I have taken some time to read the articles you have referred to. In them I have found:
that the invading placental trophoblast cells express HLA (Human Leukocyte Antigen) family known as HLA-C.
that the maternal receptors that recognize and interact with HLA-C are the KIR family (Killer Immunoglobulin-like Receptors).
that genetic differences and combinations in two gene families (HLA and KIR) are a risk factor for preeclampsia.
that during early pregnancy, trophoblast cells, invade into the uterus and tap into the mother’s blood supply to sustain the growing baby.
- The hypothesis
that initial or primary failure of the placenta to implant correctly into the uterus or womb causes insufficient blood supply to the unborn baby and could cause preeclampsia.
- The hypothesis
that sometimes the combination of these genes (HLA and KIR) from mother and baby could result in inadequate invasion and lead to preeclampsia.
I would have to agree with you that when there is evidence of failure of the placenta to implant normally in very early stages of the pregnancy in PE, this would be an important argument against the renal vein compression hypothesis. (Or, at least it would mean renal compression is not involved in all “forms” of preeclampsia) However, I didn’t find this evidence.
An alternative is not impossible: The placenta keeps on growing during a normal pregnancy. When a normal developing placenta and unborn baby are confronted with vasoconstrictive spinal arteries and arteriole and are deprived of oxygen, this could lead to damage and cell death in the placenta. Because of be increased possibility for exudation the contact between placental trophoblast cells with maternal leukocytes could then take place. In the end this could account for the placental changes observed in preeclampsia.
I agree with you that new studies on left side sleeping have methodological difficulties. Double blind is impossible and randomization difficult. An option would be to take a large enough population of pregnant women and study the effect of advising left side sleeping on the incidence of preeclampsia. If this results in a clear drop in incidence this could become an treatment option.
There already have been studies in the past that had encouraging results in al small population of women at risk of preeclampsia. http://www.ncbi.nlm.nih.gov/pubmed/6846433
The renal compression hypothesis itself could be confirmed by studying the renal vein diameter, RAS reaction and blood pressure in reaction on different women body positions. But read the references of the article, a lot of evidence is already available
. There is for instance a clear dilatation of the left renal vein in preeclampsia. (Just before it crosses between the aorta and the superior mesenteric artery.)http://www.ncbi.nlm.nih.gov/pubmed/11243294
This would be difficult to explain without the renal vein compression hypthesis.
Stenting could become an option in women in which the renal vein blockage is clearly visualized.
Finally, as you state preeclampsia is very much a human disease. This is (in my opinion) because animals do not tend to sleep on their back.