Kidney Week

Abstract: FR-OR068

Effects of the Potassium Binding Polymer Patiromer on Markers of Mineral Metabolism

Session Information

• Mineral Disease: FGF23 and Mineral Metabolism
  November 03, 2017 | Location: Room 273, Morial Convention Center
  Abstract Time: 04:30 PM - 04:42 PM

Category: Mineral Disease

• 1201 Mineral Disease: Ca/Mg/PO4

Authors

• Bushinsky, David A., University of Rochester Medical Center, Rochester, New York, United States

David A. Bushinsky, MD

• Spiegel, David M., Relypsa, Inc., a Vifor Pharma Company, Redwood City, California, United States

David M. Spiegel,

• Yuan, Jinwei, Relypsa, Inc., a Vifor Pharma Company, Redwood City, California, United States

Jinwei Yuan,

• Warren, Suzette, Relypsa, Inc., a Vifor Pharma Company, Redwood City, California, United States

Suzette Warren,

• Pergola, Pablo E., Renal Associates, PA, San Antonio, Texas, United States

Pablo E. Pergola,

Background

Patiromer is a non-absorbed potassium (K)-binding polymer approved for treatment of hyperkalemia (HK), which uses calcium (Ca) as the counter-exchange ion. The 4-week TOURMALINE study in patients with HK demonstrated that patiromer once-daily (QD) reduces serum K when given without food similarly to when given with food. Here we report data from TOURMALINE on markers of mineral metabolism.

Methods

Initial patiromer dose was 8.4 g QD and was adjusted to achieve and maintain serum K between 3.8-5.0 mEq/L. In this prespecified analysis, baseline and week 4 (wk 4) serum and 24-hour urine (u) markers of mineral metabolism normalized for u-creatinine (Cr) excretion, to correct for collection errors, are reported for the overall population of 112 patients. All values are mean ± SE; p values are for change from baseline by paired t-test.

Results

Baseline serum Ca and phosphate (P) were 9.31 ± 0.06 and 4.10 ± 0.07 mg/dL, respectively, and were not different at wk 4 (9.34 ± 0.06 and 3.99 ± 0.07 mg/dL, respectively). In the 16 patients with elevated serum P (> 4.8 mg/dL) at baseline, patiromer decreased P from 5.32 ± 0.11 to 4.68 ± 0.26 mg/dL at wk 4 (p<0.02). In the overall population, Cr-normalized uP decreased from 628.2 ± 28.2 at baseline to 573.6 ± 29.4 mg/24 hr at wk 4 (p<0.01). Cr-normalized uCa was 50.8 ± 6.4 at baseline and did not change at wk 4 (58.5 ± 6.7 mg/24 hr; p=0.1). Serum 1,25(OH)₂D levels decreased from 37.3 ± 1.6 at baseline to 34.1 ± 1.7 pg/mL at wk 4 (p<0.05), while PTH decreased from 85.1 ± 5.6 at baseline to 65.2 ± 4.5 pg/mL at wk 4 (p<0.0001). There were no changes in mean levels of FGF-23 or 25(OH)D.

Conclusion

In addition to lowering serum K, patiromer decreased mean uP excretion in the overall population and mean serum P in patients with hyperphosphatemia, while not changing mean uCa or mean serum Ca. PTH and 1,25(OH)₂D both decreased. These findings suggest that when patiromer exchanges intestinal K for Ca, some of the released Ca binds to intestinal P lowering uP and serum P in hyperphosphatemic patients and some of the Ca is absorbed, lowering PTH and 1,25(OH)₂D without changing serum Ca.

Funding

• Commercial Support –