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Hypertensive disorders in pregnancy are a leading cause of peripartum morbidity and mortality. Preeclampsia is a heterogeneous maternal syndrome. Large studies have pointed out the association of impaired spiral artery remodeling at the fetomaternal interphase in preeclampsia, but how exactly is the fetomaternal dialogue mediated and what are the biomarkers to detect the subclinical disease in various subsets of high-risk pregnancies is still a challenge. These biomarkers can finally be used to diagnose renal function (Kallikrein-creatinine ratio), vascular resistance (uterine artery Doppler), coagulation disorders (platelet volume, fibronectin, prostacyclin, thromboxane, oxidant stress (lipid peroxidase, 8-isoprostane, antioxidants, anticardiolipin antibodies, homocysteine, serum uric acid), vascular adaptation (Placental growth factor, Vascular endothelial growth factor, s-flt, s-eng) and markers ofplacental function and ischemia (placental CRH, CRH bp, activin, inhibin, hCG).Post partum preeclampsia can be predicted by identifying the factors preventing the excretion of sodium, puerperal diuresis and shift of intravascular fluid into the extra vascular compartment compartment(atrial natriuretic peptide in the first week after delivery, natriuresis and inhibition of aldosterone, angiotensin II, vasopressin). Preeclampsia is a heterogeneous disease. The late onset preeclampsia at or near term has low fetal and maternal morbidity. But the early onset preeclampsia (1%) of all preeclampsia has significant risks. Prediction of risks and identification of subclinical disease is mandatory. The majority of at risk groups in multigravida are chronic hypertension, pregestational and gestational diabetes, age and multiple fetuses. Whereas, in primi only 14% have these risks. This suggests that there are multiple underlying etiologies of different clinical presentations. A clinical algorithm based on clinical, biochemical and ultrasound markers is outlined. Post partum eclampsia can be predicted and monitored with central venous pressure and pulmonary capillary wedge pressure. The maternal syndrome (proteinuria, edema and hypertension) also has differences in time of onset, severity and organ system involvement as highlighted in several studies. These clinical subpopulations need to be identified and preeclampsia predicted with rigorous definition of different biomarkers of different clinical phenotypes. The future endeavors should be to identify subclinical disease in various clinical phenotypes with these potential biomarkers in prospective longidunal studies.
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