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The mechanism involved in the onset of hyperkalemia is the inhibition of the sodium channels present in the epithelium of the distal renal tubule, which results in altered potassium secretion and sodium reabsorption.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">This drug-induced hyperkalemia is further aggravated in certain situations such as an impaired kidney function, diabetes, heart failure, or combined treatment with other drugs, mainly renin-angiotensin system inhibitors.</p><p id="par0035" class="elsevierStylePara elsevierViewall">We hereby describe the case of a 71-year-old woman admitted to our clinic with <span class="elsevierStyleItalic">P. jirovecii</span> pneumonia and secondary hyperkalemia following treatment with trimethoprim-sulfamethoxazole, and propose a therapeutic alternative that could be used in similar cases.</p><p id="par0040" class="elsevierStylePara elsevierViewall">In terms of her medical history, this was a hypertensive, dyslipidemic patient with a diagnosis of Crohn’s disease and spondyloarthritis associated with an inflammatory bowel disease. Her usual treatment consisted of methotrexate, prednisone, and valsartan/amlodipine/hydrochlorothiazide.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Thirteen days after being discharged from the hospital after being treated for community-acquired pneumonia, she visited the Emergency Room complaining of an increase in her usual dyspnea. Given that a chest X-ray showed an area of increased density in her middle lung lobe, she was admitted to the Pulmonology ward with a diagnosis of community-acquired pneumonia. Empirical antibiotic therapy with piperacillin-tazobactam was started and pneumococcal and <span class="elsevierStyleItalic">Legionella</span> antigen testing, blood cultures, and serology tests were requested, all of which yielded negative results. After spending 48 h on the ward, she developed a respiratory deterioration because of which she required orotracheal intubation and admission to the Intensive Care Unit, where her antibiotic treatment was modified to a combination of linezolid and trimethoprim-sulfamethoxazole. A bronchoscopy was also performed, together with a bronchoalveolar lavage and aspiration. Given that the cultured samples were positive for <span class="elsevierStyleItalic">P. jirovecii</span>, monotherapy with trimethoprim-sulfamethoxazole was continued.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Three days later, the follow-up blood tests performed revealed hyperkalemia of 7 mmol/L. Because this finding was also associated with episodes of sustained, self-limiting ventricular tachycardia, an emergency hemodialysis session was required. The patient’s kidney function was normal at all times. A review of her medication revealed that she was not taking any other drug that could explain the hyperkalemia, as the renin-angiotensin system inhibitors that she took on an outpatient basis had been discontinued on her admission to the clinic.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Given the suspected diagnosis of hypokalemia secondary to trimethoprim-sulfamethoxazole, which was deemed to be a probable cause according to Naranjo’s algorithm (7 points),<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> the antibiotic was discontinued. In addition, based on the recommendations of the experts of the Infectious Diseases Department, we assessed starting treatment with pentamidine, but this option was subsequently ruled out due to the fact that both medications share the same mechanism of action. We finally decided to start treatment with a combination of clindamycin and primaquine, which is considered to be the third therapeutic option.</p><p id="par0060" class="elsevierStylePara elsevierViewall">The patient subsequently experienced an improvement from a respiratory point of view, remaining afebrile, with decreasing levels of infectious parameters, and low oxygen requirements. Her potassium levels also returned to normal after discontinuing trimethoprim-sulfamethoxazole.</p><p id="par0065" class="elsevierStylePara elsevierViewall">In spite of the above, her clinical evolution was unfavorable, as she developed a left frontoparietal ischemic stroke with bilateral occipital ischemic lesions, which kept her in a persistent coma. She eventually passed away after the decision was made to limit the therapeutic efforts owing to the irreversibility of her brain lesions.</p><p id="par0070" class="elsevierStylePara elsevierViewall">In conclusion, we would like to emphasize that trimethoprim-sulfamethoxazole is the first drug of choice in the treatment of <span class="elsevierStyleItalic">P. jirovecii</span> infections.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> As in the case of our patient, who came to require a hemodialysis session, an association between this drug and hypokalemia has been observed.</p><p id="par0075" class="elsevierStylePara elsevierViewall">Our patient had no other risk factors for hyperkalemia (treatment with renin-angiotensin system inhibitors, impaired kidney function, diabetes, or heart failure), which was an important aspect considered before starting treatment with said antibiotic.</p><p id="par0080" class="elsevierStylePara elsevierViewall">Thus, we recommend monitoring potassium levels in patients receiving antibiotic therapy with trimethoprim-sulfamethoxazole and considering the use of other therapeutic alternatives, such as the combination of clindamycin and primaquine.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Fernández Rui D, Merino Bueno MC, Sádaba Acuña MA. 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