Tetteh Paul Winston, Antwi-Boasiako Charles, Gyan Ben, Antwi Daniel, Adzaku Festus, Adu-Bonsaffoh Kwame, Obed Samuel
Department of Physiology.
Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, Utrecht, The Netherlands.
Res Rep Trop Med. 2013 Jun 18;4:7-13. doi: 10.2147/RRTM.S40450. eCollection 2013.
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.
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.
The pre-eclampsia group had significantly ( = 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 ( = 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 ( < 0.001), indicating more renal impairment.
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.
先兆子痫的病因在很大程度上仍不清楚，但氧化应激（氧化剂与抗氧化剂力量失衡，氧化剂占优势）被认为与高血压和蛋白尿等临床症状的发生有关。使用尿中异前列腺素评估先兆子痫中的氧化应激产生了相互矛盾的结果，而且肾功能可能会影响异前列腺素的排泄。本研究的目的是确定氧化应激在先兆子痫病理生理学中的作用，并评估肾功能对加纳人群先兆子痫中异前列腺素排泄的影响。
这是一项病例对照研究，包括103例先兆子痫妇女和107例正常孕妇作为对照，于2006年12月至2007年5月在科勒-布教学医院进行。研究参与者在符合纳入标准并签署书面知情同意书后被纳入研究。通过使用酶联免疫吸附测定技术测量尿中异前列腺素排泄和总抗氧化能力来确定氧化应激。通过使用肾脏病饮食改良公式计算估计的肾小球滤过率来评估肾功能。
先兆子痫组尿中异前列腺素排泄量（2.81±0.14 ng/mg肌酐）显著高于对照组（2.01±0.18 ng/mg肌酐）（P = 0.0006），总抗氧化能力（1.68±0.05 mM）显著低于对照组（1.89±0.04 mM）（P = 0.0008）。在先兆子痫病例中，尿中异前列腺素排泄与平均动脉压（r = 0.261）和微量白蛋白尿（r = 0.510）均呈正相关。先兆子痫组的估计肾小球滤过率显著低于对照组（P < 0.001），表明肾功能损害更严重。
先兆子痫组尿中异前列腺素排泄增加和总抗氧化能力降低表明氧化剂生成增加以及母体抗氧化剂消耗和/或减少。氧化应激增加可能通过导致内皮功能障碍、蛋白尿和高血压在先兆子痫的病理生理学中起重要作用。
