Renal injury is a common pathophysiological feature in women with
preeclampsia as evidenced by increased
protein leakage (
proteinuria) and glomerular injury (glomerular endotheliosis). Recently, podocyturia was found in
preeclampsia, suggesting podocyte shedding occurs in this pregnancy disorder. However, podocyte function in
preeclampsia is poorly understood. In this study, the authors have examined podocyte-specific
protein expressions for
nephrin,
glomerular epithelial protein 1 (GLEPP-1), and
ezrin in kidney biopsy tissue sections from women with
preeclampsia. Expressions for
vascular endothelial growth factor (
VEGF) and its receptor Flt-1 and oxidative stress marker
nitrotyrosine and
antioxidant CuZn-
superoxide dismutase (CuZn-SOD) were also examined. Kidney tissue sections from nonhypertensive and chronic hypertensive participants were stained as controls. The findings were (1)
nephrin and GLEPP-1 were mainly expressed in glomerular podocytes; (2)
ezrin was expressed in both glomerular podocytes and tubular epithelial cells; (3) compared to tissue sections from nonhypertensive and chronic hypertensive participants,
nephrin and GLEPP-1 expressions were much reduced in tissue sections from
preeclampsia and
ezrin expression was reduced in podocytes; (4) enhanced
VEGF, Flt-1, and
nitrotyrosine, but reduced CuZn-SOD, expressions were observed in both glomerular podocytes and endothelial cells in tissue sections from
preeclampsia; and (5) the expression pattern for
nephrin, GLEPP-1,
ezrin,
VEGF, Flt-1, and CuZn-SOD were similar between tissue sections from nonhypertensive and chronic hypertensive participants. Although the authors could not conclude from this biopsy study whether the podocyte injury is the cause or effect of the
preeclampsia phenotype, the data provide compelling evidence that podocyte injury accompanied by altered angiogenesis process and increased oxidative stress occurs in kidney of patients with
preeclampsia.