Hyperkalemia is a known adverse effect of trimethoprim-sulfamethoxazole, usually occurring at high doses. However, fatal hyperkalemia at low doses has rarely been reported. We present the case of an 80-year-old Japanese woman who experienced a cardiac arrest due to severe hyperkalemia after starting low-dose trimethoprim-sulfamethoxazole. This case suggests that trimethoprim-sulfamethoxazole can cause severe hyperkalemia and sudden death, even at low doses. When trimethoprim-sulfamethoxazole is administered, even at low doses, periodic monitoring of electrolyte levels is necessary, with the interval depending on concomitant medications and renal function.

Trimethoprim/sulfamethoxazole (TMP/SMX) is an antimicrobial agent used worldwide for the treatment and prophylaxis of Pneumocystis pneumonia (PCP), urinary tract infections, and other infections. Its antimicrobial action is brought about by TMP and SMX inhibiting deoxyribonucleic acid synthesis [1, 2]. The most common side effects are rash and gastrointestinal symptoms, with hyperkalemia being a serious side effect.

Multiple cases of fatal hyperkalemia caused by high-dose TMP/SMX, such as those used to treat PCP, have been reported and several cases have been reported of hyperkalemia at conventional doses, such as those used in common infectious diseases [3, 7]. However, few cases caused by low-dose TMP/SMX have been reported [8]. We report a case of cardiac arrest due to severe hyperkalemia that developed after starting low-dose TMP/SMX. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see www.karger.com/doi/10.1159/000530450).

An 80-year-old Japanese woman weighing 48 kg, with a body surface area of 1.394 m2, was admitted to our hospital for a suspected brain tumor. She had a history of gastric ulcer and heart failure (HF). On admission, she was receiving azosemide, spironolactone, bisoprolol, atorvastatin, and vonoprazan. After admission, she was diagnosed with non-small cell lung cancer and a metastatic brain tumor. Echocardiography showed diffuse hypokinesis and left ventricular enlargement with a reduced left ventricular ejection fraction of 21%. The patient’s clinical course is shown in Figure 1. Laboratory data on admission were as follows: sodium, 141 mEq/L; potassium, 3.9 mEq/L; chloride, 106 mEq/L; blood urea nitrogen, 27.4 mg/dL; creatinine, 0.92 mg/dL (Table 1). On day 7, prednisolone and levetiracetam were initiated to prevent cerebral edema and seizures, respectively. On day 14, low-dose TMP/SMX (80 mg/400 mg/day) was initiated for PCP prophylaxis, and radiation therapy was used to treat the patient’s brain metastases. On day 15, her serum potassium level was elevated to 5.4 mEq/L, but her creatinine level remained stable. Her dietary intake did not change and she did not receive any infusions. On day 21, she experienced a sudden cardiac arrest requiring immediate cardiopulmonary resuscitation. The initial electrocardiogram showed ventricular tachycardia; hence, she was defibrillated until the return of spontaneous circulation was achieved. Laboratory findings at the time of cardiac arrest were as follows: blood urea nitrogen, 100.2 mg/dL; creatinine, 1.78 mg/dL; potassium, 7.4 mEq/L; sodium, 123 mEq/L; pH, 7.28; PCO2, 26.7 mm Hg; HCO3, 12.2 mmol/L. Echocardiographic findings were unchanged, with no dilatation of the inferior vena cava, and no pulmonary congestion was observed on chest radiography. A 12-lead electrocardiogram performed after resuscitation was unchanged from that on admission, and echocardiography and medical history did not reveal any sign of ischemic heart disease. Hyperkalemia was suspected as the cause of cardiac arrest; therefore, 10 mL of 8.5% calcium gluconate, 40 mL of 8.4% sodium bicarbonate, 20 mL of 50% glucose solution, and 4 units of human insulin were administered slowly intravenously. The patient was immediately admitted to the intensive care unit and 90 min after the cardiac arrest, arterial blood gas analysis showed potassium 5.3 mEq/L, sodium 124 mEq/L, pH 7.43, PCO2 32.4 mm Hg, HCO3 21.2 mmol/L. Urinalysis revealed urinary sodium 95 mmol/L, potassium 32.8 mmol/L, and chloride 97 mmol/L. Proteinuria was absent, urinary creatinine was 10 mg/dL, fractional excretion of sodium 13.6%, fractional excretion of potassium 110.2%, transtubular potassium gradient 6.3. TMP/SMX and spironolactone were discontinued because of the hyperkalemia. On day 22, the patient’s serum potassium and sodium levels had improved to 5.3 mEq/L and 130 mEq/L, respectively, and she was discharged from the intensive care unit. On day 49, she was transferred to another hospital for palliative care.

Fig. 1.

Treatments administered in the hospitalization course and changes in serum potassium and serum sodium levels. TMP/SMX, trimethoprim-sulfamethoxazole.

Fig. 1.

Treatments administered in the hospitalization course and changes in serum potassium and serum sodium levels. TMP/SMX, trimethoprim-sulfamethoxazole.

Close modal
Table 1.

Laboratory findings after the sudden cardiac arrest

ParametersValuesUnitsReference range
Day 1Day 6Day 15Day 21aDay 22Day 23Day 27Day 31
Aspartate aminotransferase 17 18 25 26 29 26 24 24 U/L 13–30 
Alanine aminotransferase 27 25 26 21 22 26 U/L 7–23 
Alkaline phosphatase 202 217 216 256 NM NM 172 215 U/L 106–322 
Lactate dehydrogenase 199 208 195 342 285 258 257 288 U/L 124–222 
Gamma-glutamyl transpeptidase 17 15 21 30 NM NM 25 29 U/L 9–32 
Creatine kinase 70 61 NM 39 59 41 33 34 U/L 41–153 
Total bilirubin 0.4 0.5 0.5 0.7 1.2 1.3 0.4 0.5 mg/dL 0.4–1.5 
Total protein 6.6 NM 6.5 6.4 6.1 5.1 4.8 NM g/dL 6.6–8.1 
Albumin 3.7 3.6 NM 3.6 2.6 2.6 NM g/dL 4.1–5.1 
Sodium 141 138 134 123 130 132 134 135 mEq/L 138–145 
Potassium 3.9 4.2 5.4 7.4 5.3 4.7 4.7 4.3 mEq/L 3.6–4.8 
Chloride 106 103 99 93 97 103 102 102 mEq/L 101–108 
Phosphorus NM 4.4 NM 8.6 4.5 2.6 mg/dL 2.7–4.6 
Calcium NM 9.3 NM 9.3 8.1 7.6 8.1 8.3 mg/dL 8.8–10.1 
Blood urea nitrogen 27.4 34.7 41.9 100.2 81.5 52.1 29.3 30.6 mg/dL 8–20 
Creatinine 0.92 0.94 0.91 1.78 1.35 0.92 0.64 0.64 mg/dL 0.46–0.79 
Estimated glomerular filtration rate 45 44 45 22 29 45 66 66 mL/min/1.73 m2  
Uric acid NM 6.9 NM 10.6 NM NM 3.7 4.3 mg/dL 2.6–5.5 
C-reactive protein 0.1 NM 0.01 0.01 NM NM 0.19 0.72 mg/dL 0–0.14 
Glucose 116 147 131 241 NM NM 211 161 mg/dL 73–109 
White blood cells 4,300 6,260 10,000 19,240 19,500 11,400 8,870 8,280 /μL 3,300–8,600 
Red blood cells 3.31 3.24 3.68 4.39 3.97 3.36 3.02 3.07 ×106/μL 3.86–4.92 
Hemoglobin 9.6 10 10.8 13.5 11.8 10 9.2 9.3 g/dL 11.6–14.8 
Hematocrit 30.2 29.7 33.6 40.8 36.7 31 28.1 28.5 35.1–44.4 
Platelets 197,000 217,000 223,000 230,000 178,000 143,000 136,000 149,000 /μL 158,000–348,000 
ParametersValuesUnitsReference range
Day 1Day 6Day 15Day 21aDay 22Day 23Day 27Day 31
Aspartate aminotransferase 17 18 25 26 29 26 24 24 U/L 13–30 
Alanine aminotransferase 27 25 26 21 22 26 U/L 7–23 
Alkaline phosphatase 202 217 216 256 NM NM 172 215 U/L 106–322 
Lactate dehydrogenase 199 208 195 342 285 258 257 288 U/L 124–222 
Gamma-glutamyl transpeptidase 17 15 21 30 NM NM 25 29 U/L 9–32 
Creatine kinase 70 61 NM 39 59 41 33 34 U/L 41–153 
Total bilirubin 0.4 0.5 0.5 0.7 1.2 1.3 0.4 0.5 mg/dL 0.4–1.5 
Total protein 6.6 NM 6.5 6.4 6.1 5.1 4.8 NM g/dL 6.6–8.1 
Albumin 3.7 3.6 NM 3.6 2.6 2.6 NM g/dL 4.1–5.1 
Sodium 141 138 134 123 130 132 134 135 mEq/L 138–145 
Potassium 3.9 4.2 5.4 7.4 5.3 4.7 4.7 4.3 mEq/L 3.6–4.8 
Chloride 106 103 99 93 97 103 102 102 mEq/L 101–108 
Phosphorus NM 4.4 NM 8.6 4.5 2.6 mg/dL 2.7–4.6 
Calcium NM 9.3 NM 9.3 8.1 7.6 8.1 8.3 mg/dL 8.8–10.1 
Blood urea nitrogen 27.4 34.7 41.9 100.2 81.5 52.1 29.3 30.6 mg/dL 8–20 
Creatinine 0.92 0.94 0.91 1.78 1.35 0.92 0.64 0.64 mg/dL 0.46–0.79 
Estimated glomerular filtration rate 45 44 45 22 29 45 66 66 mL/min/1.73 m2  
Uric acid NM 6.9 NM 10.6 NM NM 3.7 4.3 mg/dL 2.6–5.5 
C-reactive protein 0.1 NM 0.01 0.01 NM NM 0.19 0.72 mg/dL 0–0.14 
Glucose 116 147 131 241 NM NM 211 161 mg/dL 73–109 
White blood cells 4,300 6,260 10,000 19,240 19,500 11,400 8,870 8,280 /μL 3,300–8,600 
Red blood cells 3.31 3.24 3.68 4.39 3.97 3.36 3.02 3.07 ×106/μL 3.86–4.92 
Hemoglobin 9.6 10 10.8 13.5 11.8 10 9.2 9.3 g/dL 11.6–14.8 
Hematocrit 30.2 29.7 33.6 40.8 36.7 31 28.1 28.5 35.1–44.4 
Platelets 197,000 217,000 223,000 230,000 178,000 143,000 136,000 149,000 /μL 158,000–348,000 

NM, not measured.

aCardiac arrest occurred on day 21, and laboratory values were recorded immediately after the cardiac arrest.

Hyperkalemia is a common electrolyte abnormality in clinical practice and has been reported to occur in 1–10% of hospitalized patients [9]. It is also more frequent in patients with chronic kidney disease, diabetes, HF, and certain medications such as renin-angiotensin-aldosterone system (RAAS) inhibitors and nonsteroidal anti-inflammatory drugs [10, 12].

TMP/SMX is also known to cause hyperkalemia. The mechanism is as follows: TMP acts like the potassium-sparing diuretic amiloride and blocks epithelial sodium channels (ENaC) in the distal nephron, reducing transepithelial voltage and inhibiting potassium secretion [13]. Recent reviews have reported that TMP/SMX-induced hyperkalemia is dose-dependent, potentiated by RAAS inhibitors and other agents, and impaired renal function also increases the propensity for hyperkalemia. However, severe hyperkalemia with serum potassium levels exceeding 6 mEq/L is rare, occurring in only 0.2% of patients [14]. In this case, the acute onset of hyperkalemia after TMP/SMX was initiated, suggests that the hyperkalemia was probably triggered by TMP/SMX, despite the low dosage. The following factors could explain why low-dose TMP/SMX caused life-threatening hyperkalemia:

The first factor is the concomitant use of spironolactone. Spironolactone, a mineralocorticoid receptor antagonist, is widely used because it improves the prognosis of patients with HF and reduced left ventricular ejection fraction [15], but it can cause hyperkalemia. Concomitant use of spironolactone, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers with TMP/SMX is associated with an increased risk of hospitalization and sudden death due to hyperkalemia in older adult patients [16, 19].

A study found that renal failure with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers use was a risk factor for low-dose TMP/SMX-induced hyperkalemia [20], but concomitant use of potassium-sparing diuretics was not. This may be because only 6 of the 186 eligible patients were concomitantly treated with potassium-sparing diuretics. Although there are insufficient data to support the effect of spironolactone on low-dose TMP/SMX-induced hyperkalemia, considering previous reports [16, 17], an effect of spironolactone on hyperkalemia is possible in this case. Further investigation of the interaction between low-dose TMP/SMX and spironolactone is warranted.

The second factor is renal failure with dehydration. The patient was taking azosemide, a loop diuretic, before starting TMP/SMX. However, her electrolyte balance was maintained. This is because ENaC reabsorption in the renal collecting duct counteracts the increased sodium excretion caused by loop diuretics [21]. However, the patient’s serum sodium levels decreased after TMP/SMX was initiated. Hyponatremia due to TMP/SMX is more common at higher doses [22], reportedly occurring in 72.3% of patients at doses of TMP ≥8 mg/kg/day [23] but can also occur at lower doses [24]. TMP/SMX may have inhibited ENaC-mediated sodium reabsorption in the collecting ducts and disrupted the compensatory effect of loop diuretic-induced sodium excretion. This may have increased sodium excretion and the diuretic effects, and gradual progression of dehydration may have induced renal dysfunction with abnormal electrolyte levels. Concomitant use of loop diuretics increases the risk of acute kidney injury in patients receiving TMP/SMX [25]. As the combination of diuretics and TMP/SMX can induce hypovolemia, it may be clinically important to monitor physical findings such as body weight, thirst, and changes in vital signs, to detect adverse effects [26].

Third, the dosage of TMP/SMX may not have been a low dose for this patient. TMP/SMX was initiated at the recommended dose for PCP prophylaxis (80 mg/400 mg/day) [27]. Both TMP and SMX are primarily renally eliminated drugs, with half-lives of 11 and 9 h, respectively, but in severe renal failure the elimination half-life of both drugs can increase to 45–60 h [28]. Therefore, 50% dose reduction is generally recommended for patients with creatinine clearance of 15–30 mL/min. The patient’s eGFR was reported as 45 mL/min/1.73 m2, but, considering her body surface area, her actual eGFR was 36.3 mL/min, and the creatinine clearance calculated by the Cockcroft-Gault equation [29] was 37 mL/min, which is close to the value at which dose reduction of TMP/SMX should be considered.

Thrice weekly TMP/SMX is thought to be as effective as once-daily administration [27] for PCP prophylaxis, and if such a reduced regimen had been chosen, severe hyperkalemia could have been avoided. As it has been reported that electrolyte imbalances occur 7 days after initiating TMP/SMX [30], electrolytes should be checked within a week and a decision should be made whether to reduce the dosage.

Finally, tumor lysis syndrome (TLS) should also be considered, as the patient had undergone corticosteroid treatment and radiotherapy. However, the transtubular potassium gradient did not show a trend toward potassium overload, although fractional excretion of potassium was overestimated, and it could not be determined whether there was excess potassium supply due to TLS. Although hyperkalemia due to TLS cannot be ruled out, considering the rarity of TLS in patients with solid tumors [31] and the clinical course of the disease, TMP/SMX is most likely to have been the trigger.

In conclusion, TMP/SMX, even at low doses, can cause severe hyperkalemia, which can lead to sudden death. Therefore, treatment with low-dose TMP/SMX should be accompanied by periodic monitoring of electrolytes, with the frequency depending on renal function and the concomitant medications administered.

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. This case report was approved by the Institutional Ethics Committee of Niigata City General Hospital (No. 21-080).

The authors have no conflicts of interest to declare.

This research received no specific grants from any funding agency in the public, commercial, or not-for-profit sectors.

H.K. conceived the work, drafted the manuscript, and takes responsibility for the entire paper. N.S., Y.I., and Y.H. supervised this study. N.S., Y.I., K.M., H.T., and Y.H. contributed substantially to its revision. All authors have read and approved the final manuscript.

The data used in this case report will not be shared because of the risk of identifying the individual. Further inquiries can be directed to the corresponding author.

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