Clinical StudiesHyponatremia: evaluating the correction factor for hyperglycemia☆
Section snippets
Subjects
Six (5 men, 1 woman) young [32 ± 2 (mean ± SD) years], healthy, normal-weight (70 ± 4 kg) volunteers were studied. None of the subjects were taking any medication or had a family history of diabetes.
Experimental protocol
Subjects fasted overnight, and baseline plasma glucose and serum sodium concentrations were obtained. Somatostatin was infused (300 μg/h) throughout the study to suppress endogenous insulin secretion. Glucose (20% dextrose given with 0.45% saline) was infused to increase the plasma glucose
Results
Acute hyperglycemia decreased the serum sodium concentration in all subjects. There was no delay in the hyponatremic effect of hyperglycemia, demonstrating that the extracellular shift of water was essentially immediate (Figure 1 ). Similarly, normalization of serum sodium concentration mirrored the time course of normalization of serum glucose concentration in the second phase of the study (Figure 1). The volume of fluid infused to increase plasma glucose concentrations averaged 805 mL (n =
Discussion
These results demonstrate that hyperglycemia rapidly and profoundly decreases the serum sodium concentration in healthy subjects rendered acutely insulin deficient. Moreover, this hyponatremic effect is quickly reversed with normalization of the glucose concentration (Figure 1). This is consistent with earlier observations that the primary mechanism of hyponatremia is the forced extracellular flux of water induced by acute hyperglycemia 2, 3. It is the magnitude of this osmotic shift that Katz
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Supported by USPHS Grants DK38578 and RR00847 to the University of Virginia General Clinical Research Center and in part by a Research Centers in Minority Institutions Award (P20 RR 11091) from the National Institutes of Health to the University of Hawaii and the Kapiolani Medical Center for Women and Children.