A 57-year-old man comes to the emergency department due to a week of progressive shortness of breath and nonproductive cough. The patient has a history of HIV and type 2 diabetes mellitus. He does not regularly go to follow-up appointments or adhere to medication prescriptions. His last CD4 cell count 3 months ago was 120/mm³. Temperature is 38.9 C (102 F), blood pressure is 120/80 mm Hg, pulse is 110/min, and respirations are 24/min. Oxygen saturation is 86% on room air. Lung examination is notable for diffuse rales bilaterally. The abdomen is soft and nontender. Laboratory results are as follows: Chest x-ray reveals bilateral patchy opacities in the lower lung fields. The patient is treated with azithromycin, ceftriaxone, trimethoprim-sulfamethoxazole, prednisone, and albuterol. He is also given insulin before meals for his diabetes mellitus. On the third day of hospitalization, the patient's serum potassium is 5.9 mEq/L, and his creatinine is 1.5 mg/dL. Which of the following medications is most likely responsible for these laboratory changes?

Question

Quizplus · Accepted Answer

11ec25c8_d4e3_5dfb_bc81_0550838976c0_MD0003_00 This patient with untreated AIDS has evidence of acute hypoxemic respiratory failure due to pneumonia. Because he is at risk for infection with both common and opportunistic pulmonary pathogens, he was treated with antibiotics for community-acquired (azithromycin plus ceftriaxone) and Pneumocystis (trimethoprim-sulfamethoxazole) pneumonia. The patient subsequently developed hyperkalemia and elevated creatinine, likely due to trimethoprim (TMP). TMP is excreted via the urine and commonly exerts a potassium-sparing diuretic effect (similar to amiloride) by blocking the epithelial sodium channel in the collecting tubule. Blockade of the epithelial sodium channel prevents reabsorption of sodium from the urine, which reduces the electrochemical gradient for potassium to leave epithelial cells and move into the lumen of the collecting tubule. Patients with HIV who are treated with high doses of TMP are at greatest risk for hyperkalemia, but even normal doses can produce a modest elevation in the plasma potassium concentration. TMP also competitively inhibits renal tubular creatinine secretion, which may cause an artificial increase in serum creatinine; however, glomerular filtration rate is unchanged. TMP and sulfamethoxazole (SMX) work sequentially to block the bacterial synthesis of tetrahydrofolic acid. They are commonly used together (ie, TMP-SMX) to treat uncomplicated urinary tract infection (eg, gram-negative rods), Pneumocystis pneumonia, and infections caused by Nocardia and community-acquired methicillin-resistant Staphylococcus aureus. (Choices A and D) Inhaled beta-2 agonists (eg, albuterol) and insulin move potassium intracellularly by activating the Na⁺/K⁺-ATPase in skeletal muscle. They are often used to rapidly reduce serum potassium in hyperkalemic emergency; they do not increase serum potassium. (Choices B and C) Macrolide antibiotics (eg, azithromycin) can cause prolonged QT interval and cholestasis. Ceftriaxone is also associated with cholestasis and is contraindicated in neonates at high risk of developing cholestasis. Neither drug significantly affects potassium levels. (Choice E) Prednisone has some mineralocorticoid activity, but it would cause potassium loss, not retention. Educational objective: Trimethoprim can cause hyperkalemia due to blockade of the epithelial sodium channel in the collecting tubule. Trimethoprim also competitively inhibits renal tubular creatinine secretion and may cause an artificial increase in serum creatinine without affecting the glomerular filtration rate. References: Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose. (http://www.ncbi.nlm.nih.gov/pubmed/8879854)

A 57-Year-Old Man Comes to the Emergency Department Due to a Week