The role of hyperuricemia in the pathophysiology of preeclampsia

Preeclampsia (PE) is a human pregnancy disorder that begins with high blood pressure. This disorder occurs after 20 weeks of pregnancy and is defined by the high pressure of blood and proteinuria symptoms. Also, PE is recognized as a multifactorial disease that causes damage to some systemic organs including the lungs, brain, kidneys and liver. In some cases, high blood pressure might happen without proteinuria but includes complications including acute renal failure, thrombocytopenia, and fetal growth limitations. Hyperuricemia is known as a serum urate concentration of more than 6.8 mg/dL. Uric acid, which is mainly synthesized in the liver, is released into the bloodstream, only a small percentage of which binds to proteins. Thus, most circulating urate is readily available for filtration in the glomerulus and for participation in a number of complex renal mechanisms. Uric acid amounts in non-pregnant women usually range from 0.3 up to 6.0 mg/dL. Surprisingly, the levels of uric acid in pregnant women up to the twentieth week of pregnancy are 20 to 25 percent lower than in non-pregnant women. This reduction in levels of uric acid in the first trimester is due to hemodilution because of increased blood levels due to elevated filtration rate of glomeruli and decreased proximal tubular reabsorption. Uric acid is an identified biomarker for oxidative stress, kidney damage, and placental ischemia. Specifically, these are also the properties of PE. However, uric acid is sometimes referred to as a biomarker of PE. Elevated levels of serum uric acid in PE vs. usual pregnancies have been shown and recommend levels of serum uric acid as a risk indicator for progression of PE. According to the above discussion, the objective of this study was to review the role of hyperuricemia in the pathophysiology of PE. As a conclusion, PE is specified by hyperuricemia and signs of elevated creation of ROS and reduced antioxidants levels. There are GCKR, PDZK1, LRP2, ABCG2, SLC2A9, SLC17A1, LRRC16, SLC22A12, SLC17A3, SLC22A11, and SF1 genes involved in the uric acid transport that may contribute in the hyperuricemia during PE and Alterations in the function of these genes might increase the risk of this disease.