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ePublished: 01 Dec 2014
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J Renal Inj Prev. 2014;3(4): 83-86.
doi: 10.12861/jrip.2014.24
PMID: 25610884
PMCID: PMC4301390
  Abstract View: 2982
  PDF Download: 1830

Editorial

Renal dysfunction in fetal alcohol syndrome: a potential contributor on developmental disabilities of offspring

Farahnak Assadi*

1 Section of Nephrology, Rush University Medical Center, Chicago, Illinois, UA
*Corresponding Author: *Corresponding author: Prof. Farahnak Assadi, , Email: fassadi@rush.edu

Implication for health policy/practice/research/medical education

Alcohol consumption during pregnancy is teratogennic. The affects of prenatal alcohol exposure on offspring range from growth retardation, facial dysmorphism, and central nervous involvements. Impaired renal acidification has been documented in infants with fetal alcohol syndrome (FAS). The high urinary zinc excretion could deplete the zinc stores of the body leading to zinc deficiency. Zinc deficiency in pregnant mothers is also associated with fetal dysmorphogenesis. It is therefore possible that the increased zinc excretion in FAS is a spectrum of the impaired tubular dysfunction. The finding of low plasma zinc levels in infants with FAS suggest the possibility of preventing the alcohol-related birth defects by educating women of child bearing age to refrain drinking alcohol during pregnancy and by supplementing alcoholic pregnant women and their newborns with zinc. Further studies of zinc metabolism in alcoholic women and their neonates seem justified. 

Please cite this paper as: Assadi F. Renal dysfunction in fetal alcohol syndrome: a potential contributor on developmental disabilities of offspring. J Renal Inj Prev 2014; 3(4): 83-86. DOI: 10.12861/jrip.2014.24

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