Patiromer eliminates potassium through the gastrointestinal (GI) tract and reduces serum potassium in patients on hemodialysis (HD), but the binder also appears to affect serum and stool levels of other electrolytes, according to a new study.
Investigators measured serum and fecal electrolytes in 27 anuric patients with hyperkalemia (defined as predialysis serum potassium levels of 5.1 mEq/L or higher) receiving HD (mainly 2 mEq/L dialysate) during 20 weeks: 2 weeks of no treatment, 12 weeks of patiromer (16.8 g/d), and 6 weeks of no treatment. Patients were asked to keep a consistent diet throughout the study period. Dietary potassium intake was 1500 to 1600 mg/d throughout. Dietary calcium, magnesium, and phosphorus remained stable. Only sodium intake decreased during the treatment phase.
Serum potassium significantly declined then rebounded from a mean of 5.7 mEq/L before treatment to 5.1 mEq/L with patiromer to 5.4 mEq/L after treatment (P <.001), Dominic Raj, MD, of George Washington University in Washington DC, and colleagues reported in Kidney International. During treatment, 42% of patients had serum potassium within a range of 3.5 to 5.0 mEq/L (and no one had levels less than 3.5 mEq/L).
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Patiromer effectively eliminated potassium through the GI tract. Stool potassium significantly increased from 4132 mg/g before treatment to 5923 mg/g with patiromer, then decreased to 4246 mg/g after treatment (P =.009). For each 1 mg/g increase in stool potassium, serum potassium significantly declined by 0.05 mEq/L. The team estimated that 16.8 g of patiromer is needed to increase fecal potassium by 1880 mg/g and reduce serum potassium by 0.5 mEq/L.
Patiromer, which exchanges calcium for potassium in the colon, increased serum calcium. During the treatment phase, serum calcium significantly increased from 8.9 to 9.1 mg/dL (P =.02). Fecal calcium also was significantly higher during treatment 13017 mg/g vs 7874 pre- and 7635 mg/g post-treatment (P <.001).
The binder also appeared to decrease magnesium. Serum magnesium decreased significantly from 2.6 to 2.4 mg/dL with patiromer (P=.003). In contrast, a 1 mEg/L increase in serum magnesium was associated with a serum potassium increase of 1.07 mEq/L. The investigators observed no significant increase in fecal magnesium and found no significant changes in serum phosphorus.
“These results indicate that patiromer safely eliminates [potassium] through the GI tract and effectively reduces [serum potassium] in HD patients,” Dr Raj’s team stated. “Our results also suggest that although the affinity of patiromer is probably highest for [potassium], it also affects other electrolytes directly or indirectly through other mechanisms.”
No patient experienced clinically significant hypokalemia, hypercalcemia, or hypomagnesemia during patiromer treatment. Still, the investigators recommended that patients at risk for hypercalcemia be carefully monitored while treated with patiromer and advised that serum magnesium be periodically assessed in patients, especially in those at risk for cardiac arrhythmia.
Disclosure: This clinical trial was supported by Relypsa Inc, the makers of patiromer (Veltassa®). Please see the original reference for a full list of authors’ disclosures.
Reference
Amdur RL, Paul R, Barrows ED, et al. The potassium regulator patiromer affects serum and stool electrolytes in patients receiving hemodialysis. Kidney Int. Published online July 31, 2020. doi:10.1016/j.kint.2020.06.042
