**5. Conclusion**

*Prediction of Maternal and Fetal Syndrome of Preeclampsia*

*smooth muscle reflexes, and the endothelium influence vascular tone.*

angiotensin II (AGII) rises and leads to the synthesis and release of aldosterone from the zona glomerulosa in the adrenal cortex. The pregnant women do not develop hypertension from the presser effects of AGII due to the downregulation of ATR1 receptors. The vessel responsive to adrenal cortisol is usually unaltered in

*Pathogenesis of preeclampsia in a nonresilient cardiovascular system. The autonomic nervous system, intrinsic* 

Angiotensin II is very peculiar because its action depends on which of its two receptors it is acting. When AGII binds with AGI receptors, it causes vasoconstriction, but when it binds to AGII receptors, it causes vasodilation. If angiotensin I receptors are downregulated during pregnancy or by angiotensin receptor blockers like telmisartan or if angiotensin II receptors are upregulated during fetal life, it is a

Villous syncytiotrophoblast has high density of angiotensinase A (aminopeptidase A) which converts angiotensin II to angiotensin III [22, 23]. The increase in this angiotensinase activity is also responsible for downregulation of ATR1 receptors in normal pregnancy [24]. It was observed that during cesarean section in normal pregnancy, the uterine venous AGII is lower than the peripheral venous AGII. In preeclampsia pregnancy, uterine venous AGII are higher than peripheral

In prospective studies it has been demonstrated that aminopeptidase A levels were high before the clinical syndrome of preeclampsia but levels were lower after preeclampsia clinically developed [24]. The initial rise in trophoblastic aminopeptidase could be an initial homeostatic response protecting placenta from the harmful

The receptor for angiotensin IV is also called as insulin-regulated aminopeptidase (IRAP). High concentrations of IRAP are present on human placenta [26]. In the second half of pregnancy, the extracellular domain of this receptor is shed off. Angiotensin IV acts as an endogenous inhibitor of angiotensin-converting enzyme. It stimulates both RNA and DNA synthesis in endothelial cells and proliferation of endothelial cells. It can also increase the levels of plasminogen activator inhibitor

**14**

pregnancy [20, 21].

vasodilator.

**Figure 7.**

AGII level [25].

effects of locally generated AGII.

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 are mandatory. The majority of at-risk groups in multigravida are chronic hypertension, pregestational and gestational diabetes, age, and multiple fetuses, whereas in primigravida only 14% have these risks. If there is preeclampsia in a multigravida, a nonplacental cause should be definitely considered. This suggests that there are multiple underlying etiologies of different clinical presentations. **Table 1** summarizes the likely etiopathogenesis in different clinical scenarios. Postpartum eclampsia can be predicted and monitored with central venous pressure and pulmonary capillary wedge pressure [34–36]. The maternal syndrome (proteinuria, edema, and hypertension) also has differences in time of onset, severity, and organ system involvement as highlighted in several studies [37–39]. There is a rising interest in galectin molecules for prediction of these subtypes (**Figure 8**). These clinical subpopulations need to be identified and preeclampsia predicted with rigorous definition of different biomarkers of different clinical phenotypes [40–44]. The future endeavors should be to identify subclinical disease in various clinical phenotypes with these potential biomarkers in prospective longitudinal studies.
