Incidence and Predictors of Hyperkalemia in Patients With Heart Failure

Desai, Akshay S.; Swedberg, Karl; McMurray, John J.V.; Granger, Christopher B.; Yusuf, Salim; Young, James B.; Dunlap, Mark E.; Solomon, Scott D.; Hainer, James W.; Olofsson, Bertil; Michelson, Eric L.; Pfeffer, Marc A.; Investigators, Charm

doi:10.1016/j.jacc.2007.07.067

Cited by 159 publications

(86 citation statements)

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“…In some clinical studies of hyperkalemic events, the causal role of ␤-blockers has been assumed without the presence of a referent group (2,48), and in other studies their role has been examined only in high-risk patient populations (49 -51). Conversely, in more rigorously conducted clinical studies, ␤-blockers were not associated with hyperkalemia (6,52,53). Our study does not refute the physiologic effects of ␤-blockers, but does suggest their contribution to hyperkalemia in ambulatory patients may be relatively minor.…”

Section: Discussioncontrasting

confidence: 80%

“…We adjusted for characteristics that may have predisposed to hyperkalemia in the multivariable model using all available data in the 3 years preceding the index date, including the Charlson comorbidity score (0, 1, Ն2) (38;39), the number of distinct prescriptions in the preceding year (Յ5, 6 to 10, 11 to 15, 16 to 20, 21 to 25, Ն26) (40), socioeconomic status (quintiles 1 to 2, quintiles 3 to 5), congestive heart failure, coronary artery disease, and previous episodes of hyperkalemia. We adjusted for medications used within the 120-day interval before the index date that may have influenced serum potassium concentrations: Nonpotassium-sparing diuretics, potassium-sparing diuretics (7,8), potassium supplements, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors (9), and angiotensin receptor blockers (6). We assessed for a statistical interaction by comparing the OR from the two cohorts using the technique of Altman and Bland, the OR from the first cohort reflected the risk of hyperkalemia among users of both ␤-blockers and TMP-SMX, and the OR from the second cohort reflected the same risk among users of TMP-SMX alone (41).…”

Section: Methodsmentioning

confidence: 99%

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Beta-Blockers, Trimethoprim-Sulfamethoxazole, and the Risk of Hyperkalemia Requiring Hospitalization in the Elderly

Weir¹,

Juurlink²,

Gomes³

et al. 2010

Clinical Journal of the American Society of Nephrology

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Background and objectives:The simultaneous use of beta adrenergic receptor blockers (␤-blockers) and trimethoprimsulfamethoxazole (TMP-SMX) may confer a high risk of hyperkalemia.Design, setting, participants, & measurements: Two nested case-control studies were conducted to examine the association between hospitalization for hyperkalemia and the use of TMP-SMX in older patients receiving ␤-blockers. Linked health administrative records from Ontario, Canada, were used to assemble a cohort of 299,749 ␤-blockers users, aged 66 years or older and capture data regarding medication use and hospital admissions for hyperkalemia.Results: Over the study period from 1994 to 2008, 189 patients in this cohort were hospitalized for hyperkalemia within 14 days of receiving a study antibiotic. Compared with amoxicillin, the use of TMP-SMX was associated with a substantially greater risk of hyperkalemia requiring hospital admission (adjusted odds ratio, 5.1; 95% confidence interval [CI], 2.8 to 9.4). No such risk was identified with ciprofloxacin, norfloxacin, or nitrofurantoin. When dosing was considered, the association was greater at higher doses of TMP-SMX. When the primary analysis was repeated in a cohort of non-␤-blocker users, the risk of hyperkalemia comparing TMP-SMX to amoxicillin was not significantly different from that found among ␤-blocker users.Conclusions: Although TMP-SMX is associated with an increased risk of hyperkalemia in older adults, these findings show no added risk when used in combination with ␤-blockers.

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Section: Discussioncontrasting

confidence: 80%

Section: Methodsmentioning

confidence: 99%

Beta-Blockers, Trimethoprim-Sulfamethoxazole, and the Risk of Hyperkalemia Requiring Hospitalization in the Elderly

Weir¹,

Juurlink²,

Gomes³

et al. 2010

Clinical Journal of the American Society of Nephrology

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“…Rates of serum potassium Ն6.0 mmol/L were also higher with candesartan than with placebo (Table 2). Moreover, in a post hoc analysis of data from the CHARM program, single-site RAAS inhibition with candesartan was associated with a higher incidence of "clinically important" hyperkalemia (fatal hyperkalemia, or hyperkalemia requiring dose reduction, study discontinuation, or hospitalization) than was placebo (4.0% versus 1.5%; odds ratio: 2.7; 95% confidence interval (95% CI): 1.5 to 5.0) (24).…”

Section: Hyperkalemia Risk With Raas Inhibitor Monotherapymentioning

confidence: 99%

“…Moreover, a post hoc analysis of the CHARM program data showed that adding candesartan to ACEI therapy increased the combined incidence of fatal hyperkalemia and hyperkalemia requiring dose reduction, study discontinuation, or hospitalization from 2.9% to 8.4% (P Ͻ 0.0001) (24). Importantly, however, the addition of candesartan to ACEI therapy reduced cardiovascular death and HF hospitalizations in the subgroups of patients at high risk of hyperkalemia, such as those with CKD (serum creatinine Ͼ2.0 mg/dl) (24).…”

Section: Hyperkalemia Risk With Dual Raas Inhibitionmentioning

confidence: 99%

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Weir

Rolfe²

2010

Clinical Journal of the American Society of Nephrology

218

138

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Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension and cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This review evaluates the effects on serum potassium levels of RAAS inhibitors. Using PubMed, we searched for clinical trials published up to December 2008 assessing the effects on serum potassium levels of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors, alone and in combination, in patients with hypertension, heart failure (HF), or chronic kidney disease (CKD); 39 studies were identified. In patients with hypertension without risk factors for hyperkalemia, the incidence of hyperkalemia with RAAS inhibitor monotherapy is low (<2%), whereas rates are higher with dual RAAS inhibition (Ϸ5%). The incidence of hyperkalemia is also increased in patients with HF or CKD (5% to 10%). However, increases in serum potassium levels are small (Ϸ0.1 to 0.3 mmol/L), and rates of study discontinuation due to hyperkalemia are low, even in high-risk patient groups (1% to 5%). Patients with HF or CKD are at greater risk of hyperkalemia with RAAS inhibitors than those without these conditions. However, the absolute changes in serum potassium are generally small and unlikely to be clinically significant. Moreover, these patients are likely to derive benefit from RAAS inhibition. Rather than denying them an effective treatment, electrolyte levels should be closely monitored in these patients.Clin J Am Soc Nephrol 5: 531-548, 2010. doi: 10.2215/CJN.07821109 T he renin-angiotensin-aldosterone system (RAAS) plays key roles in the regulation of blood volume, BP, and cardiovascular function. Therapeutic manipulation of the RAAS is an important treatment strategy for hypertension, chronic kidney disease (CKD), heart failure (HF), and diabetes. It is generally accepted, however, that RAAS inhibitors, such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), aldosterone receptor antagonists (ARAs), and direct renin inhibitors (DRIs), are associated with an increased risk of hyperkalemia, particularly when administered in combination (1,2). ACEIs, ARBs, and DRIs increase serum potassium levels by interfering with angiotensin II-mediated stimulation of aldosterone secretion from the adrenal gland and by decreasing renal blood flow and GFR in special patient populations. ARAs increase the risk of hyperkalemia by blocking interaction of aldosterone with its receptor, reducing renal potassium excretion.ACEIs, ARBs, ARAs, and DRIs may have different effects on potassium levels, reflecting the differences in their actions on potassium homeostasis. This raises the question of what effect different combinations of these agents might have on serum potassium levels-...

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“…The paucity of existing data on long term mortality in hyperkalemia precludes the accurate future assessment of mortality benefits of these new drugs. Most published literature focuses on the effects of hyperkalemia on short-term mortality [1,7]. There is a paucity of published literature on the outcomes of hyperkalemia in survivors from the index episode.…”

Section: Archives Of Medicine Issn 1989-5216mentioning

confidence: 99%

Long-term Mortality Outcomes of Hyperkalemic Patients in the Emergency Department Setting: A Case Control Study

Velagapudi¹,

O’Horo²,

Glinskii³

et al. 2017

Arch Med

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Background: The impact of an episode of hyperkalemia on long term mortality is not well studied. Such a study is vital for development of a utilization strategy for new drugs for the treatment of hyperkalemia. To study the long term impact of hyperkalemia on mortality, we conducted a retrospective, observational casecontrol study in a tertiary care emergency department. We compared cases of non-hemolyzed serum potassium >5.3 mEq/L with normokalemic controls. Allcause mortality and causes of death were determined from social security death index, national death index, and medical record review over a follow-up period of 490 patient years. Methods and Findings:A total of 287 consecutive subjects (223 cases, 64 controls) were identified among 14,483 patients. Cox proportional hazard regression showed that for each 1 mEq/L increase in admit potassium, all-cause mortality Hazard Ratio was 1.54, 95% Confidence Interval: 1.22-1.96. Subgroup analyses showed higher mortality in acute kidney injury and heart failure patients. Conclusion:Hyperkalemia predicted all-cause mortality, when adjusted for age, sex, Charlson comorbidity index, and significant covariates (heart failure and end stage renal disease). The deleterious effect of admit hyperkalemia persisted in survivors from index episode throughout the study period. Cardiovascular mortality was statistically more prevalent. Future studies are needed for risk stratification strategies and mortality impact of newer drugs.

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Incidence and Predictors of Hyperkalemia in Patients With Heart Failure

Cited by 159 publications

References 18 publications

Beta-Blockers, Trimethoprim-Sulfamethoxazole, and the Risk of Hyperkalemia Requiring Hospitalization in the Elderly

Beta-Blockers, Trimethoprim-Sulfamethoxazole, and the Risk of Hyperkalemia Requiring Hospitalization in the Elderly

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Long-term Mortality Outcomes of Hyperkalemic Patients in the Emergency Department Setting: A Case Control Study

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