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Third, renal gluconeogenesis is reduced. In the fasting state, the kidney contributes 10�C25% of glucose production [9]. This protective process is lost in ESRD and predisposes these patients to fasting hypoglycemia [10]. Fourth, uremia can blunt the release of counter-regulatory hormones such as glucagon and catacholamines further limiting the body's defense against hypoglycemia [11]. Schafers et al. [12] examined the incidence of hypoglycemia after treatment of hyperkalemia with insulin in hospitalized adults. This study found that hypoglycemia [blood glucose check details occurred with the commonly used regimen of 10 units of IV insulin with 25 g of dextrose. The results of their study and our study suggest the need for additional dextrose. Their study population included 67% of patients with acute renal injury or ESRD, and the risk of hypoglycemia was higher in this subset. Our study focused solely on patients with ESRD, likely explaining the higher frequency of hypoglycemia. Our study showed a 13% risk of hypoglycemia despite dextrose with insulin, demonstrating that one dose of dextrose is not sufficient in some patients. This suggests the need for additional dextrose support. The administration of dextrose alone to stimulate endogenous insulin secretion is not advised because, if there is inadequate insulin secretion such as with insulin-dependent diabetes, the resultant hyperglycemia could increase plasma UNC2881 osmolarity, promote the exit of potassium from cells and worsen hyperkalemia [13]. We suggest administering 25 g of dextrose with insulin and 25 g of dextrose 1 h after insulin based on our result that hypoglycemia occurred 1�C3 h after insulin with dextrose. We think this regimen is superior to 50 g of dextrose with insulin because it may lessen the initial hyperglycemia, and the second dose may be more effective at preventing hypoglycemia in the following 1�C3 h. Another potential solution is to treat with the standard 10 units of regular insulin and dextrose 25 g followed by an infusion of 10% dextrose at 50 mL/h with close monitoring of blood glucose for at least 3 h or until dialysis is initiated [13]. Hypoglycemia in our study persisted for 2�C3 h after insulin. This suggests the need for blood glucose monitoring STI571 solubility dmso for 3 h after insulin. Since three episodes of hypoglycemia in our study occurred despite dextrose with insulin and dextrose 1 h after insulin, extending blood glucose monitoring for 3 h after insulin will hopefully identify the patients who require additional dextrose. Our study has limitations. It is a retrospective study that includes data from a time period when there was no set protocol to treat hyperkalemia. Therefore, glucose monitoring varied according to the treating physicians.