd was prescribed to enable RAS blockade. Five months later, sK remained elevated at 5.0 mEq/L. Patiromer dosage was thus increased to 16.8 g qd. Three months later, sK fell to 4.1 mEq/L. Hence, patiromer was maintained at 16.8 g qd and irbesartan initiated. At that time, corrected serum calcium (sCa) was 9.3 mg/dL and serum bicarbonate (sHCO₃) 26 mEq/L. Five months later, routine laboratory tests revealed a sK 2.5 mEq/L, sCa 12.6 mg/dL and sHCO₃ 34 mEq/L. The patient denied recreational or over-the-counter drugs, diuretics or calcium supplements. Patiromer was discontinued. Thorough investigation (PTH, PTH-related peptide, 1,25-OH-vitamin D, 25-OH-vitamin D, TSH, serum protein electrophoresis, free light chains, cortisol and ACTH) was negative for other causes of hypercalcemia. Five days later, sK was 4.1 mEq/L, sCa 7.7 mg/dL and sHCO₃ 32 mmol/L.

Discussion

Patiromer promotes gastrointestinal elimination of potassium by binding of the molecule to potassium in exchange for calcium. Increased in intestinal absorption of calcium results in hypercalciuria but not sustained hypercalcemia. The clinical course of our patient suggests that the increased dose of patiromer led to a profound exchange of calcium and potassium ions leading to hypercalcemia, iatrogenic hypokalemia and resulting metabolic alkalosis. The role of secondary hyperparathyroidism in this case remains unclear. We recommend cautious vigilance of patients receiving patiromer and undergoing dose escalation