Various pathways have been proposed to be linked to the production of
soluble pathogenic factors by the placenta. These include deficient haeme
oxygenase expression, placental hypoxia, genetic factors, autoantibodies
against the angiotensin receptor, oxidative stress, inflammation, altered natural killer cell signalling, and,more recently, deficient catechol-O-methyl
transferase.4While there is compelling evidence in animal studies demonstrating
an important role for these upstream pathways, the underlying
events that induce placental disease activating the cascade of placental
damage and anti-angiogenic factor production remain unknownin humans.
The cause of gestational hypertension is unclear, but it is believed that
this entity occurs inwomendestined to have essential hypertension later
in life (analogous to women with gestational hyperglycaemia who eventually
develop type 2 diabetes). A significant proportion of patients with
gestational hypertension may represent an early phase of pre-eclampsia
in which proteinuria has not yet appeared. Renal biopsy studies support
the latter hypothesis.12