Abstract: TH-PO199

Effects of Patiromer on Markers of Mineral Metabolism in Patients with Hyperkalemia and Hyperphosphatemia

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Bushinsky, David A., University of Rochester Medical Center, Rochester, New York, United States
  • Spiegel, David M., Relypsa, Inc., a Vifor Pharma Group Company, Redwood City, California, United States
  • Yuan, Jinwei, Relypsa, Inc., a Vifor Pharma Group Company, Redwood City, California, United States
  • Warren, Suzette, Relypsa, Inc., a Vifor Pharma Group Company, Redwood City, California, United States
  • Fogli, Jeanene, Relypsa, Inc., a Vifor Pharma Group Company, Redwood City, California, United States
  • Pergola, Pablo E., Renal Associates, PA, San Antonio, Texas, United States
Background

Patiromer (PAT) is a once-daily K binder for hyperkalemia (HK) treatment; Ca is the counterexchange ion. In TOURMALINE (NCT02694744) patients (pts) with serum K >5.0 mEq/L were randomized to PAT 8.4 g QD without/with food for 4 wks, with doses adjusted to achieve/maintain serum K 3.8-5.0 mEq/L (target range). The primary endpoint (% of pts in target range at wk 3/4) was met in 83% dosed without food and 87% with food, with overlapping 95% CIs. We report the effects of PAT on markers of mineral metabolism in the pts with baseline (BL) hyperphosphatemia (HyperP, serum phosphate >4.8 mg/dL).

Methods

BL and wk 4 serum and 24-hr urine phosphate and Ca, and other markers, are reported for all HyperP pts combined (without/with food). Time-corrected 24-hr urine phosphate/Ca values were normalized to each pt’s mean of the time-corrected urine creatinine (Cr) level.

Results

16 pts had HyperP; 11 dosed without and 5 with food. All had CKD (median [Q1, Q3] eGFR 18.0 [11.5, 20.5] mL/min/1.73m2) and hypertension; 14/16 had diabetes. Two pts were on stable doses of sevelamer during the study. The primary endpoint was met in 14/16 pts (10/11 without and 4/5 with food in target range). There were significant reductions in serum and 24-hr urine phosphate (Table). Mean serum Mg decreased significantly. Mean serum Ca and 24-hr urine Ca were not different from BL at wk 4. Serum PTH levels decreased at wk 4 (P=0.19). Overall, 15/16 had ≥1 post-BL serum phosphate assessment; 9/15 had serum phosphate in the normal range by wk 4.

Conclusion

The decrease in serum and urine phosphate in the small number of HyperP pts in this study supports that intestinal phosphate is bound to some of the released Ca when PAT is used to lower serum K. These findings suggest that PAT may aid in the management of HyperP in pts with CKD requiring both K and phosphate binders.

Funding

  • Commercial Support