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      Trimethoprim/Sulfamethoxazole-Induced Bradycardia, Renal Failure, AV-Node Blockers, Shock and Hyperkalemia Syndrome

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          Abstract

          BRASH (bradycardia, renal failure, atrioventricular-node blockers, shock, and hyperkalemia) syndrome is a recently coined term for a condition that describes the severe bradycardia and shock associated with hyperkalemia in patients on atrioventricular (AV)-node blocking agents. The proposed pathophysiology involves a precipitating event that exacerbates renal dysfunction with resulting AV-node blocker and potassium accumulation that act synergistically to precipitate bradycardia and hypotension. This syndrome may be refractory to the usual management of bradycardia. This case describes BRASH syndrome precipitated by trimethoprim/sulfamethoxazole.

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          Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: a population-based study.

          Trimethoprim therapy can cause hyperkalemia and is often coprescribed with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). The objective of this study was to characterize the risk of hyperkalemia-associated hospitalization in elderly patients who were being treated with trimethoprim-sulfamethoxazole along with either an ACEI or an ARB. We conducted a population-based, nested case-control study of a cohort of elderly patients 66 years or older who were residents of Ontario, Canada, and who were receiving continuous therapy with either an ACEI or an ARB. Case patients were those with a hyperkalemia-associated hospitalization within 14 days of receiving a prescription for trimethoprim-sulfamethoxazole, amoxicillin, ciprofloxacin, norfloxacin, or nitrofurantoin. For each case, we identified up to 4 control patients from the same cohort matched for age, sex, and presence or absence of chronic renal disease and diabetes. Odds ratios were determined for the association between hyperkalemia-associated hospitalization and previous antibiotic use. During the 14-year study period, we identified 4148 admissions involving hyperkalemia, 371 of which occurred within 14 days of antibiotic exposure. Compared with amoxicillin, the use of trimethoprim-sulfamethoxazole was associated with a nearly 7-fold increased risk of hyperkalemia-associated hospitalization (adjusted odds ratio, 6.7; 95% confidence interval, 4.5-10.0). No such risk was found with the use of comparator antibiotics. Among older patients treated with ACEIs or ARBs, the use of trimethoprim-sulfamethoxazole is associated with a major increase in the risk of hyperkalemia-associated hospitalization relative to other antibiotics. Alternate antibiotic therapy should be considered in these patients when clinically appropriate.
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            Renal mechanism of trimethoprim-induced hyperkalemia.

            1) To determine the incidence and severity of hyperkalemia during trimethoprim therapy. 2) To test the hypothesis that trimethoprim inhibits renal potassium excretion by blocking sodium channels in the mammalian distal nephron. Thirty consecutive patients who were treated with trimethoprim-containing drugs. All patients included in the study had the acquired immunodeficiency syndrome (AIDS). Thirty-nine male Sprague-Dawley rats receiving normal rat chow and tap water (allowed free access). Humans: high dose (20 mg/kg per day) of trimethoprim therapy. Rats: trimethoprim (9.6 mg/h per kg body weight) was infused intravenously or into the renal distal tubules (1 mmol/L). Humans: Serum and urine electrolyte levels, serum creatinine, renin, aldosterone, and cortisol levels were measured, and the transtubular potassium gradient was calculated. Rats: The effects of trimethoprim infusion on urinary sodium, chloride, and potassium concentration and urine volume were measured. Sodium, chloride, potassium, and inulin concentrations were measured in fluid samples obtained from kidney distal tubules. The voltage across the wall of the distal tubule was measured. Humans: Trimethoprim increased the serum potassium concentration by 0.6 mmol/L (95% Cl, 0.29 to 0.95 mmol/L) despite normal adrenocortical function and glomerular filtration rate. Serum potassium levels greater than 5 mmol/L were observed during trimethoprim treatment in 15 of 30 patients. Rats: Intravenous trimethoprim inhibited renal potassium excretion by 40% (Cl, 21% to 60%) and increased renal sodium excretion by 46% (Cl, 9% to 83%). Trimethoprim (1 mmol/L) in tubule fluid inhibited distal tubule potassium secretion by 59% (Cl, 26% to 92%) and depolarized the lumen-negative transepithelial voltage by 66% (Cl, 46% to 85%). Trimethoprim (an organic cation) acts like amiloride and blocks apical membrane sodium channels in the mammalian distal nephron. As a consequence, the transepithelial voltage is reduced and potassium secretion is inhibited. Decreased renal potassium excretion secondary to these direct effects on kidney tubules leads to hyperkalemia in a substantial number of patients being treated with trimethoprim-containing drugs.
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              Brief report: trimethoprim-induced hyperkalemia in a patient with AIDS.

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                Author and article information

                Journal
                Clin Pract Cases Emerg Med
                Clin Pract Cases Emerg Med
                Clinical Practice and Cases in Emergency Medicine
                University of California Irvine, Department of Emergency Medicine publishing Western Journal of Emergency Medicine
                2474-252X
                August 2019
                22 July 2019
                : 3
                : 3
                : 282-285
                Affiliations
                Desert Regional Medical Center, Department of Emergency Medicine, Palm Springs, California
                Author notes
                Address for Correspondence: Nnaemeka Diribe, DO, Desert Regional Medical Center, Department of Emergency Medicine, 1180 N. Indian Canyon Dr. Suite E418, Palm Springs, CA 92262. Email: nnaemeka.diribe@ 123456tenethealth.com .
                Article
                cpcem-3-282
                10.5811/cpcem.2019.5.43118
                6682249
                31403103
                a4062c2e-a29a-4aef-ad91-5eb76d4fef3f
                Copyright: © 2019 Diribe et al

                This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) License. See: http://creativecommons.org/licenses/by/4.0/

                History
                : 17 March 2019
                : 06 May 2019
                : 20 May 2019
                Categories
                Case Report

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