Hyperkalemia With High-Dose Trimethoprim-Sulfamethoxazole Therapy

Greenberg, Sheldon; Reiser, Ira W.; Chou, Shyan–Yih

doi:10.1016/s0272-6386(12)80937-1

Cited by 28 publications

(9 citation statements)

References 19 publications

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“…Various reports reveal that hyperkalemia secondary to these effects is associated with both high-dose therapy in patients with AIDS 18–21 and in patients receiving standard doses of TMP/SMX. 22–28 Hyperkalemia is also a common finding in type 4 RTA.…”

Section: Antimicrobial Agentsmentioning

confidence: 99%

Antimicrobial-Associated Renal Tubular Acidosis

Hemstreet

2004

Ann Pharmacother

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Given that antimicrobial-associated RTA is a relatively uncommon adverse effect, review of the patient's drug regimen may reveal these agents as otherwise unrecognized causes of RTA. Likewise, underlying causes of RTA other than medications must be ruled out. Diagnosing antimicrobial-induced RTA may be difficult, given many of these agents may be used in combination and some are intrinsically nephrotoxic.

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Section: Antimicrobial Agentsmentioning

confidence: 99%

Antimicrobial-Associated Renal Tubular Acidosis

Hemstreet

2004

Ann Pharmacother

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“…The adverse effect of hyperkalemia has been reported in acquired immunodeficiency syndrome patients 7–10 days after the start of high doses of TMP-SMX therapy for treatment of Pneumocystitis carinii pneumonia [1,2,3] and in hospitalized patients treated with standard doses of TMP-SMX [4]. The hyperkalemia appears to be reversible as it ameliorates after withdrawal of the drug [1, 2]. …”

Section: Introductionmentioning

confidence: 99%

Effect of Trimethoprim-Sulfamethoxazole on Na<sup>+</sup> and K<sup>+</sup> Transport Properties in the Rabbit Cortical Collecting Duct Perfused in vitro

et al. 2006

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Background: In this study, the membrane mechanisms of hyperkalemia caused by trimethoprim-sulfamethoxazole (TMP-SMX) combination antibiotics were assessed in the cortical collecting duct (CCD). Methods: We used the microelectrode technique and flux measurements, and examined the effects of TMP and SMX on electrical properties of the apical and basolateral membranes in the rabbit CCD perfused in vitro. Results: TMP in the lumen caused increases in apical membrane voltage, fractional apical membrane resistance (fR_A), and transepithelial resistance (R_T), all effects which were completely inhibited by luminal amiloride, but not by luminal Ba²⁺. The luminal TMP inhibited both net Na⁺ reabsorption and K⁺ secretion in the CCD. TMP in the bath slightly but significantly depolarized transepithelial voltage and basolateral membrane voltage without influencing fR_A or R_T. SMX in the lumen or bath had no effect on barrier voltages or resistances. Conclusion: TMP mainly acts on the apical membrane of the CCD, inhibits the amiloride-sensitive macroscopic Na⁺ conductance in this membrane, and thereby decreases the net driving force for K⁺ exit across the membrane, resulting in an inhibition of K⁺ secretion. SMX in the lumen or bath had no effect on the CCD.

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“…Cotrimoxazol también se asocia a nefritis intersticial, leucopenia, neutropenia o trombocitopenia. A pesar que las reacciones alérgicas y las molestias digestivas son reportadas hasta en 20% de los pacientes adultos que reciben este compuesto por períodos prolongados 8,9 , el desarrollo de hiperkalemia o aumento en la creatininemia ha recibido menos atención 4,5,10,11 . Contribuye a una falsa percepción de seguridad, el uso infrecuente que tiene esta molécula actualmente, la que además es aplicada en bajas dosis y en forma intermitente en casos de profilaxis (Pneumocystis jiroveci, por ejemplo) o por períodos cortos.…”

Section: Discussionunclassified