Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge

Orlando, Marc P.; Dillon, Mary E.; O’Dell, Michael W.

doi:10.1097/00002060-200001000-00019

Cited by 21 publications

(8 citation statements)

References 13 publications

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“…Patients with diabetes, HF, or CKD are at an increased risk of hyperkalemia compared with those without these conditions (4). Furthermore, a number of medications are known to cause hyperkalemia, including nonsteroidal anti-inflammatory drugs (NSAIDs) (5), ␤-blockers (2), heparin (6), and calcineurin inhibitors (7).…”

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confidence: 99%

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Weir

Rolfe²

2010

Clinical Journal of the American Society of Nephrology

216

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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confidence: 99%

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Weir

Rolfe²

2010

Clinical Journal of the American Society of Nephrology

216

138

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“…Three cases of HIH are reported for subcutaneous heparin, whereby resolution usually occurs within 24 hours of heparin discontinuation, as described by Thomas and colleagues. 27 The observation of resolution and rise in potassium after a rechallenge with heparin has been described by Orlando and colleagues, 28 which supports reduced aldosterone synthesis as the driving mechanism. 28,29 However, in patients at high risk for thrombosis, discontinuing heparin because of HIH can be problematic.…”

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confidence: 70%

Heparin-Induced Hyperkalemia in a Patient Diagnosed with Thyroid Storm

2013

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“…Heparin-induced increases in serum potassium are mediated by a reversible effect of heparin on aldosterone leading to hypoaldosteronism [ 2 , 3 ]. It is effected by both a reduction of the number and affinity of angiotensin II receptors in the zona glomerulosa [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of 8,000 IU aXa long-term prophylaxis with certoparin on the incidence of hyperkalemia in patients with coronary heart disease – a post-hoc analysis of the PARAT trial

2014

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BackgroundHyperkalemia is an infrequent but potentially serious complication of low molecular weight heparin (LMWH) use. While there are a number of trials comparing LMWH to unfractionated heparin (UFH) there is no comparison of the risk with LMWH versus placebo. Aim of the present post-hoc analysis of the PARAT trial was the description of serum potassium levels with certoparin compared to placebo.ResultsPARAT was a double-blind, placebo-controlled, randomized trial in patients with coronary artery disease receiving either 8,000 I.U. aXa per day or placebo. Serum potassium was monitored at baseline and at scheduled follow-up visits at 2 and 4–6 weeks and 3 and 4–6 months. Statistical evaluation included paired, two sided t-test for each of the treatment groups to compare baseline and follow-up values. A total of 117 patients (59 certoparin, 58 placebo) were included with a mean age of 59 years and 84.6% male gender. There was a statistically significant increase in serum potassium at two weeks after discharge compared to baseline (p < 0.001) in either group which remained elevated throughout the three months treatment phase. Differences between treatment groups were not statistically significant. After treatment discontinuation at the three months’ visit serum potassium returned to normal values (p = n.s. vs. baseline) in both groups. Overall 12 out of 59 patients receiving certoparin (20.3%) and 11 out of 58 patients receiving placebo (19.0%) experienced hyperkalemia based on threshold of >5.0 mmol/l at any time during the observation.ConclusionsWe conclude that there is no incremental risk of hyperkalemia with certoparin up to 8,000 I.U. aXa per day versus placebo in patients with coronary artery disease. The increase in serum potassium values in either group calls for clinical surveillance and the consideration of further risk factors predisposing to hyperkalemia.

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Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge

Cited by 21 publications

References 13 publications

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Potassium Homeostasis and Renin-Angiotensin-Aldosterone System Inhibitors

Heparin-Induced Hyperkalemia in a Patient Diagnosed with Thyroid Storm

Effects of 8,000 IU aXa long-term prophylaxis with certoparin on the incidence of hyperkalemia in patients with coronary heart disease – a post-hoc analysis of the PARAT trial

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