Pregnancy induced hypertension (PIH) in current healthcare practice continues to be a major obstetric dilemma. Preeclampsia is a multifactorial, pregnancy specific vascular disorder characterized by hypertension and proteinuria. It affects around 3-5% of pregnancies worldwide. There is a wide range of phenotypes from mild form developing in the end of pregnancy, to severe forms with extremely high blood pressure that in worst cases could lead to eclampsia, the occurrence of seizures. It is associated with high maternal mortality and morbidity as well as risk of perinatal death, preterm birth and intrauterine growth restriction. Preeclampsia remains a serious and poorly understood complication of pregnancy; identification of epidemiological and clinical risk factors to predict it, before it threatens the survival of both mother and fetes is required. In Pakistan, maternal mortality is very high where 1 in 89 women die during pregnancy because of eclampsia or preeclampsia. Changes in the adipocytokines levels during pregnancy have been reported some of which have pathogenic effect including preeclampsia and eclampsia. Adipocytokines include metabolic regulators (leptin, adiponectin and visfatin) angiogenic proteins (VEGF) and inflammatory mediators (IL-6, IL-8). Human adipose tissue is an important regulator of endocrine functions through its multisystem effects such as through the secretion of plasma adipocytokines. Out of these visfatin, dysregulation participates in the pathogenesis of obesity-associated disorders such as hyperlipidemia or hypertension, preeclampsia and small for gestational age. Visfatin gene is named nicotinamide phosphorybosyl transferase (NMAPT) due to its probable cardiovascular role. The circulating visfatin levels have also shown influence in polymorphism of visfatin gene. In this study we investigated the relationship of serum visfatin level with preeclampsia and eclampsia in 3rd trimester women in Pakistani cohort. The polymorphism in NAMPT/visaftin gene with preeclamsia was also performed. This was a cross sectional study conducted in three tertiary care hospitals of Peshawar. Total 234 subjects have participated; that were subdivided into preeclampsia (80), eclampsia (74) and healthy pregnant women (74). Serum visfatin levels (ng/mL) were determined by enzyme linked immune sorbent assay. Haematological parameters, liver function tests and serum electrolytes were determined and calculated by Sysmex haematology analyzer (Automated haematology analyzer). The blood urea and Lipid parameters were determined by automated chemistry analyzer in PGMI-LRH by using enzymatic kits of Roche diagnostics. BMI was calculated using weight and height values. For data MINITAB® version 17 was used for further analysis. High levels of visfatin (P<0.05) found in patients group, preeclampsia and eclampsia when compared with control while among patient group no significant differences in visfatin levels were found. A strong positive and statistically significant association of visfatin was observed for monthly income (R2=7.75 and p-value <0.001). Similarly, significant results were obtained for still birth, caesarean section, low birth babies, family history of BP, systolic and diastolic BP, serum albumin, serum ALP, serum chloride, serum HDL and LDL. Among all the three ratios, TC:HDL-C ratio, LDL:HDL,TG:HDL and VLDL:HDL was having a positive and significant correlation. Out of the 11 exons (exon 2-6) the visfatin gene was sequenced and were analyzed for polymorphisms by PCR direct sequencing. We found no polymorphism in the exons region of visfatin gene in present study. Our data suggest that circulating NAMPT/visfatin levels may be associated with pregnancy induced hypertension when compared with normotensive pregnant women.In the current study we symmetrically investigated the polymorphism of the coding region and found no polymorphism. Our finding suggests that polymorphism may not affect the NAMPT/visfatin levels in preeclampsia and eclampsia patients.