To investigate kidney injury in preeclampsia, we analyzed 14 biomarkers in urine specimen from 4 groups of pregnant women (normotensive, pregnancy-complicated with chronic hypertension, mild or severe preeclampsia). These biomarkers were podocyte glycoproteins nephrin and podocalyxin; matrix metallopeptidases MMP2 and MMP9, and their inhibitor TIMP2; inflammatory molecules and cytokines sVCAM-1, TNFα, sTNFR-1, IL-6, IL-8, IL-10, and IL-18; and kidney injury biomarkers NGAL and KIM-1. Postpartum urine specimens (6-8 weeks) from normotensive and severe preeclampsia were also evaluated. We found 1) urine levels of nephrin, MMP2, MMP9, and KIM-1 were significantly higher before delivery in severe preeclampsia than in normotensive controls. The increased levels were all reduced to the levels similar to that of normotensive controls in postpartum specimens from severe preeclampsia; 2) sVCAM-1, sTNFR-1, and NGAL levels were significantly increased in severe preeclampsia compared to normotensive controls before delivery, but levels of these molecules were significantly reduced in postpartum specimens in both groups; 3) IL-6 and IL-8 levels were not different between preeclampsia and normotensive groups, but significantly increased in pregnancy-complicated with chronic hypertension; 4) TIMP2 and IL-18 levels were not different among the study groups before delivery, but significantly reduced in postpartum specimens from normotensive controls. Our results indicate that kidney experiences an increased inflammatory response during pregnancy. Most interestingly, tubular epithelial cell injury may also occur in severe preeclampsia. These biomarkers could be used to assess podocyte or tubular injury, and kidney inflammatory responses during pregnancy and to evaluate postpartum kidney injury recovery in pregnancy-complicated disorders.