Effect of low-molecular-weight heparin on serum potassium

Canova, Corina; Fischler, Manuel; Reinhart, Walter H.

doi:10.1016/s0140-6736(05)63723-3

Cited by 28 publications

(13 citation statements)

References 5 publications

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“…Heparin probably interferes with adrenal aldosterone production through several different mechanisms, the most important appears to involve reduction in both the number and affinity of the angiotensin II receptors in the zona glomerulosa [2]. Although previous reports have shown LMWH therapy to increase serum potassium concentration [6,7], others failed to show similar results [8]. Conflicting data regarding the effect of LMWH on aldosterone secretion exist as well [7,9].…”

Section: Discussionmentioning

confidence: 99%

Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis

Abdel-Raheem

Potti

Tadros

et al. 2002

Pathophysiol Haemos Thromb

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Background: Low-molecular-weight heparins (LMWHs) are being preferred to unfractionated heparin (UFH) because of their superior convenience and a comparable or slightly better toxicity profile. Whether LMWH has an inhibitory effect on aldosterone that causes hyperkalemia is yet uncertain. Methods: Twenty-eight patients (all male; mean age: 70 years, range 52–87 years) placed on LMWH therapy (40 mg subcutaneously every 12 h) for deep venous thrombosis prophylaxis after an operation were included in the study. Transtubular potassium concentration gradient (TTKG) was calculated 1 day prior to LMWH therapy and again after 4 days of treatment. Of the 28 patients enrolled in the study, we were able to calculate the TTKG in only 19 patients: 9 had a urinary osmolarity (either before or after LMWH therapy) less than the serum osmolarity, making the TTKG calculation unreliable. The Wilcoxon signed-rank test was used to analyze differences in the median serum potassium levels and TTKG before and after LMWH therapy. Results: All patients had adequate renal function (creatinine clearance >90 ml/min). Mean (± SD) serum potassium concentration before LMWH was 4.25 (± 0.40) mmol/dl. It increased to 4.35 (± 0.41) mmol/dl after initiating LMWH therapy (p = 0.09). Similarly, the mean (± SD) TKKG calculated was 5.52 (± 2.33) before and 5.97 (± 3.06) after 4 days of LMWH (p = 0.54). Conclusions: Unlike UFH, LMWH (Lovenox^®) in doses used for postoperative prophylaxis against deep venous thrombosis does not seem to have a significant effect on potassium homeostasis.

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Section: Discussionmentioning

confidence: 99%

Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis

Abdel-Raheem

Potti

Tadros

et al. 2002

Pathophysiol Haemos Thromb

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“…Additionally, heparin can decrease the number and affinity of angiotensin II receptors in the adrenal zona glomerulosa [75,76]. There is also an effect of lowmolecular-weight heparin on K + levels [77,78]. ACE inhibitors and AT2RA can cause hyperkalemia and acidosis, particularly in patients with advanced renal insufficiency [79][80][81].…”

Section: Inhibition Of the Aldosterone Axis (Angiotensin Inhibition Amentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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“…Greater than normal potassium levels occur in about 7% of patients, and this has occurred with unfractionated doses as low as 5000 units twice daily (91). Elevations in serum potassium have ranged from 0.2 mEq/L to 1.7 mEq/L with an onset 1 to 3 days after drug exposure (91,92). Succinylcholine has been reported to cause severe hyperkalemia in patients with burns, trauma, and severe infection (93,94).…”

Section: Drug-induced Hyperkalemiamentioning

confidence: 99%

Electrolyte disturbances associated with commonly prescribed medications in the intensive care unit

Buckley

LeBlanc²,

Cawley³

2010

Critical Care Medicine

110

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Electrolyte imbalances are common in critically ill patients. Although multiple disease states typically encountered in the intensive care unit may be responsible for the development of electrolyte disorders, medications may contribute to these disturbances as well. Medications can interfere with the absorption of electrolytes, alter hormonal responses affecting homeostasis, as well as directly impact organ function responsible for maintaining electrolyte balance. The focus on this review is to identify commonly prescribed medications in the intensive care unit and potential electrolyte disturbances that may occur as a result of their use. This review will also discuss the postulated mechanisms associated with these drug-induced disorders. The specific drug-induced electrolyte disorders discussed in this review involve abnormalities in sodium, potassium, calcium, phosphate, and magnesium. Clinicians encountering electrolyte disturbances should be vigilant in monitoring the patient's medications as a potential etiology. Insight into these drug-induced disorders should allow the clinician to provide optimal medical management for the critically ill patient, thus improving overall healthcare outcomes.

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Effect of low-molecular-weight heparin on serum potassium

Cited by 28 publications

References 5 publications

Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis

Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis

Drug-induced acid-base disorders

Electrolyte disturbances associated with commonly prescribed medications in the intensive care unit

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