Abstract
Preeclampsia (PE) is a disorder that affects 3–5% of normal pregnancies. It was believed for a long time that the kidney, similarly to all vessels in the whole system, only sustained endothelial damage. The current knowledge gives rise to a presumption that the main role in the development of proteinuria is played by damage to the podocytes and their slit diaphragm. The podocyte damage mechanism in preeclampsia is connected to free VEGF and nitric oxide (NO) deficiency, and an increased concentration of endothelin-1 and oxidative stress. From national cohort studies, we know that women who had preeclampsia in at least one pregnancy carried five times the risk of developing end-stage renal disease (ESRD) when compared to women with physiological pregnancies. The focal segmental glomerulosclerosis (FSGS) is the dominant histopathological lesion in women with a history of PE. The kidney’s podocytes are not subject to replacement or proliferation. Podocyte depletion exceeding 20% resulted in FSGS, which is a reason for the later development of ESRD. In this review, we present the mechanism of kidney (especially podocytes) injury in preeclampsia. We try to explain how this damage affects further changes in the morphology and function of the kidneys after pregnancy.
Highlights
According to state-of-the-art research and current knowledge, generalized endothelial damage caused by factors excreted by the placenta into the maternal circulation is the cause of preeclampsia (PE)
In his experiment on murine models in which preeclampsia was caused by the administration of a nitric oxide analog, Baijnath identified the mRNA of podocin and nephrin in the urine [29]
Preeclampsia is known to be accompanied by increased levels of the soluble form of the vascular endothelial growth factor (VEGF) receptor, i.e., fms-like tyrosine kinase-1, a compound that competes with VEGFR1 for VEGF, which is why podocytes are so exposed to damage in preeclampsia [37]
Summary
According to state-of-the-art research and current knowledge, generalized endothelial damage caused by factors excreted by the placenta into the maternal circulation is the cause of preeclampsia (PE). The imbalance is caused by decreased concentrations of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), and increased concentrations of soluble fms-like tyrosine kinase-1 (sFlt-1)—a VEGF receptor, and endoglin [1]. The development of preeclampsia is associated with arterial hypertension, proteinuria—usually nephrotic, and decreased glomerular filtration often meeting the criteria for acute kidney injury
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