Severe hyperkalaemia induced by trimethoprim in combination with an angiotensin‐converting enzyme inhibitor in a patient with transplanted lungs

Bugge, J. F.

doi:10.1046/j.1365-2796.1996.43869000.x

Cited by 18 publications

(8 citation statements)

References 11 publications

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“…competitive inhibition of the renal tubular secretion. Besides this effect, trimethoprim can also cause hyperkalaemia [34,35]. Cotrimoxazole and trimethoprim can also induce real renal toxicity: acute tubular necrosis and acute interstitial nephritis are reported [7,36,37].…”

Section: Trimethoprimmentioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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Abstract. Andreev E, Koopman M, Arisz L (Medical University-Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247±252. This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide±creatinine interaction is not fully explained. These drug-induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine.

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Section: Trimethoprimmentioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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“…We have previously shown that the use of co-trimoxazole with angiotensin converting enzyme inhibitors or angiotensin receptor blockers results in an almost sevenfold increase in the risk of hyperkalemia related hospital admission relative to amoxicillin. 14 Case reports show that this drug interaction can cause life threatening hyperkalemia, 15 16 but whether it can increase the risk of sudden death in clinical practice is unknown. This is an important question, because sudden death due to hyperkalemia in the pre-hospital setting is likely to be misattributed to intrinsic heart disease, particularly in older patients with existing cardiovascular disease or diabetes.…”

Section: Introductionmentioning

confidence: 99%

Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study

Fralick

Macdonald

Gomes

et al. 2014

BMJ

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Objective To determine whether the prescription of co-trimoxazole with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker is associated with sudden death. Design Population based nested case-control study. Setting Ontario, Canada, from 1 April 1994 to 1 January 2012. Participants Ontario residents aged 66 years or older treated with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker. Cases were those who died suddenly shortly after receiving an outpatient prescription for one of co-trimoxazole, amoxicillin, ciprofloxacin, norfloxacin, or nitrofurantoin. Each case was matched with up to four controls on age, sex, chronic kidney disease, and diabetes. Main outcome measure Odds ratio for the association between sudden death and exposure to each antibiotic relative to amoxicillin, after adjustment for predictors of sudden death according to a disease risk index. Results Of 39 879 sudden deaths, 1027 occurred within seven days of exposure to an antibiotic and were matched to 3733 controls. Relative to amoxicillin, co-trimoxazole was associated with an increased risk of sudden death (adjusted odds ratio 1.38, 95% confidence interval 1.09 to 1.76). The risk was marginally higher at 14 days (adjusted odds ratio 1.54, 1.29 to 1.84). This corresponds to approximately three sudden deaths within 14 days per 1000 co-trimoxazole prescriptions. Ciprofloxacin (a known cause of QT interval prolongation) was also associated with an increased risk of sudden death (adjusted odds ratio 1.29, 1.03 to 1.62), but no such risk was observed with nitrofurantoin or norfloxacin. Conclusions In older patients receiving angiotensin converting enzyme inhibitors or angiotensin receptor blockers, co-trimoxazole is associated with an increased risk of sudden death. Unrecognized severe hyperkalemia may underlie this finding. When appropriate, alternative antibiotics should be considered in such patients.

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“…Calcineurin inhibitors, such as cyclosporine or tacrolimus, are associated with as high as a 73% incidence of hyperkalemia 36–37 . Finally, trimethoprim/sulfamethoxazole (Bactrim) has been associated with the development of hyperkalemia 38–39 . Trimethoprim reduces renal K + excretion through the competitive inhibition of epithelial Na + channels in the distal nephron in a manner identical to the K + ‐sparing diuretic, amiloride.…”

Section: Concomitant Medications/conditionsmentioning

confidence: 99%

Aldosterone Receptor Antagonism: Interface With Hyperkalemia in Heart Failure

Sica

Heß

2004

Congestive Heart Failure

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Aldosterone receptor antagonism (ARA) is an increasingly well-accepted element of heart failure therapy. The experimental underpinnings for the use of ARA in heart failure are strong being linked to a variety of tissue-based cardiac effects characteristic of drugs in this class. However, the benefits of ARA therapy do not come without some risk since drugs in this class are potent inhibitors of renal potassium (K+) elimination. Thus, some increment in serum K+, up to and including the development of overt hyperkalemia (typically defined as a serum K+ value in excess of 6.0 mEq/L), is to be expected whenever they are used. Hyperkalemia attributable to ARA relates to several factors including ARA dose, patient predisposition to hyperkalemia, as in the case of renal failure, and dietary intake of K+. The risk of some change in serum K+ with ARA should not be a deterrent to use of drugs in this class but, rather should prompt careful surveillance for the onset of this potentially life-threatening electrolyte disturbance. The frequency of such scrutiny should be patient-specific and based on the constellation of risk factors for hyperkalemia.

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Severe hyperkalaemia induced by trimethoprim in combination with an angiotensin‐converting enzyme inhibitor in a patient with transplanted lungs

Cited by 18 publications

References 11 publications

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study

Aldosterone Receptor Antagonism: Interface With Hyperkalemia in Heart Failure

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