Long-Term Effects of Patiromer for Hyperkalaemia Treatment in Patients with Mild Heart Failure and Diabetic Nephropathy on Angiotensin-Converting Enzymes/Angiotensin Receptor Blockers: Results from AMETHYST-DN

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  Figure 1. AMETHYST‐DN study design. *eGFR 15 to <60 mL/min/1.73 m2. †Primary endpoint. ‡RAASi therapy was continued after patiromer discontinuation only in patients who were normokalaemic (serum K+ ≤ 5.0 mEq/L) at the last on‐treatment visit. ACR, albumin‐to‐creatinine ratio; BID, twice daily; BP, blood pressure; CKD, chronic kidney disease; DM, diabetes mellitus; eGFR, estimated glomerular filtration rate; K+, potassium; PRN, as needed; RAASi, renin–angiotensin–aldosterone system inhibitors; spiro, spironolactone; Wk, week.

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  Figure 2. Least squares mean (95% CI) serum potassium levels over 52 weeks and during the follow‐up period in patients with (A) or without (B) HF. Serum potassium values [mmol/L (95% CI)] at baseline were as follows: in the HF subgroup, 5.11 (5.03, 5.20) for mild and 5.61 (5.28, 5.94) for moderate hyperkalaemia; and in the non‐HF subgroup, 5.16 (5.08, 5.23) for mild and 5.74 (5.59, 5.89) for moderate hyperkalaemia. All serum potassium analyses are based on central laboratory values. P‐values for least squares mean changes from baseline (for 52 weeks of treatment period) and from Week 52 (or time of last dose of patiromer; for follow‐up period). Least squares mean values are based on a mixed‐effects repeated‐measures model with serum potassium value as the dependent variable, time point and starting dose as fixed‐effect predictors, baseline central laboratory serum potassium value as a continuous covariate, and patient as a random effect. A compound symmetry matrix was fit. Least squares mean values for the follow‐up period are based on the same model described, while the baseline covariate used was the last potassium value before study termination. The blue shaded area denotes the target…