Goren M P, Sibai B M, el-Nazar A
Department of Pathology and Laboratory Medicine, St. Jude Children's Research Hospital, Memphis, TN 38101.
Am J Obstet Gynecol. 1987 Oct;157(4 Pt 1):906-8. doi: 10.1016/s0002-9378(87)80084-4.
The pathophysiology of preeclampsia includes ischemia and microinfarctions of the kidney, which could induce renal tubular cells to release enzymes into urine. We therefore measured the concentrations of two markers of renal tubular damage, N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase, in urine specimens from women with mild or severe preeclampsia and compared the results with those from healthy pregnant and nonpregnant women. The median urinary concentrations of N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase in women without preeclampsia increased progressively through the first, second, and third trimesters and reached maximum values of 1.12 and 0.77 U/mmol creatinine, respectively. Median concentrations of the two enzymes were significantly higher in women with mild preeclampsia (N-acetyl-beta-D-glucosaminidase = 1.40, alanine aminopeptidase = 1.12 U/mmol creatinine) or severe preeclampsia (N-acetyl-beta-D-glucosaminidase = 2.90, alanine aminopeptidase = 1.26 U/mmol creatinine). This increased enzyme excretion indicates subclinical preeclamptic renal tubular damage.
