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A Journal on Obstetrics and Gynecology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Scopus, Emerging Sources Citation Index
Minerva Ginecologica 1999 October;51(10):373-8
Markers of tubular damage in pre-eclampsia
Paternoster D. M., Stella A., Babbo G. L., Pignataro R., Mussap M., Plebani M.
Background. The aim of this study is to investigate the tubular damage markers in pre-eclampsia and in pregnancy induced hypertension (PIH).
Methods. This transversal study involved 111 women admitted to the Department of Obstetric and Gynaecology, University Hospital, Padua (Italy) and was conducted from the 24th week until delivery: 23 had normal pregnancies, 54 manifest pre-eclampsia, and 34 manifested pregnancy-induced hypertension (PIH) without superimposed pre-eclampsia. The following laboratory tests were performed: U-a1 microglobulin, U-NAG, uric acid and microalbuminuria. The four groups were compared using the Mann-Whitney test and the Kruskall-Wallis test for multiple comparisons. A value of p<0.05 was considered as statistically significant.
Results. As for the markers of tubular damage, the values for urinary NAG were significantly lower in the control group (0.97 U/mmol Creat) than in the pre-eclampsia group (2.89 U/mmol Creat), and the PIH group (2.12 U/mmol Creat) (p<0.01). Values for urinary a1-microglobulin were higher in the pre-eclampsia group (4.03 U/mmol Creat) than in the control (0.74 U/mmol Creat), and PIH groups (1.88 U/mmol Creat) (p<0.01). As for the markers of glomerular damage, the values of microalbuminuria were higher in the pre-eclampsia group (134 µg/min) than in the control (9.4 µg/min), and PIH groups (10 µg/min), (p<0.05). Uric acid, the marker of glomerular and tubular damage, was higher in the pre-eclampsia group (0.27 mmol/L) than in the control (0.20 mmol/L ), and PIH groups (0.24 mmol/L), (p<0.05).
Conclusions. In pre-eclampsia there is a tubular and glomerular damage to point out by an increased urinary excretion of NAG. In pre-eclampsia, an increase of urinary a1-microglobulin excretion may be considered to be partly due to the overloading of the tubule and partly due to a mixed glomerular and tubular lesion.