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Supplements Managing Hyperkalemia in High-Risk Patients in Long-Term Care
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Managing Hyperkalemia in High-Risk Patients in Long-Term Care
Rajeev Kumar, MD, FACP; Leo Kanev, MD; Steven D. Woods, PharmD; Melanie Brenner, PharmD; and Bernie Smith, RPh, MBA, MHA

Managing Hyperkalemia in High-Risk Patients in Long-Term Care

Rajeev Kumar, MD, FACP; Leo Kanev, MD; Steven D. Woods, PharmD; Melanie Brenner, PharmD; and Bernie Smith, RPh, MBA, MHA
Potassium-Restricted Diet
A K+-restricted diet is often recommended28 but is not a long-term and effective therapeutic approach to chronic hyperkalemia management. The dietary approach is difficult to comply with and may adversely affect nutrition in patients who may benefit the most from a healthy diet, such as the Dietary Approaches to Stop Hypertension diet.65 Moreover, the clinical utility of this approach has not been tested in randomized controlled trials.66

Although loop and/or thiazide diuretics have long been used to treat hyperkalemia, and may be a feasible choice in some patients with CKD, use of these agents may not be possible or may be inappropriate in others.32,66-68 Factors such as extracellular volume, distal delivery of sodium, and kidney function may play a role in the effectiveness of diuretic-induced K+ excretion but are impaired in patients with advanced CKD and/or HF.32,69-71 In addition, a high dose or combination of diuretics may cause adverse effects such as volume depletion and gout.72,73 Diuretics may be overused in the elderly74 and contribute to adverse effects and drug-drug interactions in this patient population.75,76

Potassium Binders
Until recently, the only available treatment option specifically indicated for hyperkalemia in the United States was sodium polystyrene sulfonate (SPS).77 Although SPS was developed more than 50 years ago, it lacks sufficient clinical trial data with appropriate controls and its efficacy has not been rigorously evaluated.78-80 A short-term (7 days) and small placebo-controlled study (n = 33) assessed the efficacy and safety of SPS in treating mild-to-moderate hyperkalemia (serum K+ level 5.0-5.9 mEq/L) in outpatients with CKD.81 Treatment with SPS resulted in a significantly greater reduction in serum K+ level compared with placebo, but the percentage of patients achieving normokalemia at the end of treatment was similar in the 2 groups.81 The rates of electrolyte disturbances and GI adverse events (AEs) were higher in the SPS group, but the small sample size precluded broad conclusions.

A prominent concern about the safety of SPS appears in its prescribing information, which includes a warning for the infrequent but potentially fatal AE of intestinal necrosis.77,82,83 A systematic review of biomedical databases identified 58 cases of severe GI AEs associated with SPS use in 30 reports; these included 36 (62%) cases of intestinal necrosis and 5 (9%) cases of perforation.83 Necrosis was reported with the use of SPS given both with and without sorbitol. Additionally, death due to GI injury was reported in 33% of these cases.83 The prescribing information further warns to reserve the use of SPS for patients who have normal bowel function and to avoid use in patients who are at risk of developing constipation or impaction. Another important concern is the presence of sodium as the counter-exchange ion in SPS, which may contribute to volume overload in patients who cannot tolerate even a small increase in sodium load, such as those with severe HF or hypertension.65

Newly Approved and Investigational K+ Binders

Patiromer is a K+-binding polymer approved by the FDA to treat hyperkalemia with a once-daily dosing regimen.84 Patiromer exchanges K+ for calcium and promotes fecal excretion of K+ in a dose-dependent manner, leading to a concordant reduction in serum K+ level.85-87 The exchange occurs throughout the gut, but predominantly in the colon where the K+ concentration is high and pH is optimal for exchange.87 Animal studies using the radiolabeled drug have shown that patiromer is not absorbed into the systemic circulation.87 A rigorously designed study of patients with CKD admitted to a clinical research unit showed that a single dose of patiromer reduces serum K+ level significantly within 7 hours following administration.88 Patiromer is administered as a powder mixed with 1/3 cup of water.84

Patiromer uses calcium rather than sodium as the counter-exchange ion to bind K+, thus avoiding sodium overload.84,87,89 The calcium released from K+ binding with patiromer has the potential to be absorbed or to bind to phosphate. In healthy volunteers, a total daily dose of patiromer 25.2 g (the maximum recommended dose) led to an increase in urine calcium of 73 mg/d and a decrease in urine phosphate of 64 mg/d.90 These data suggest that only a small fraction of calcium released from patiromer is available for absorption and some binds to intestinal phosphate.

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