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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