Effect of Patiromer on Hyperkalemia Recurrence in Older Chronic Kidney Disease Patients Taking RAAS Inhibitors

Weir, Matthew R.; Bushinsky, David A.; Benton, Wade W.; Woods, Steven D.; Mayo, Martha; Arthur, Susan; Pitt, Bertram; Bakris, George L.

doi:10.1016/j.amjmed.2017.11.011

Cited by 42 publications

(37 citation statements)

References 41 publications

(45 reference statements)

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“…Although a cause-effect relationship can only be proven by a trial [46], it is interesting that a post-hoc analysis of RENAAL trial in diabetic CKD patients has shown the nephroprotective efficacy of losartan was in part offset by the hyperkalemic effect of this drug [47]. Furthermore, a 8-week trial testing a new K binder in hyperkalemic ND-CKD patients showed that more patients could continue the nephroprotective therapy with ARB in the K-binder arm (95%) than in the placebo arm (50%) [48].…”

Section: Discussionmentioning

confidence: 99%

Competing-Risk Analysis of Death and ESKD by Hyperkalemia Status in Non-Dialysis CKD Patients Receiving Stable Nephrology Care

Provenzano¹,

Minutolo²,

Chiodini³

et al. 2018

Preprint

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Hyperkalemia burden in non-dialysis CKD under nephrology care is undefined. We prospectively followed 2443 patients with two visits (referral and control with 12-month interval) in 46 nephrology clinics. Patients were stratified in four categories of hyperkalemia (sK≥5.0 mEq/L) by sK at visit 1 and 2: Absent (no-no), Resolving (yes-no), New Onset (no-yes), Persistent (yes-yes). We assessed competing risks of ESKD and death after visit 2. Age was 65±15 y, eGFR 35±17 mL/min/1.73 m 2 , proteinuria 0.40 (0.14-1.21) g/24h. In the two visits sK was 4.8±0.6 and levels ≥6 mEq/L were observed in  4%. Hyperkalemia was absent in 46%, resolving 17%, new onset 15% and persistent 22%. Renin-angiotensin-system inhibitors (RASI) were prescribed in 79% patients. During 3.6-year follow-up, 567 patients reached ESKD and 349 died. Multivariable competing risk analysis [subhazard ratio-sHR, 95%Confidence Interval-CI] evidenced that new onset [sHR 1.34, 95%CI 1.05-1.72] and persistent [sHR 1.27, 95%CI 1.02-1.58] hyperkalemia predicted higher ESKD risk versus absent,independently from main determinants of outcome including eGFR change. Conversely, no effect on mortality was observed. Results were confirmed by testing sK as continuous variable. Therefore, in CKD under nephrology care, mild-to-moderate hyperkalemia status is common (37%) and predicts per se higher ESKD risk but not mortality.

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Section: Discussionmentioning

confidence: 99%

Competing-Risk Analysis of Death and ESKD by Hyperkalemia Status in Non-Dialysis CKD Patients Receiving Stable Nephrology Care

Provenzano¹,

Minutolo²,

Chiodini³

et al. 2018

Preprint

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“…15 Given the integral role of RAAS inhibitor therapy in reducing CV risk and slowing the progression of CKD, the use of new K þ binders to lower serum K þ and thereby maintain optimal RAAS inhibitor therapy is expected to improve long-term clinical outcomes in patients with CKD. 9,15,51 Although studies evaluating SZC and patiromer included patients receiving RAAS inhibitor therapy and appeared to permit continued use without hyperkalemia, 52,53,55,56,62 the direct effects of these agents on the optimization of RAAS inhibitor dose have not been clearly delineated. Although evidence is emerging on the sustained benefits of K þ binders, 63 additional studies are necessary to evaluate these effects long term.…”

Section: Effect On Raas Inhibitor Therapy Optimizationmentioning

confidence: 99%

“…53 In prespecified subgroup analyses, 100% of patiromer recipients with HF and 100% of patiromer recipients aged 65 years or older continued RAAS inhibitor therapy while maintaining K þ control. 62,86 A post hoc analysis of OPAL-HK found that the efficacy and safety of patiromer were not compromised by background diuretic therapy, which is often required in patients with CKD. 87 In the AMETHYST-DN study (Patiromer in the Treatment of Hyperkalemia in Patients With Hypertension and Diabetic Nephropathy; ClinicalTrials.gov Identifier: NCT01371747), serum K þ concentrations were reduced with patiromer through week 4 of treatment, and K þ was maintained in a normal range over 52 weeks.…”

Section: Patiromermentioning

confidence: 99%

Potassium Binders for Hyperkalemia in Chronic Kidney Disease—Diet, Renin-Angiotensin-Aldosterone System Inhibitor Therapy, and Hemodialysis

Palmer

2020

Mayo Clinic Proceedings

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Hyperkalemia is a potentially life-threatening complication of chronic kidney disease (CKD). The management of CKD requires balancing the benefits of specific treatments, which may exacerbate the potential for hyperkalemia, with the risks of hyperkalemia itself. Renin-angiotensin-aldosterone system (RAAS) inhibitors, which slow CKD progression and improve cardiovascular outcomes, are often discontinued if hyperkalemia develops. Patients with hyperkalemia are frequently advised to restrict dietary potassium (K þ), depriving these patients of many heart-healthy foods. Patients receiving hemodialysis are particularly susceptible to hyperkalemia during long interdialytic intervals, and managing this risk without causing hypokalemia can be challenging. Recently, 2 K þ-binding agents were approved for the treatment of hyperkalemia: sodium zirconium cyclosilicate and patiromer. These agents offer alternatives to sodium polystyrene sulfonate, which is associated with serious gastrointestinal adverse effects. For this review, PubMed was searched for English-language articles published in 2014-2018 using the terms patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate, hyperkalemia, renin-angiotensin-aldosterone, diet, and dialysis. In randomized controlled studies of patients with hyperkalemia, sodium zirconium cyclosilicate and patiromer effectively reduced serum K þ and were generally well tolerated. Furthermore, patients in these studies could maintain RAAS inhibitor therapy and, in some studies, were not required to limit dietary K þ. There may also be a role for these agents in preventing hyperkalemia in patients receiving hemodialysis. Thus, K þ-binding agents may allow patients with CKD at risk for hyperkalemia to optimize RAAS inhibitor therapy, receive benefits of a K þ-rich diet, and experience improved hemodialysis outcomes. Additional longterm studies are necessary to confirm these effects.

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“…Two potential alternatives to SPS have recently emerged, patiromer calcium (RLY5016, Vifor Pharma, Bern, Switzerland) and sodium zirconium cyclosilicate (ZS‐9, AstraZeneca, Cambridge, UK) . Patiromer has been evaluated in short‐term studies of CKD patients treated with RAAS inhibitors and in a longer, 52‐week, phase 2 study of patients with diabetes and CKD . Patiromer appears to be generally well tolerated, with major adverse effects consisting of constipation, hypomagnesaemia and hypokalaemia .…”

Section: Management Of Chronic Hyperkalaemia In Ckdmentioning

confidence: 99%

“…2 Patiromer has been evaluated in short-term studies of CKD patients treated with RAAS inhibitors and in a longer, 52-week, phase 2 study of patients with diabetes and CKD. [18][19][20] Patiromer appears to be generally well tolerated, with major adverse effects consisting of constipation, hypomagnesaemia and hypokalaemia. [18][19][20] ZS-9 is another cation exchanger that is reported to have greater selectivity for monovalent cations than divalent cations (e.g.…”

Section: Management Of Chronic Hyperkalaemia In Ckdmentioning

confidence: 99%

Potassium control in chronic kidney disease: implications for neuromuscular function

Arnold

Pianta

Pussell

et al. 2019

Internal Medicine Journal

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In Australia approximately 1.7million adults have evidence of chronic kidney disease (CKD). This complex disease can result in a multitude of complications, including hyperkalaemia which common and well recognised. . The advent of new therapeutics aimed at lowering serum potassium have raised the possibility of optimising potassium control to enable greater use of renin-angiotensin-aldosterone system inhibitors in the management of CKD. Recent studies suggest that hyperkalaemia also has implications for peripheral neuropathy in CKD, a complication that substantially contributes to patient morbidity. This review examines evidence of the relationship between potassium and peripheral neuropathy with discussion of clinical implications. We searched PubMed for original and review articles using prespecified key words, clinical guidelines and population data. The major findings were that contemporary CKD cohorts demonstrate a high prevalence of peripheral neuropathy, even in stage 3-4 CKD, including those without diabetes. The severity of the problem has been emphasized by an ominous rise in foot complications and amputation rates in dialysis patients, highlighting the need for increased awareness of the condition in earlier stages of CKD and targeted treatment strategies. It is likely that the pathophysiology of peripheral neuropathy in CKD is multifaceted with potential influences from potassium, vascular abnormalities, diabetes, inflammation and unknown middle molecules. Despite these complexities, the relationship between potassium and nerve function in dialysis has been well established and recent research in stage 3-4 CKD suggests that assertive potassium control may improve neuromuscular outcomes in CKD. These small studies should be confirmed in large, multicenter settings. This article is protected by copyright. All rights reserved.

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Effect of Patiromer on Hyperkalemia Recurrence in Older Chronic Kidney Disease Patients Taking RAAS Inhibitors

Abstract: Patiromer reduced recurrent hyperkalemia and was well tolerated in older chronic kidney disease patients taking RAASi.

Cited by 42 publications

References 41 publications

Competing-Risk Analysis of Death and ESKD by Hyperkalemia Status in Non-Dialysis CKD Patients Receiving Stable Nephrology Care

Competing-Risk Analysis of Death and ESKD by Hyperkalemia Status in Non-Dialysis CKD Patients Receiving Stable Nephrology Care

Potassium Binders for Hyperkalemia in Chronic Kidney Disease—Diet, Renin-Angiotensin-Aldosterone System Inhibitor Therapy, and Hemodialysis

Potassium control in chronic kidney disease: implications for neuromuscular function

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