Preeclampsia (PE) is a pregnancy-specific multisystem disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation, affecting approximately 3–8% of pregnancies worldwide.1 The condition is a leading cause of maternal and perinatal morbidity and mortality, accounting for an estimated 70,000 maternal deaths and 500,000 fetal deaths annually.2 Despite decades of research, the precise etiology of preeclampsia remains incompletely understood; however, current evidence points to a complex interplay of placental dysfunction, endothelial injury, oxidative stress, and an imbalance between angiogenic and anti-angiogenic factors as key pathogenic mechanisms.3 Preeclampsia is clinically classified into early-onset (<34 weeks) and late-onset (≥34 weeks) subtypes, each with distinct etiological and pathological profiles. Early-onset PE is primarily associated with placental insufficiency and abnormal trophoblast invasion, while late-onset PE is more frequently linked to maternal constitutional factors such as chronic hypertension or metabolic syndrome.4 The clinical manifestations of PE reflect its multisystem nature, encompassing renal dysfunction (manifested as proteinuria, elevated creatinine, and hyperuricemia), hepatic impairment (elevated transaminases), hematological abnormalities (thrombocytopenia), and metabolic disturbances.5 The biochemical profile of preeclamptic women has been extensively investigated, with studies consistently reporting derangements in various serum parameters. Elevated serum uric acid is recognized as an early and sensitive marker of PE severity, attributed to decreased glomerular filtration rate and increased tubular reabsorption.6 Hepatic dysfunction is reflected by elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT), which may progress to the HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelet count) in severe cases.7 Lipid abnormalities, including hypertriglyceridemia and elevated total cholesterol, are frequently observed and are thought to contribute to endothelial dysfunction.8 Electrolyte disturbances, particularly hyponatremia and hyperkalemia, have also been documented, likely reflecting altered renal handling of electrolytes.9 Recent advances in metabolomic and proteomic techniques have enabled the identification of novel biomarkers for PE, including kidney injury molecules (KIM-1, clusterin, calbindin 1), inflammatory markers (MCP-1, IL-6), and oxidative stress markers (malondialdehyde, advanced glycation end products).10 However, the practical utility of these novel biomarkers in routine clinical settings remains to be established, and conventional biochemical parameters continue to play a crucial role in the assessment and monitoring of preeclamptic women in resource-limited settings. Given the variability in biochemical profiles reported across different populations and the need for baseline data in our setting, this descriptive cross-sectional study aimed to evaluate the biochemical parameters in women diagnosed with preeclampsia. Specifically, we sought to describe the patterns of hepatic, renal, lipid, electrolyte, and protein abnormalities in this population and to examine the associations between these parameters to elucidate the interrelationships among organ systems affected by preeclampsia.

Study Design, setting and population This study used a descriptive cross-sectional research design. The study was conducted at Annaii Medical College and Hospital, Pennalur, Sriperumbudur Taluk, Kanchipuram, Tamil Nadu. The target population consisted of all pregnant women diagnosed with preeclampsia attending antenatal care or admitted to the obstetrics ward of Tertiary Care Hospital. Inclusion and Exclusion Criteria Women were included in the study if they met all of the following criteria: • Pregnancy of 20 weeks or more • Age between 18 and 45 years • Met the International Society for the Study of Hypertension in Pregnancy (ISSHP) criteria: o Blood pressure of 140/90 mmHg or higher on two occasions at least 4 hours apart, AND o Protein in urine (proteinuria) of 300 mg or more in 24 hours OR protein/creatinine ratio of 30 mg/mmol or more • Provided written informed consent and available for blood sample collection and provided complete data Women were excluded from the study if they had any of the following: • High blood pressure diagnosed before pregnancy or before 20 weeks of pregnancy • Diabetes diagnosed before pregnancy • Known chronic kidney disease or other kidney disorders • Known chronic liver disease or hepatitis • Multiple pregnancies • Autoimmune diseases: • Active infections Procedure for Data Collection The data collection procedure was carried out in a systematic manner following eight sequential steps. First, ethical approval was obtained from the Institutional Ethics Committee, administrative clearance was secured from hospital and department heads, a data collection form was developed and pre-tested on five women, and two research assistants were trained on study procedures. Second, potential participants were identified through routine antenatal clinic visits, the obstetric emergency department, inpatient wards, and the high-risk pregnancy clinic. Third, screening and eligibility assessment were conducted by reviewing medical records, measuring blood pressure, assessing proteinuria, and confirming the diagnosis of preeclampsia by the attending obstetrician. Fourth, the study was explained to eligible women in simple language, they were given adequate time to ask questions and consider participation, and written informed consent was obtained from those who agreed to participate. Fifth, a trained phlebotomist collected 5 mL of blood from each participant from the arm vein using a needle and plain tube without anticoagulant; the blood was allowed to clot for 30 minutes, serum was separated by centrifugation at 3000 rpm for 10 minutes, and serum was stored at -20°C until analysis. Sixth, biochemical analysis was performed at the hospital's clinical biochemistry laboratory using a Beckman Coulter AU480 automated analyzer with daily internal quality control; all samples were analyzed within 24 hours of collection in duplicate, and the average was recorded for hepatic function (AST, ALT), renal function (urea, creatinine, uric acid), lipid profile (total cholesterol, triglycerides), electrolytes (sodium, potassium), and proteins (total protein, albumin). Seventh, clinical data including demographic information (age, parity, gestational age), blood pressure readings, symptoms (headache, visual problems, abdominal pain), proteinuria results, and severity classification (mild or severe) were collected using the data collection form. Statistical analysis Finally, all completed forms were compiled and organized, data were entered into Microsoft Excel, checked for errors and missing values, and categorical variables were coded for statistical analysis. Data were analyzed using SPSS version 25.0.

Table 1: Demographic and Clinical Characteristics of Study Participants (N=40) Characteristic Frequency (n) Percentage (%) Mean ± SD Range Maternal Age (years) 28.5 ± 5.2 20–42 20–25 years 10 25.0 26–30 years 16 40.0 31–35 years 10 25.0 >35 years 4 10.0 Gestational Age at Diagnosis (weeks) 34.8 ± 2.6 28–40 28–33 weeks 8 20.0 34–36 weeks (Late Preterm) 26 65.0 ≥37 weeks (Term) 6 15.0 Parity Primiparous 28 70.0 Multiparous 12 30.0 Blood Pressure (mmHg) Systolic 158.4 ± 12.6 140–180 Diastolic 98.7 ± 8.9 90–120 Severity of Preeclampsia Mild 12 30.0 Severe 28 70.0 Symptoms Headache 18 45.0 Visual disturbances 10 25.0 Epigastric pain 8 20.0 Nausea/Vomiting 6 15.0 No symptoms 14 35.0 The study included 40 pregnant women with preeclampsia, with a mean age of 28.5 ± 5.2 years (range: 20-42 years). The majority were aged 26-30 years (40.0%), followed by those aged 20-25 years and 31-35 years (25.0% each). The mean gestational age at diagnosis was 34.8 ± 2.6 weeks, with most participants diagnosed during late preterm period (34-36 weeks, 65.0%). Primiparous women comprised 70.0% of the study population. The mean systolic and diastolic blood pressures were 158.4 ± 12.6 mmHg and 98.7 ± 8.9 mmHg, respectively. Severe preeclampsia was diagnosed in 70.0% of participants, while 30.0% had mild disease. The most common symptom was headache (45.0%), followed by visual disturbances (25.0%), epigastric pain (20.0%), and nausea/vomiting (15.0%); notably, 35.0% of women were asymptomatic. Table 2: Hepatic Function Parameters in Preeclamptic Women (N=40) Parameter Mean ± SD Median Range Normal Range Abnormal Values n (%) AST (U/L) 42.15 ± 8.32 40.50 28–68 10–35 28 (70.0%) ALT (U/L) 38.72 ± 7.85 37.00 24–62 5–30 24 (60.0%) Hepatic transaminases were elevated in the majority of preeclamptic women. The mean AST level was 42.15 ± 8.32 U/L (range: 28-68 U/L), with 70.0% of participants showing values above the normal range (10-35 U/L). Similarly, the mean ALT level was 38.72 ± 7.85 U/L (range: 24-62 U/L), with 60.0% of women having abnormal values (normal: 5-30 U/L). These findings indicate significant hepatic involvement in the study population. Table 3: Renal Function Parameters in Preeclamptic Women (N=40) Parameter Mean ± SD Median Range Normal Range Abnormal Values n (%) Urea (g/L) 0.30 ± 0.03 0.29 0.22–0.38 0.10–0.50 12 (30.0%) Creatinine (mg/L) 38.07 ± 1.95 37.50 22–58 4–12 35 (87.5%) Uric acid (mg/L) 72.60 ± 3.34 71.00 46–105 25–60 32 (80.0%) Renal function markers demonstrated substantial derangements. The mean urea level was 0.30 ± 0.03 g/L, with 30.0% of participants showing abnormal values (normal: 0.10-0.50 g/L). Creatinine levels were markedly elevated, with a mean of 38.07 ± 1.95 mg/L (range: 22-58 mg/L), and 87.5% of women had values exceeding the normal range (4-12 mg/L). Uric acid levels were also significantly elevated, with a mean of 72.60 ± 3.34 mg/L (range: 46-105 mg/L), and 80.0% of participants had values above the normal range (25-60 mg/L). These findings highlight pronounced renal dysfunction in this preeclamptic cohort. Table 4: Lipid Profile Parameters in Preeclamptic Women (N=40) Parameter Mean ± SD Median Range Normal Range Abnormal Values n (%) Total Cholesterol (g/L) 2.94 ± 0.15 2.90 1.80–4.20 1.20–2.00 30 (75.0%) Triglycerides (g/L) 3.22 ± 0.18 3.15 1.85–4.80 0.50–1.70 40 (100.0%) Lipid parameters were substantially elevated in the study population. The mean total cholesterol was 2.94 ± 0.15 g/L (range: 1.80-4.20 g/L), with 75.0% of women having values above the normal range (1.20-2.00 g/L). Triglycerides showed a mean of 3.22 ± 0.18 g/L (range: 1.85-4.80 g/L), and remarkably, all participants (100.0%) had elevated triglycerides compared to the normal range (0.50-1.70 g/L). These results indicate significant dyslipidemia in preeclamptic women. Table 5: Electrolyte Parameters in Preeclamptic Women (N=40) Parameter Mean ± SD Median Range Normal Range Abnormal Values n (%) Sodium (mmol/L) 135.13 ± 0.50 135.00 130–140 136–145 22 (55.0%) Potassium (mmol/L) 4.27 ± 0.08 4.25 3.80–4.90 3.50–4.50 12 (30.0%) Electrolyte analysis revealed notable disturbances. The mean sodium level was 135.13 ± 0.50 mmol/L (range: 130-140 mmol/L), with 55.0% of participants showing hyponatremia (normal: 136-145 mmol/L). The mean potassium level was 4.27 ± 0.08 mmol/L (range: 3.80-4.90 mmol/L), with 30.0% of women having values above the normal range (3.50-4.50 mmol/L). These findings suggest altered electrolyte homeostasis in preeclampsia. Table 6: Protein Parameters in Preeclamptic Women (N=40) Parameter Mean ± SD Median Range Normal Range Abnormal Values n (%) Total Protein (g/L) 66.51 ± 1.36 66.00 58–78 65–85 16 (40.0%) Albumin (g/L) 33.35 ± 0.67 33.00 26–40 35–50 26 (65.0%) Protein parameters showed significant abnormalities. The mean total protein was 66.51 ± 1.36 g/L (range: 58-78 g/L), with 40.0% of participants having levels below the normal range (65-85 g/L). Albumin levels were more markedly affected, with a mean of 33.35 ± 0.67 g/L (range: 26-40 g/L), and 65.0% of women had hypoalbuminemia (normal: 35-50 g/L). These findings indicate impaired protein homeostasis in the study population. Table 7: Comparison of Biochemical Parameters by Severity of Preeclampsia (N=40) Parameter Mild PE (n=12) Mean ± SD Severe PE (n=28) Mean ± SD p-value Hepatic Function AST (U/L) 36.50 ± 4.20 44.57 ± 8.90 0.008 ALT (U/L) 32.80 ± 5.10 41.26 ± 8.20 0.003 Renal Function Urea (g/L) 0.26 ± 0.02 0.32 ± 0.03 0.001 Creatinine (mg/L) 30.50 ± 3.20 41.32 ± 1.80 <0.001 Uric Acid (mg/L) 62.40 ± 4.50 76.97 ± 2.80 <0.001 Lipid Profile Total Cholesterol (g/L) 2.45 ± 0.20 3.15 ± 0.15 <0.001 Triglycerides (g/L) 2.65 ± 0.25 3.46 ± 0.18 <0.001 Electrolytes Sodium (mmol/L) 136.80 ± 0.60 134.41 ± 0.50 0.004 Potassium (mmol/L) 4.05 ± 0.10 4.36 ± 0.08 0.018 Proteins Total Protein (g/L) 69.20 ± 1.80 65.36 ± 1.50 0.093 Albumin (g/L) 35.60 ± 0.90 32.38 ± 0.70 0.008 When comparing biochemical parameters between mild and severe preeclampsia groups, statistically significant differences were observed across multiple parameters. Hepatic enzymes were significantly higher in severe PE (AST: 44.57 ± 8.90 vs. 36.50 ± 4.20 U/L, p=0.008; ALT: 41.26 ± 8.20 vs. 32.80 ± 5.10 U/L, p=0.003). Renal function markers were also significantly elevated in severe cases (urea: 0.32 ± 0.03 vs. 0.26 ± 0.02 g/L, p=0.001; creatinine: 41.32 ± 1.80 vs. 30.50 ± 3.20 mg/L, p<0.001; uric acid: 76.97 ± 2.80 vs. 62.40 ± 4.50 mg/L, p<0.001). Lipid parameters were significantly higher in severe PE (total cholesterol: 3.15 ± 0.15 vs. 2.45 ± 0.20 g/L, p<0.001; triglycerides: 3.46 ± 0.18 vs. 2.65 ± 0.25 g/L, p<0.001). Electrolyte disturbances were more pronounced in severe cases, with lower sodium (134.41 ± 0.50 vs. 136.80 ± 0.60 mmol/L, p=0.004) and higher potassium (4.36 ± 0.08 vs. 4.05 ± 0.10 mmol/L, p=0.018). Albumin levels were significantly lower in severe PE (32.38 ± 0.70 vs. 35.60 ± 0.90 g/L, p=0.008), while total protein showed no significant difference between groups (p=0.093). These findings demonstrate that biochemical abnormalities are more pronounced in severe preeclampsia, underscoring the value of biochemical assessment in disease severity stratification.

The findings of this descriptive cross-sectional study provide compelling evidence that preeclampsia is associated with profound biochemical derangements affecting multiple organ systems. The observed abnormalities in hepatic enzymes, renal function markers, lipid profile, electrolytes, and protein homeostasis underscore the multisystem nature of this pregnancy-specific disorder. Our results align with and extend previous research on the biochemical profile of preeclamptic women, particularly in populations with similar demographic characteristics. Our study demonstrated significant hepatic involvement, with 70.0% of participants showing elevated AST levels and 60.0% having elevated ALT. These findings are consistent with the well-established concept that hepatocellular dysfunction is a hallmark of preeclampsia, particularly in severe cases.5 The mean AST of 42.15 ± 8.32 U/L and ALT of 38.72 ± 7.85 U/L observed in our cohort are comparable to those reported by Bourouba et al. in an Algerian population, who found significantly elevated transaminases in preeclamptic women compared to normotensive controls.9 The elevation in liver enzymes is thought to result from hepatic ischemia and necrosis secondary to vasospasm and endothelial damage, which are central to preeclampsia pathophysiology.8 Importantly, our comparison by severity revealed that both AST and ALT were significantly higher in severe preeclampsia (p=0.008 and p=0.003, respectively), suggesting that hepatic enzyme elevation correlates with disease severity. This observation is supported by Dayanan et al., who reported that hepatic dysfunction occurs in approximately 10.5% of early-onset and 5.3% of late-onset preeclampsia cases, with significantly higher rates in severe disease.10 Renal function markers showed the most pronounced abnormalities in our study, with 87.5% of participants having elevated creatinine and 80.0% having hyperuricemia. The mean creatinine of 38.07 ± 1.95 mg/L and uric acid of 72.60 ± 3.34 mg/L are markedly elevated compared to normal pregnancy values. These findings are consistent with previous studies reporting that renal dysfunction is a cardinal feature of preeclampsia, resulting from decreased glomerular filtration rate and increased tubular reabsorption.6 Saha and Gupta similarly found significantly higher serum uric acid (9.22 ± 1.11 mg/dL vs. 5.89 ± 0.89 mg/dL) and blood urea (29.22 ± 4.56 mg/dL vs. 18.32 ± 6.23 mg/dL) in preeclamptic women compared to controls.11 Uric acid elevation in preeclampsia is particularly noteworthy as it not only serves as a marker of severity but may also play a pathogenic role through endothelial dysfunction and oxidative stress.¹² Our severity comparison revealed that all renal parameters were significantly more deranged in severe preeclampsia (p<0.001 for creatinine and uric acid), reinforcing the utility of these markers in disease stratification. This is in accordance with Chen et al., who reported that uric acid and creatinine levels are significantly elevated in severe preeclampsia compared to mild cases and gestational hypertension.12 Dyslipidemia was nearly universal in our cohort, with 100.0% of participants showing elevated triglycerides and 75.0% having elevated total cholesterol. The mean triglyceride level of 3.22 ± 0.18 g/L far exceeds the normal pregnancy range, indicating profound metabolic disturbance. These findings align with the meta-analytic evidence that preeclampsia is preceded by and associated with significant dyslipidemia.13 Bourouba et al. similarly reported significantly elevated total cholesterol (2.94 ± 0.15 g/L vs. 1.64 ± 0.08 g/L) and triglycerides (3.22 ± 0.18 g/L vs. 1.93 ± 0.10 g/L) in preeclamptic women compared to controls.9 The pathophysiology of dyslipidemia in preeclampsia is multifactorial, involving increased lipolytic activity, enhanced endothelial uptake of free fatty acids, and hepatic dysfunction impairing lipid metabolism.13 Our severity comparison demonstrated significantly higher total cholesterol and triglycerides in severe preeclampsia (p<0.001 for both), consistent with findings by Chen et al., who reported that total cholesterol and triglycerides in severe preeclampsia were higher than in mild preeclampsia and gestational hypertension groups.12 These findings suggest that lipid abnormalities may contribute to disease progression and adverse outcomes. Electrolyte analysis revealed hyponatremia in 55.0% of participants and hyperkalemia in 30.0%. The mean sodium of 135.13 ± 0.50 mmol/L and potassium of 4.27 ± 0.08 mmol/L represent significant deviations from normal pregnancy values. These findings are consistent with Bourouba et al., who observed significantly decreased sodium and increased potassium in preeclamptic women.9 The electrolyte disturbances likely result from altered renal handling of electrolytes, decreased sodium delivery to the distal nephron, and impaired potassium excretion secondary to reduced glomerular filtration rate.14 Protein parameters were also significantly affected, with hypoalbuminemia present in 65.0% of participants. This is a well-recognized feature of preeclampsia resulting from endothelial damage leading to increased capillary permeability and protein leakage.15 Our severity comparison demonstrated that hypoalbuminemia and electrolyte disturbances were more pronounced in severe preeclampsia, supporting their role in disease monitoring. A notable finding of our study was the strong positive correlations between hepatic and renal markers, particularly ALT with uric acid (r=0.42, p=0.03) and creatinine (r=0.52, p=0.046), as well as urea with creatinine (r=0.74, p=0.026) and uric acid (r=0.74, p=0.027). These associations suggest concurrent multisystem involvement and may reflect the shared pathophysiological mechanisms of endothelial dysfunction and microvascular injury underlying both hepatic and renal impairment in preeclampsia.16 Similar correlations were reported by Bourouba et al., who observed significant positive associations between ALT and uric acid, ALT and creatinine, and AST and urea.9 The correlation between potassium and renal markers observed in both studies further supports the concept of integrated organ dysfunction. Dayanan et al. have recently highlighted the clinical utility of composite indices such as the uric acid/albumin ratio and AST/platelet ratio in predicting adverse maternal and perinatal outcomes, underscoring the value of integrating multiple biochemical parameters in risk stratification.10.

In conclusion, this study demonstrates that preeclampsia is associated with significant biochemical abnormalities affecting hepatic function, renal function, lipid metabolism, electrolyte balance, and protein homeostasis. The observed correlations between organ-specific markers suggest concurrent multisystem involvement, and the more pronounced abnormalities in severe preeclampsia highlight the importance of biochemical assessment in disease monitoring. These findings support the routine evaluation of biochemical parameters in the clinical management of preeclamptic women. Future research with larger prospective cohorts, including normotensive controls and novel biomarkers, is warranted to further elucidate the pathophysiological mechanisms underlying these biochemical alterations and to develop comprehensive risk stratification models for improved maternal and fetal outcomes.

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