Kinetic behavior of the erythrocyte sodium-lithium countertransporter in nonnephropathic diabetic twins

Elevated erythrocyte sodium-lithium countertransport activity occurs in diabetes and may be genetically mediated. The relation of this abnormality to the disease and its complications is unclear. To remove confounding genetic factors and the impact of complications, we studied sodium-lithium countertransport activity together with its kinetic components, maximal rate of turnover (V max) and external affinity for sodium (k Na), in identical-twin pairs discordant for insulin-dependent diabetes who were normotensive and had no evidence of nephropathy. Fifteen twin pairs were studied along with the same number of healthy control subjects matched with the twins for gender, age, and body mass index. Clinical and laboratory characteristics of the twins and controls were similar, with the exception that whole blood glucose and glycated hemoglobin concentrations were higher in diabetic twins ( P < .001). Comparison of countertransport activity between nondiabetic and diabetic twin groups failed to uncover any significant differences ( P = .30, Wilcoxon). Similarly, there were no differences in countertransport activity between the nondiabetic twin group and the controls ( P = .38, Mann-Whitney). Furthermore, no associations were noted between residual activity values and residual data of any of the other clinical or laboratory characteristics measured. Comparison of V max between nondiabetic and diabetic twin groups showed a significant elevation in the diabetic twins (0.515 + 0.220 v 0.439 + 0.229 mmol Li L RBC · h, P = .049, paired t test). By contrast, no significant differences were noted between the nondiabetic twin group and the controls ( P = .15, unpaired t test). Comparison of k Na between nondiabetic and diabetic twin groups found no significant differences in k Na ( P = .42, Wilcoxon). Similarly, there were no differences in k Na between nondiabetic twins and controls ( P = .14, Mann-Whitney). Neither the residual data for V max nor k Na showed any association with the residual data of any of the other clinical or laboratory characteristics measured. When intertwin correlations were examined, all three parameters describing the behavior of the sodium-lithium countertransporter showed significant intertwin correlations (activity, r = .51, P = .04; V max, r = .82, P = .001; k Na, r = .76, P = .001). In conclusion, the diabetic state has a small effect on the V max of the sodium-lithium countertransporter. Failure to consider the complex nature of the activ