Abstract
Objectives: To compare the levels of podocyte damage markers nephrin and podocalyxin in urine samples taken at the time of gestational diabetes mellitus (GDM) diagnosis and at birth. Amniotic fluid podocalyxin (pdx) and nephrin levels were also analyzed to determine whether GDM had an impact on fetal glomeruli. Methods: A total of 50 patients, including 24 patients diagnosed with gestational diabetes and 26 healthy pregnant women whose gestational weeks were matched, were included in the study. GDM was diagnosed with a 75 g oral glucose tolerance test (OGTT). Fresh morning urine samples from patients diagnosed with GDM were collected. The second urine sample was collected with the help of a catheter during birth. Amniotic fluid samples were taken from patients who gave birth by cesarean section. The urinary podocalyxin and nephrin levels were measured via the quantitative sandwich enzyme immunoassay. Albumin-creatinine ratio (uACR) was also calculated in urine samples. Results: Urinary nephrin and pdx levels on the day of GDM diagnosis were similar in the GDM and control groups. Microalbuminuria was detected in only one patient from each group at the time of GDM diagnosis. In the urine samples taken from the time of birth, pdx and nephrin levels of the GDM group were significantly higher than the control group (p < 0.001 for each). While microalbuminuria was detected in five patients (20.8%) at the time of birth in the GDM group, it was detected in only two patients (7.7%) in the control group. In the GDM group, a significant increase was detected between the urine pdx and nephrin levels measured at diagnosis and those measured at birth. In the control group, measurements at baseline and at birth were similar. There was no significant difference between the GDM and control groups in terms of amniotic fluid pdx and nephrin levels. A positive and significant correlation was detected between urinary pdx, nephrin, SBP, and uACR. Conclusions: While GDM triggers podocyte damage in maternal glomeruli, it does not cause significant change in fetal glomeruli.