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In this uncontrolled, retrospective study, Apel et al found a 13% incidence of hypoglycemia (defined as blood glucose ankyrin learn more of overall gluconeogenesis, and is therefore as important as the liver in carbohydrate metabolism [29, 30]. The kidney also plays a critical role in insulin metabolism. Even though evidence implies that CKD creates an insulin-resistant state, hypoglycemia can ensue due to decreased gluconeogenesis and insulin degradation [31]. Other factors such as altered drug metabolism, malnutrition, decreased hepatic gluconeogenesis, and infection also increase the risk of hypoglycemia in this population [27, 32]. In hemodialysis patients, the use of glucose-free dialysis solution increases the risk of hypoglycemia due to transfer of plasma glucose to the dialyzate. Addition of glucose to dialysis solution significantly decreases this risk [33, 34]. Apel et al do not specify in their study whether there is a difference between hemodialysis and peritoneal dialysis patients. Theoretically, the incidence of hypoglycemia is lower in peritoneal dialysis due GSK-3 activation to the presence of dextrose in the dialysis solution. The results from Apel's study emphasize the importance of intense blood glucose monitoring after insulin administration. Apel's study defined hypoglycemia as ��60 mg/dL [3.33 mmol/L] and even with this conservative definition, the incidence was 13%. Since IV insulin is a commonly used therapy for severe hyperkalemia in ESRD patients in the hospital setting, we agree with Apel et al that a protocol-driven approach may be able to decrease the incidence of hypoglycemia. Published literature indicates that the insulin and dextrose regimen varies from center to center. Dose of insulin ranges from 5�C10 units and amount of glucose ranges from 25 to 60 g [35]. Others have recommended additional dextrose infusion after intravenous push of dextrose and insulin to prevent hypoglycemia [17, 20]. Due to risks of hypoglycemia, some have advocated the use of glucose alone in the treatment of hyperkalemia. The rationale is based on the theory that exogenous glucose stimulates insulin secretion which shifts potassium into the cell.