Exploring the Spectrum of Electrolyte Imbalances in Preeclampsia: Mechanisms, Implications, and Clinical Insights

Abstract

Preeclampsia, a complex and perplexing disorder unique to pregnancy, is widely recognized as primarily originating from placental dysfunction and can only be resolved by the delivery of the fetus in severe cases. Preeclampsia is a prevalent medical issue during pregnancy and is associated with elevated rates of maternal and infant mortality and morbidity. The exact cause of preeclampsia remains uncertain, although multiple factors have been implicated in its development based on current knowledge. Preeclampsia is characterized by maternal endothelial dysfunction due to the presence of fetal-derived circulatory substances from the placenta. The condition is associated with various risk factors, including maternal comorbidities such as chronic renal disease, hypertension (HTN), and obesity. Additionally, a family history of preeclampsia, nulliparity, multiple gestations, previous instances of preeclampsia, or intrauterine fetal growth restriction (IUGR) are considered risk factors. Electrolytes, including sodium, potassium, and chloride, play a critical role in the function of vascular smooth muscles and may potentially contribute to the pathophysiology of hypertension. In this review, we have summarized the literature on electrolytes in preeclampsia by conducting an extensive systematic search of databases such as PubMed, Excerpta Medica database (EMBASE), and Medical Literature Analysis and Retrieval System Online (MEDLINE).

Keywords: derangement; electrolyte; gestational hypertension; preeclampsia; pregnancy-induced hypertension.

Figure 1. A two-stage model illustrating the cause and development of preeclampsia

Acquired, genetic, and immune risk factors contribute to early placental dysfunction (Stage 1). Placental dysfunction results in the release of anti-angiogenic factors, leading to later multiorgan dysfunction (Stage 2). Solid arrows represent the progression of the disease. Dashed arrows represent the SNS effect on respective organs. Ang II: anqiotensin II; ER: endoplasmic reticulum; HA: headache; HIF: hypoxia-inducible transcription factor; NO: nitric oxide; PIGF: placental growth factor; PRES: posterior reversible encephalopathy syndrome; RAAS: renin-angiotensin-aldosterone system; Eng: endoglin; FIt: fms like tyrosine kinase; SNS: sympathetic nervous system; TGF: transforming growth factor; VEG: vascular endothelial growth factor Reprinted from the Journal of the American College of Cardiology, Volume 76, Ives CW, Sinkey R, Rajapreyar I, Tita ATN, Oparil S,  "Preeclampsia—Pathophysiology and Clinical Presentations: JACC State-of-the-Art Review", Pages 1690-1702, Copyright 2020, with permission from Elsevier [40].

Figure 2. A PRISMA flowchart representing the data collection process

PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-Analyses