Good question, and the answer is probably more complicated than even this explanation. I'm kind of rusty on my explanations and I don't mind corrections, but let me give it a shot:
One of the things in a PE pregnancy that deprives the placenta of oxygen, releasing all those nasty factors into our bloodstreams, is that the spiral arteries that attach the placenta to the uterus don't get deep enough, and as the placenta gets bigger it demands more and more blood (because that's what feeds the placenta), but the spiral arteries aren't able to supply enough, so the placenta ends up getting more and more hypoxic (lack of oxygen) and we get more PE symptoms.
If I'm understanding right, that's one of the prime theories for what happens in early-onset (before 34 weeks) PE.
Late-onset PE (37 weeks+? what is it between 34-37weeks? I'll see if I can get a reference on that...) *might* be due to something other than problems with the spiral arteries. Same with post-partum PE.
The factors - sFlt-1 and sEng - are produced in every normal pregnancy, it's just that they are produced a lot *more* in PE pregnancies. So to get PE at all there is something going on, but it might be something different in early-onset vs late-onset or pp PE. The thing to remember, though, is that the disease is the same and it's just as dangerous no matter what causes it.
Heather, mom to
#1 7-18-03 - 5#8oz 37 weeks PE/PIH
#2 8-11-06 - 6#14oz 37 weeks PE/PIH
#3 9-10-09 - 5#10oz 37 weeks PE/PIH