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Decreased urine albumin:creatinine ratios in infants of diabetic mothers: does exposure to diabetic pregnancies alter fetal renal development?

Published online by Cambridge University Press:  22 August 2011

R. F. Dyck*
Affiliation:
Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada Department of Community Health and Epidemiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
W. T. Bingham
Affiliation:
Department of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
H. Lim
Affiliation:
Department of Community Health and Epidemiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
Y. Jiang
Affiliation:
Department of Community Health and Epidemiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
N. D. Osgood
Affiliation:
Department of Community Health and Epidemiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada Department of Computer Science, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
*
*Address for correspondence: Dr R. F. Dyck, MD, Department of Medicine, Royal University Hospital, 103 Hospital Drive, Saskatoon, Saskatchewan S7N 0W8, Canada. (Email [email protected])

Abstract

Offspring of diabetic mothers experience an increased risk for type 2 diabetes but it is not known whether diabetic pregnancies also confer a higher inter-generational risk for diabetic complications. Because microalbuminuria is a sensitive indicator of glomerular damage, we compared the urine albumin:creatinine ratios (ACRs) between 65 infants of diabetic mothers (InfDM+) and 59 infants of non-diabetic mothers (InfDM−), and repeated the comparisons in 21 InfDM+ and 19 InfDM− when children were 5–19 months old. ACRs were higher among neonates compared with normal reference values for adults, but declined with increasing age. The only independent predictor of higher ACRs in a logistic regression model (⩾13 mg/mmol v. <13 mg/mmol) was the presence of delivery complications (odds ratio 2.95; P = 0.015). Neither high nor low birth weight was associated with higher neonatal ACRs. The most unique finding of the study was that InfDM+ had significantly lower ACRs than InfDM− [mean = 12.9 (median = 6.0) v. mean = 16.6 (median = 11.5), respectively at P = 0.05] even after adjusting for other variables using logistic regression (odds ratio 0.25; P = 0.001). In contrast, by 5–19 months, there was a trend toward higher ACRs among InfDM+ compared with InfDM− [mean = 6.3 mg/mmol (median = 1.9) v. mean = 3.0 mg/mmol (median = 2.5), respectively at P = 0.25]. Lower ACRs in InfDM+ may be due to developmental changes in fetal kidneys induced by hyperinsulinemia. Although the implications of this observation are unclear, it is possible that exposure to a diabetic intrauterine environment might influence the later risk for renal disease.

Type
Original Articles
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2011

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