BACKGROUND: The renal threshold for glucose (RT(G)) is determined by the nephron's reabsorptive capacity. Glucose is reabsorbed through sodium-coupled glucose cotransporters in the proximal tubules. During pregnancy, renal glucose reabsorptive capacity decreases, possibly, due to reduced glucose transporter expression. Our hypothesis is that inadequate decrease in RT(G) during pregnancy will make women more prone to develop gestational diabetes mellitus (GDM). METHODS: Pregnant women (n = 40) who were referred to our center for oral glucose tolerance test (OGTT) were included in the analysis. Plasma glucose levels and urinary glucose excretion were measured for 4 h after 100 g oral glucose load. These data were used to calculate RT(G) . The subjects were divided into two cohorts, GDM and non-GDM, according to the OGTT results. Mean RT(G) was compared between the two groups. RESULTS: Fifteen (37.5%) of the women were diagnosed with GDM. Seventeen participants had only trace amounts of urinary glucose excretion, and no value of RT(G) could be determined; RT(G) was determined in the other 23 subjects. Among these 23 women, 13 were diagnosed as GDM, and 10 had normal OGTT. RT(G) was lower in the non-GDM women (146 ± 14 mg/dL) than in the GDM women (182 ± 18 mg/dL), p < 0.001. CONCLUSIONS: Gestational diabetes mellitus is associated with higher RT(G) during pregnancy compared with non-GDM. These results support our hypothesis that inadequate decrease of the RT(G) may have a pathophysiological role in the development of GDM.
BACKGROUND: The renal threshold for glucose (RT(G)) is determined by the nephron's reabsorptive capacity. Glucose is reabsorbed through sodium-coupled glucose cotransporters in the proximal tubules. During pregnancy, renal glucose reabsorptive capacity decreases, possibly, due to reduced glucose transporter expression. Our hypothesis is that inadequate decrease in RT(G) during pregnancy will make women more prone to develop gestational diabetes mellitus (GDM). METHODS: Pregnant women (n = 40) who were referred to our center for oral glucose tolerance test (OGTT) were included in the analysis. Plasma glucose levels and urinary glucose excretion were measured for 4 h after 100 g oral glucose load. These data were used to calculate RT(G) . The subjects were divided into two cohorts, GDM and non-GDM, according to the OGTT results. Mean RT(G) was compared between the two groups. RESULTS: Fifteen (37.5%) of the women were diagnosed with GDM. Seventeen participants had only trace amounts of urinary glucose excretion, and no value of RT(G) could be determined; RT(G) was determined in the other 23 subjects. Among these 23 women, 13 were diagnosed as GDM, and 10 had normal OGTT. RT(G) was lower in the non-GDM women (146 ± 14 mg/dL) than in the GDM women (182 ± 18 mg/dL), p < 0.001. CONCLUSIONS:Gestational diabetes mellitus is associated with higher RT(G) during pregnancy compared with non-GDM. These results support our hypothesis that inadequate decrease of the RT(G) may have a pathophysiological role in the development of GDM.