Preeclampsia is a heterogeneous disorder in which maternal and placental factors lead to endothelial dysfunction, which manifests in the kidney as glomerular endotheliosis and proteinuria.
Given its heterogeneity, it is possible that the relationship between preeclampsia and ESRD is mediated by different mechanisms in different women. First, conditions such as obesity or kidney disease prior to pregnancy may be significant cofounders, leading to preeclampsia and ESRD at different times of a woman's life. Second, it is plausible that kidney damage that occurs at the time of preeclamptic pregnancies may have an independent effect on kidney function later in life.
There is a growing body of evidence suggesting that podocyturia, the urinary loss of viable podocytes, may disrupt the glomerular filtration barrier and lead to proteinuria in preeclampsia. Although this injury is thought to be transient, some evidence suggests that moderately increased albuminuria is present for up to twenty years after the hypertensive pregnancy.
Podocyturia may be sustained in the postpartum period in some women with preeclampsia, which could reflect ongoing kidney damage or even systemic endothelial dysfunction.
Third, women with preeclampsia are at increased risk for hypertension and may develop hypertension earlier than women with normotensive pregnancies, suggesting that hypertension may be an important mediating factor on the casual pathway from preeclampsia to ESRD.
It is unknown to what extent preeclampsia increases the risk for ESD independent of shared risk factors.