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Letter

Safety, Effectiveness, and Tolerability of Patiromer in Kidney Transplant Recipients

Lim, Mary Ann MD1; Sawinski, Deirdre MD1; Trofe-Clark, Jennifer Pharm D1,2

Author Information
doi: 10.1097/TP.0000000000002829
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To the Editor

Hyperkalemia is common in kidney transplant recipients (KTRs), resulting from impaired tubular potassium secretion due to kidney dysfunction or medication side effects (calcineurin inhibitors, trimethoprim or renin-angiotensin-aldosterone blockers).1,2 Patiromer, a nonabsorbable cation-exchanger, is an effective treatment for chronic hyperkalemia.3,4 Despite Food and Drug Administration-approval in 2015, concerns regarding its impact on drug absorption have limited patiromer use in KTRs. To date, there is only one published report of patiromer use involving 2 KTRs.5 We conducted this study to determine the safety, effectiveness, and tolerability of patiromer in our KTRs.

In this IRB-approved, single-center, retrospective review of all adult KTRs started on patiromer between January 1, 2016, and January 25, 2019, 19 participants were included (10 Caucasians, 7 African Americans, 2 Asians). Median age was 61 years and median follow-up was 45 days. Most were men (n = 15) and had deceased donors (n = 13) and diabetic kidney disease (n = 9) and started patiromer within the first posttransplant year (n = 10). Five patients were on sulfamethoxazole-trimethoprim for prophylaxis, and all were on a potassium-restricted diet (<2 g/day). Data were collected through February 7, 2019.

Fifteen participants (79%) were previously on sodium polystyrene sulfonate (SPS), while 4 started de novo during SPS market shortage (Figure 1). For those previously on SPS, most common final dose of patiromer was 8.4 g for every 30 g of SPS.

FIGURE 1.
FIGURE 1.:
Tacrolimus doses (a), tacrolimus levels (b), and potassium levels (c) before and after patiromer initiation. Subjects 1–15 were switched from chronic sodium polystyrene sulfonate (SPS) to patiromer; subjects 16–19 were not previously on SPS.

Patiromer was started at 8.4 g/day in 14 participants (5 requiring dose escalation to 16.8 g/day, 1 requiring further escalation to 25.2 g/day), 16.8 g/day in 3 participants (1 requiring dose decrease to 8.4 g/day), 8.4 g/48 hours in 1 participant, and 8.4 g 3x/week in 1 participant. Dose changes occurred 1–4 weeks after initiation. One subject required an emergency room visit for hyperkalemia during patiromer dose adjustment. As of last follow-up, all subjects remained on patiromer and 16 (84%) had potassium levels <5.2 mmol/L. Two of the 3 participants with potassium levels ≥5.2 mmol/L had documented nonadherence to patiromer.

All participants were on immediate-release tacrolimus-based immunosuppression. All were instructed to take patiromer around noon, at least 3 hours separated from all other medications. Seven (37%) subjects, including 6 previously on SPS and 1 with prior supratherapeutic tacrolimus level, required a tacrolimus dose decrease within 1–4 weeks of patiromer initiation. None with previously therapeutic tacrolimus levels required tacrolimus dose increase. It is possible that prior SPS use may have affected tacrolimus absorption, necessitating a dose reduction after SPS-to-patiromer conversion. Although 2 subjects had constipation and 1 complained of diarrhea, none stopped patiromer because of intolerable GI side-effects. Serum creatinine levels remained within baseline ranges, except for 1 participant whose declining graft function was attributed to progressive CKD. No participants developed hypercalcemia. Unfortunately, magnesium and mycophenolic acid levels were not available for review.

Even though our study is limited by small sample size and retrospective design, it adds to the published data regarding patiromer use in the kidney transplant population.5 We demonstrated that patiromer is safe and effective for hyperkalemia in KTRs and has an acceptable side-effect profile. Tacrolimus levels should be followed closely as some of our participants required tacrolimus dose changes.

References

1. Ben Salem C, Badreddine A, Fathallah N, et al. Drug-induced hyperkalemia. Drug Saf. 2014; 37:677–692
2. Palmer BF, Clegg DJ. Hyperkalemia across the continuum of kidney function. Clin J Am Soc Nephrol. 2018; 13:155–157
3. Bakris GL, Pitt B, Weir MR, et al.; AMETHYST-DN Investigators. Effect of patiromer on serum potassium level in patients with hyperkalemia and diabetic kidney disease: the AMETHYST-DN randomized clinical trial. JAMA. 2015; 314:151–161
4. Weir MR, Bakris GL, Bushinsky DA, et al.; OPAL-HK Investigators. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. N Engl J Med. 2015; 372:211–221
5. Rattanavich R, Malone AF, Alhamad T. Safety and efficacy of patiromer use with tacrolimus in kidney transplant recipients. Transpl Int. 2019; 32:110–111
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