Objective: Clinical and experimental studies strongly suggest that
prenatal alcohol exposure is associated with zinc deficiency and
impaired renal tubular function. Whether maternal alcohol consumption
during pregnancy causes renal tubular cell injury is unknown. Material
& Methods: Renal function was studied in 8 infants with fetal
alcohol syndrome (FAS) and 8 healthy age-matched infants. Renal
function and structure were also examined in 11 offspring of rats
exposed to alcohol during gestation. Findings: Infants with FAS had
limited ability to concentrate urine after water restriction
(P<0.001) and impaired acidification after acute acid loading
(P<0.001) compared to control group. Plasma zinc levels were lower
(P<0.001) and urinary zinc excretion was higher (P<0.001) in
infants with FAS compared to control infants. Scanning electron
microscopic studiesrevealed cytoplasmic mitochondrial hypertrophy and
vacuolar structures of the epithelial cells of thecortical
collectingducts in the rat kidney following fetal exposure to alcohol.
Conclusion: These findings suggest that offspring of rats exposed to
alcohol during fetal life have renal functional and structural
abnormalities that may be responsible in the genesis of renal
functional abnormalities as described in infants with FAS
