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

*Corresponding author: Prof. Farahnak Assadi, Email: [email protected] Introduction The term fetal alcohol syndrome (FAS) signifies the triad of intrauterine growth retardation, microcephaly and short palpebral fissures, due to prenatal exposure to alcohol (1-4). Those severely affected have unusual facial dysmorphism with microcephaly, narrow forehead, short palpebral fissures with hypoplastic upper lip (5-7). In addition, they have developmental delay, behavior dysfunction or deficit, intellectual impairment and/or mental retardation (8,9). The term fetal alcohol effects (FAE) describe less extreme changes associated with prenatal alcohol exposure. Criteria have not yet been established for the diagnosis of FAE, but there is consensus that the diagnosis requires deficiencies in two of the above categories and a history of maternal alcohol abuse (1-4). Prenatal alcohol exposure has also been linked to cardiac anomalies, urinary and kidney anomalies, neural tube defects, cleft lip with or without cleft palate, gastrointestinal and genital abnormalities, dental anomalies, limb and joint abnormalities, scoliosis, ptosis, strabismus, epicanthal folds, microphthalmia, myopia, short up-turned nose, broad or low nasal bridge, low set ears and rotated ears (10-12). Renal structural anomalies of FAS include cross-fused ectopia, renal hypoplasia and urethropelvic junction obstruction have been reported in children with FAS (10,12). More recent clinical and experimental studies have also shown that fetuses exposed to ethanol perinatally have a number of renal functional abnormalities, including impairment in renal acidification and potassium excretion as well as a defect in urinary concentrating ability, even in the absence of any structural abnormalities (13-15). The scanning electron microscopy examinations of the rat kidney following fetal exposure to alcohol, showed mitochondrial swelling and cytoplasmic vacuolation of the epithelial cells of the distal nephron, suggesting the possibility of alcohol induced renal tubular cell injury (16). Assadi and Ziai also reported that offspring of alcoholic mothers particularly those children with FAS have lower plasma zinc levels and that the urinary excretion of zinc is increased in these infants, suggesting a direct relationship between urinary losses and lower plasma zinc levels (17). Farahnak Assadi*