Case Presentation: 58 year-old woman with history of chronic kidney disease, insulin dependent diabetes mellitus, and hypertension presented with three weeks of worsening generalized weakness. She denied recent vomiting, diarrhea, or polyuria. Laboratories revealed severe hypokalemia with potassium of 2.3 mEq/L, sodium of 141 mEq/L, magnesium of 1.5 mEq/L, glucose of 129 mEq/L, creatinine of 3.0 mg/dL (at baseline) and bicarbonate of 24 mEq/L. Urine potassium was 17 mEq/L. Initial aggressive potassium repletion and correction of magnesium failed to correct hypokalemia. Computerized tomography revealed a sub-centimeter right adrenal nodule, but renin/aldosterone ratio was normal. As no evident source of hypokalemia was found after extensive evaluation, we performed a detailed reconciliation of medications, which revealed that patient had recently started taking quetiapine 200mg nightly. After a trial off quetiapine, serum potassium normalized, which led to a diagnosis of quetiapine-induced hypokalemia.
Discussion: Hypokalemia is a common finding and the workup requires a detailed history, physical exam, as well as laboratory testing. Hypokalemia is the result of either decreased potassium intake, increased excretion, or transcellular shifting. The most common causes are gastrointestinal losses and diuretic use. Quetiapine induced hypokalemia however is rare and has been reported in only a few case reports. The exact mechanism of this phenomenon is not clear. Quetiapine is primarily a serotonin, adrenergic, and dopamine antagonist, but at high doses it can paradoxically cause a surge of catecholamines instead. The exact dose that this occurs is unknown. Therefore, it has been hypothesized that quetiapine can create a beta 2 adrenergic mediated influx of potassium into cells. The catecholamine rush can also increase insulin levels and resistance and therefore further promote influx of potassium into cells. Since quetiapine is a dopamine antagonist, it may inhibit centrally released ADH. As a result of a decrease in volume, the renin-angiotensin system can become activated and therefore increase urinary potassium excretion. Furthermore, quetiapine and other antipsychotic medications have been thought to display aldosterone-like effects directly on the renal tubules, therefore promoting urinary potassium excretion.
Conclusions: In conclusion, every internist should have a systematic approach to hypokalemia, especially when symptomatic. The key to figuring out the etiology of hypokalemia can be in the history, particularly when a medication is implicated. While quetiapine-induced hypokalemia is rare, internists should be aware of this potential side effect.