As a broad generalization, most cases of PE are plays in (at least) two acts -- first the spiral arteries get remodelled and the placenta embeds and grows, and then there's a symptomatic phase where that placenta has become inadequate to support preganancy and begins to release these angiogenic factors. (This isn't true in all cases of PE, like the sudden severe late cases where a clot has lodged in an umbillical artery and suddenly compromised the placenta, but it's true for most.)
These studies Karumanchi has been doing are all about the second act. But the stage is set in the first.
SFlt-1 and sEng are possibly going to be useable to prevent some of the severe maternal consequences of PE -- for example, we could possibly combat the hypertension and liver damage with supplemental VEGF -- but doing so wouldn't be likely to embed the placenta any more deeply, because it isn't one of the proteins that controls embedment (at least, as I understand things.)
In fact, lowering maternal blood pressure might *compromise* the fetus, because it would mean less blood was being forced across the placenta. It's very likely that the fetus is responsible for at least some of the increase in the maternal blood pressure, with the "goal" of increasing its blood supply.
As for the inflammation -- the question you just asked ("What adverse reactions could occur") has no known answer as I understand things. They've only just begun to understand that inflammation underpins a whole bunch of chronic diseases, and is an essential component of our innate immune system. They're starting to ask questions like, "If we shut it down to treat arthritis, will we see a vastly increased rate of death from the common cold?"