PubMed:26459796 JSONTXT

{"project":"wangzhuo19_800","denotations":[{"id":"T1","span":{"begin":10,"end":19},"obj":"CI"},{"id":"T2","span":{"begin":199,"end":208},"obj":"CI"},{"id":"T3","span":{"begin":532,"end":541},"obj":"CI"},{"id":"T4","span":{"begin":909,"end":918},"obj":"CI"},{"id":"T5","span":{"begin":1497,"end":1506},"obj":"CI"},{"id":"T6","span":{"begin":1616,"end":1625},"obj":"CI"},{"id":"T7","span":{"begin":1812,"end":1821},"obj":"CI"},{"id":"T8","span":{"begin":104,"end":117},"obj":"DP"},{"id":"T9","span":{"begin":122,"end":144},"obj":"DP"},{"id":"T10","span":{"begin":368,"end":390},"obj":"DP"},{"id":"T11","span":{"begin":392,"end":395},"obj":"DP"},{"id":"T12","span":{"begin":1768,"end":1771},"obj":"DP"},{"id":"T13","span":{"begin":1116,"end":1129},"obj":"DP"},{"id":"T14","span":{"begin":1131,"end":1133},"obj":"DP"},{"id":"T15","span":{"begin":1776,"end":1778},"obj":"DP"},{"id":"T16","span":{"begin":306,"end":319},"obj":"DP"},{"id":"T17","span":{"begin":321,"end":323},"obj":"DP"}],"text":"Effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on RAAS inhibitors.\nAIMS: We evaluated the effects of patiromer, a potassium (K(+) )-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial.\nMETHODS AND RESULTS: Chronic kidney disease (CKD) patients on renin-angiotensin-aldosterone system inhibitors (RAASi) with serum K(+) levels ≥5.1 mEq/L to \u003c6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K(+) from baseline to week 4. Eligible patients (those with baseline K(+) ≥5.5 mEq/L to \u003c6.5 mEq/L and levels ≥3.8 mEq/L to \u003c5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K(+) from baseline to week 4 was -1.06 ± 0.05 mEq/L [95% confidence interval (CI), -1.16,-0.95; P \u003c 0.001]; 76% (95% CI, 69,84) achieved serum K(+) , 3.8 mEq/L to \u003c5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K(+) from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P \u003c 0.001); recurrent hyperkalaemia (serum K(+) , ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P \u003c 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%.\nCONCLUSION: In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K(+) , and, compared with placebo, reduced recurrent hyperkalaemia."}

{"project":"luoyt2021_800_3","denotations":[{"id":"T1","span":{"begin":10,"end":19},"obj":"CI"},{"id":"T10","span":{"begin":122,"end":144},"obj":"DP"},{"id":"T11","span":{"begin":278,"end":291},"obj":"DP"},{"id":"T12","span":{"begin":306,"end":319},"obj":"DP"},{"id":"T13","span":{"begin":321,"end":323},"obj":"DP"},{"id":"T14","span":{"begin":368,"end":390},"obj":"DP"},{"id":"T15","span":{"begin":392,"end":395},"obj":"DP"},{"id":"T16","span":{"begin":1768,"end":1771},"obj":"DP"},{"id":"T17","span":{"begin":73,"end":86},"obj":"DP"},{"id":"T18","span":{"begin":148,"end":163},"obj":"CI"},{"id":"T19","span":{"begin":409,"end":456},"obj":"CI"},{"id":"T2","span":{"begin":199,"end":208},"obj":"CI"},{"id":"T20","span":{"begin":458,"end":463},"obj":"CI"},{"id":"T21","span":{"begin":1911,"end":1924},"obj":"DP"},{"id":"T22","span":{"begin":1788,"end":1801},"obj":"DP"},{"id":"T23","span":{"begin":1539,"end":1552},"obj":"DP"},{"id":"T24","span":{"begin":1776,"end":1778},"obj":"DP"},{"id":"T25","span":{"begin":1131,"end":1133},"obj":"DP"},{"id":"T26","span":{"begin":1116,"end":1129},"obj":"DP"},{"id":"T3","span":{"begin":1812,"end":1821},"obj":"CI"},{"id":"T4","span":{"begin":1616,"end":1625},"obj":"CI"},{"id":"T5","span":{"begin":1497,"end":1506},"obj":"CI"},{"id":"T6","span":{"begin":909,"end":918},"obj":"CI"},{"id":"T7","span":{"begin":532,"end":541},"obj":"CI"},{"id":"T8","span":{"begin":212,"end":245},"obj":"CI"},{"id":"T9","span":{"begin":104,"end":117},"obj":"DP"},{"id":"T27","span":{"begin":1884,"end":1891},"obj":"CI"},{"id":"T28","span":{"begin":1598,"end":1605},"obj":"CI"},{"id":"T29","span":{"begin":1475,"end":1482},"obj":"CI"},{"id":"T30","span":{"begin":932,"end":939},"obj":"CI"}],"text":"Effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on RAAS inhibitors.\nAIMS: We evaluated the effects of patiromer, a potassium (K(+) )-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial.\nMETHODS AND RESULTS: Chronic kidney disease (CKD) patients on renin-angiotensin-aldosterone system inhibitors (RAASi) with serum K(+) levels ≥5.1 mEq/L to \u003c6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K(+) from baseline to week 4. Eligible patients (those with baseline K(+) ≥5.5 mEq/L to \u003c6.5 mEq/L and levels ≥3.8 mEq/L to \u003c5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K(+) from baseline to week 4 was -1.06 ± 0.05 mEq/L [95% confidence interval (CI), -1.16,-0.95; P \u003c 0.001]; 76% (95% CI, 69,84) achieved serum K(+) , 3.8 mEq/L to \u003c5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K(+) from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P \u003c 0.001); recurrent hyperkalaemia (serum K(+) , ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P \u003c 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%.\nCONCLUSION: In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K(+) , and, compared with placebo, reduced recurrent hyperkalaemia."}

{"project":"Linmchun_800_3","denotations":[{"id":"T1","span":{"begin":10,"end":19},"obj":"CI"},{"id":"T10","span":{"begin":392,"end":395},"obj":"DP"},{"id":"T11","span":{"begin":1768,"end":1771},"obj":"DP"},{"id":"T12","span":{"begin":1812,"end":1821},"obj":"CI"},{"id":"T14","span":{"begin":1475,"end":1482},"obj":"CI"},{"id":"T15","span":{"begin":1598,"end":1605},"obj":"CI"},{"id":"T16","span":{"begin":122,"end":144},"obj":"DP"},{"id":"T17","span":{"begin":321,"end":323},"obj":"DP"},{"id":"T18","span":{"begin":306,"end":319},"obj":"DP"},{"id":"T19","span":{"begin":278,"end":291},"obj":"DP"},{"id":"T2","span":{"begin":199,"end":208},"obj":"CI"},{"id":"T20","span":{"begin":1776,"end":1778},"obj":"DP"},{"id":"T21","span":{"begin":1788,"end":1801},"obj":"DP"},{"id":"T22","span":{"begin":1911,"end":1924},"obj":"DP"},{"id":"T23","span":{"begin":104,"end":117},"obj":"DP"},{"id":"T24","span":{"begin":73,"end":86},"obj":"DP"},{"id":"T25","span":{"begin":1539,"end":1552},"obj":"DP"},{"id":"T26","span":{"begin":1884,"end":1891},"obj":"CI"},{"id":"T27","span":{"begin":409,"end":456},"obj":"CI"},{"id":"T28","span":{"begin":458,"end":463},"obj":"CI"},{"id":"T29","span":{"begin":212,"end":245},"obj":"CI"},{"id":"T3","span":{"begin":532,"end":541},"obj":"CI"},{"id":"T30","span":{"begin":148,"end":163},"obj":"CI"},{"id":"T31","span":{"begin":1131,"end":1133},"obj":"DP"},{"id":"T32","span":{"begin":1116,"end":1129},"obj":"DP"},{"id":"T4","span":{"begin":909,"end":918},"obj":"CI"},{"id":"T5","span":{"begin":932,"end":939},"obj":"CI"},{"id":"T6","span":{"begin":1497,"end":1506},"obj":"CI"},{"id":"T7","span":{"begin":1616,"end":1625},"obj":"CI"},{"id":"T9","span":{"begin":368,"end":390},"obj":"DP"}],"text":"Effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on RAAS inhibitors.\nAIMS: We evaluated the effects of patiromer, a potassium (K(+) )-binding polymer, in a pre-specified analysis of hyperkalaemic patients with heart failure (HF) in the OPAL-HK trial.\nMETHODS AND RESULTS: Chronic kidney disease (CKD) patients on renin-angiotensin-aldosterone system inhibitors (RAASi) with serum K(+) levels ≥5.1 mEq/L to \u003c6.5 mEq/L (n = 243) received patiromer (4.2 g or 8.4 g BID initially) for 4 weeks (initial treatment phase); the primary efficacy endpoint was mean change in serum K(+) from baseline to week 4. Eligible patients (those with baseline K(+) ≥5.5 mEq/L to \u003c6.5 mEq/L and levels ≥3.8 mEq/L to \u003c5.1 mEq/L at the end of week 4) entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo; the primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of that phase. One hundred and two patients (42%) had heart failure (HF). The mean [± standard error (SE)] change in serum K(+) from baseline to week 4 was -1.06 ± 0.05 mEq/L [95% confidence interval (CI), -1.16,-0.95; P \u003c 0.001]; 76% (95% CI, 69,84) achieved serum K(+) , 3.8 mEq/L to \u003c5.1 mEq/L. In the randomized withdrawal phase, the median increase in serum K(+) from baseline of that phase was greater with placebo (n = 22) than patiromer (n = 27) (P \u003c 0.001); recurrent hyperkalaemia (serum K(+) , ≥5.5 mEq/L) occurred in 52% on placebo and 8% on patiromer (P \u003c 0.001). Mild-to-moderate constipation was the most common adverse event (11%); hypokalaemia occurred in 3%.\nCONCLUSION: In patients with CKD and HF who were hyperkalaemic on RAASi, patiromer was well tolerated, decreased serum K(+) , and, compared with placebo, reduced recurrent hyperkalaemia."}