Is this the pathophysiology of preeclampsia?

[caryn]

Preeclampsia rates weren't higher in that study; it's a study of stillbirth...

Of course shallow implantation is secondary to apoptosis of placental cytotrophoblast, but that isn't secondary to compression of the renal vein by the larger pregnant uterus, because it happens right at the beginning during initial implantation. Are you suggesting randomizing women to sleep on their left side pre pregnancy, and if so, why? The weight of the uterus plus a blastocyst is negligibly different from the weight of the non pregnant uterus, right?

[rodin]

I feel we are repeating ourself.You write: it happens right at the beginning during initial implantation.
I still have not seen the evidence to prove it happens right at the beginning during initial implantation.

I'm NOT suggesting randomizing women to sleep on their left side pre pregnancy. I don't see any logic in it.
I was just referring to the only recent study I'm aware of on left side sleeping. It is indeed on stillbirth and has nothing to do with preeclampsia.
Although the underlying pathophysiology could be similar.

[caryn]

? But this is just a consequence of how placentas develop: the trophoblast burrow into the maternal spiral arteries during initial implantation. Their normal development is known to be compromised in preeclampsia; PE placentas on biopsy have developed with inadequate remodeling.

http://atvb.ahajournals.org/content/25/1/102.full.pdf is one discussion but there are hundreds if you search strings like "trophoblast spiral artery first trimester". It starts Remodeling of the uterine arteries is a key event in early pregnancy. In the first trimester of pregnancy, a subpopulation of fetal trophoblast cells, the extravillous trophoblast, invade the uterine wall (interstitial invasion) and its blood vessels (endovascular invasion) as far as the myometrial segments. In the uterine spiral arteries, the trophoblasts interdigitate between the endothelial cells (ECs), replacing the endothelial lining and most of the musculoelastic tissue in the vessel walls. This creates a high-flow, low-resistance circulation that increases maternal blood flow to the placental villi at the maternal–fetal interface... Defective remodeling of the spiral arteries is associated with pregnancies complicated by preeclampsia and intrauterine growth restriction (IUGR) and is proposed to lead to an overall state of oxidative stress or fluctuations in oxygen concentrations analogous to hypoxia-reperfusion within the placental environment...

Is that what I wasn't explaining?

ETA: also useful: a Google Image search of "spiral artery remodeling preeclampsia"

ETA: also useful: http://dmm.biologists.org/content/5/1/9.long

It is clear from placental samples examined at term, as well as from Doppler ultrasound study of placental perfusion, that the remodeling of spiral arteries is incomplete in patients with preeclampsia. Fewer trophoblast cells are present within the spiral arterioles, and the vessel walls remain stiff (Khong et al., 1986; Aquilina and Harrington, 1996). Although, by definition, preeclampsia can be diagnosed only after the 20th week of pregnancy (and clinically typically presents even later), this vascular remodeling occurs during the first two trimesters. In normal pregnancies, endovascular extravillous cytotrophoblast cells have been identified by 9 weeks of gestation (Craven et al., 1998), and intervillous blood flow is not established until 10–12 weeks of gestation (Caniggia et al., 2000; Burton et al., 2009). Thus, poor trophoblast invasion is an early event in disease progression, although it has not been determined whether it is the cause of preeclampsia or a result of another underlying problem.