Abstract

Hyperkalemia is a medical emergency that can induce deadly cardiac arrhythmias. Treatment of hyperkalemia can be thought of in three distinct steps. First, antagonize the effects of hyperkalemia at the cellular level (membrane stabilization) by administering calcium gluconate; secondly, decrease serum potassium by promoting potassium into cells through co-administration of glucose and insulin and thirdly, remove potassium from the body by dialysis or treatment with potassium-binding resins. The use of insulin to promote the movement of potassium into cells in patients with end-stage renal failure and hyperkalemia is widely supported. Administration of insulin with glucose causes the potassium to fall rapidly; however, hypoglycemia has been noted as a frequent complication [1]. Blood pressure (BP) elevation secondary to hypoglycemia has been demonstrated through the activation of the sympathoadrenal system [2]. Herein we present the case of a patient with end-stage renal failure who developed a hypertensive crisis in the setting of insulin-induced hypoglycemia following treatment for hyperkalemia.

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