Paul Winston Tetteh1,2, Charles Antwi-Boasiako1, Ben Gyan3, Daniel Antwi1, Festus Adzaku1, Kwame Adu-Bonsaffoh1,4, Samuel Obed4. 1. Department of Physiology. 2. Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, Utrecht, The Netherlands. 3. Department of Immunology, Noguchi Memorial Institute for Medical Research, University of Ghana, Legon, Ghana, bgyan@noguchi.mimcom.org. 4. Department of Obstetrics and Gynecology, University of Ghana Medical School, Accra, Ghana.
Abstract
BACKGROUND: The cause of pre-eclampsia remains largely unknown, but oxidative stress (an imbalance favoring oxidant over antioxidant forces) has been implicated in contributing to the clinical symptoms of hypertension and proteinuria. Assessment of oxidative stress in pre-eclampsia using urinary isoprostane has produced conflicting results, and it is likely that renal function may affect isoprostane excretion. The aim of this study was to determine the role of oxidative stress in the pathophysiology of pre-eclampsia and to assess the effect of renal function on isoprostane excretion in pre-eclampsia in the Ghanaian population. METHODS: This was a case-controlled study, comprising 103 pre-eclamptic women and 107 normal pregnant controls and conducted at the Korle-Bu Teaching Hospital between December 2006 and May 2007. The study participants were enrolled in the study after meeting the inclusion criteria and signing their written informed consent. Oxidative stress was determined by measuring urinary excretion of isoprostane and total antioxidant capacity using an enzyme-linked immunosorbent assay technique. Renal function was assessed by calculating the estimated glomerular filtration rate using the Modification of Diet in Renal Disease formula. RESULTS: The pre-eclampsia group had significantly (P = 0.0006) higher urinary isoprostane excretion (2.81 ± 0.14 ng/mg creatinine) than the control group (2.01 ± 0.18 ng/mg creatinine) and a significantly (P = 0.0008) lower total antioxidant power (1.68 ± 0.05 mM) than the control group (1.89 ± 0.04 mM). Urinary isoprostane excretion showed a positive correlation with both mean arterial pressure (r = 0.261) and microalbuminuria (r = 0.510) in the pre-eclampsia cases. The pre-eclampsia group had a significantly lower estimated glomerular filtration rate than the control group (P < 0.001), indicating more renal impairment. CONCLUSION: The increased urinary excretion of isoprostanes and decreased total antioxidant power in the in pre-eclampsia group suggest increased production of oxidants and depletion and/or reduction of maternal antioxidants. Increased oxidative stress may be important in the pathophysiology of pre-eclampsia by contributing to endothelial dysfunction, proteinuria, and hypertension.
BACKGROUND: The cause of pre-eclampsia remains largely unknown, but oxidative stress (an imbalance favoring oxidant over antioxidant forces) has been implicated in contributing to the clinical symptoms of hypertension and proteinuria. Assessment of oxidative stress in pre-eclampsia using urinary isoprostane has produced conflicting results, and it is likely that renal function may affect isoprostane excretion. The aim of this study was to determine the role of oxidative stress in the pathophysiology of pre-eclampsia and to assess the effect of renal function on isoprostane excretion in pre-eclampsia in the Ghanaian population. METHODS: This was a case-controlled study, comprising 103 pre-eclamptic women and 107 normal pregnant controls and conducted at the Korle-Bu Teaching Hospital between December 2006 and May 2007. The study participants were enrolled in the study after meeting the inclusion criteria and signing their written informed consent. Oxidative stress was determined by measuring urinary excretion of isoprostane and total antioxidant capacity using an enzyme-linked immunosorbent assay technique. Renal function was assessed by calculating the estimated glomerular filtration rate using the Modification of Diet in Renal Disease formula. RESULTS: The pre-eclampsia group had significantly (P = 0.0006) higher urinary isoprostane excretion (2.81 ± 0.14 ng/mg creatinine) than the control group (2.01 ± 0.18 ng/mg creatinine) and a significantly (P = 0.0008) lower total antioxidant power (1.68 ± 0.05 mM) than the control group (1.89 ± 0.04 mM). Urinary isoprostane excretion showed a positive correlation with both mean arterial pressure (r = 0.261) and microalbuminuria (r = 0.510) in the pre-eclampsia cases. The pre-eclampsia group had a significantly lower estimated glomerular filtration rate than the control group (P < 0.001), indicating more renal impairment. CONCLUSION: The increased urinary excretion of isoprostanes and decreased total antioxidant power in the in pre-eclampsia group suggest increased production of oxidants and depletion and/or reduction of maternal antioxidants. Increased oxidative stress may be important in the pathophysiology of pre-eclampsia by contributing to endothelial dysfunction, proteinuria, and hypertension.
Authors: H Li; J A Lawson; M Reilly; M Adiyaman; S W Hwang; J Rokach; G A FitzGerald Journal: Proc Natl Acad Sci U S A Date: 1999-11-09 Impact factor: 11.205
Authors: C L Regan; R J Levine; D D Baird; M G Ewell; K L Martz; B M Sibai; J Rokach; J A Lawson; G A Fitzgerald Journal: Am J Obstet Gynecol Date: 2001-09 Impact factor: 8.661