| BackgroundProteinuria is an important clinical manifestation and a diagnostic criterion in preeclampsia, but its pathogenesis is poorly understood. Previous studies suggest that a change in glomerular capillary endothelial cells is a characteristic pathological change in preeclampsia kidney. However, the endothelial cell injury can not completely explain the mechanism of proteinuria in preeclampsia. Some researchers believe that podocyte injury may play an important role in the proteinuria of preeclampsia, but its specific injuries and formation mechanism remain unclear.MethodsA rat model of preeclampsia was developed by using inhibitor of nitric oxide synthase (L-NAME). The systolic blood pressure (SBP),24h urine protein, hepatic and renal function were compared among the normal female group, the normal pregnant group, nonpregnant control group and preeclampsia group. The kidney biopsies of each group were observed by using light and electron microscopy. The glomerular nephrin was detected by Western blot and Real-time PCR. Immunofluorescence was used to detect expression of WT1 in every group.ResultsIn rat with preeclampsia, SBP and 24h urine protein were increased significantly compared with other control groups. There were no statistical significance of hepatic and renal function among four groups. In rat with preeclampsia, the level of glomerular nephrin (0.0726±0.0074) was decreased significantly compared with normal female group (0.3795±0.0509), normal pregnant group (0.2361±0.0437) and nonpregnant control group(0.7265±0.0503)(P<0.01), the mRNA level of nephrin had no significant difference among four groups. The expression of WT1 had no significant variation among four groups.ConclusionIn rat with preeclampsia, nephrin was decreased significantly compared with the other control groups. The abnormal expression of nephrin may be involved in the preeclampsia proteinuria, the underlying mechanism of this phenomenon need further research.
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