Preeclampsia (PE) is a hypertensive disorders of pregnancy that is accompanied by a combination of new-onset proteinuria, maternal organ dysfunction, or uteroplacental dysfunction at or after 20 weeks’ gestation [1]. Pregnant women with PE who develop proteinuria often show a rapid increase in proteinuria during pregnancy. The pathogenesis of PE is known to be endothelial cell damage; however, the existence of dysfunction in podocytes and tubules remains unclear. Notably, women with previous PE have been reported to have a higher incidence of future CKD [2], [3].

Damage to glomerular endothelial glycocalyx and podocytes may occur in patients with CKD, resulting in increased urinary albumin excretion. These represent significant albumin barriers. The endothelial glycocalyx layer found on the luminal surface of all endothelial cells contributes to the permeability barrier formed by the vessel wall [4], [5]. The adherent structure of the glycocalyx layer includes proteoglycans, glycoproteins, and glycolipids. Proteoglycans consist of core proteins, such as syndecans, glypicans, and biglycans with covalently bound glycosaminoglycan side chains, such as heparan sulfate and chondroitin sulfate. Proteoglycans covalently bind to the endothelial cell membrane and adhere to glycosaminoglycans, including the long chains of hyaluronan [6], [7]. We have reported that serum levels of hyaluronan could be a possible biomarker for glomerular endothelial damage [8].

Podocytes are located on the outer surface of the glomerular basement membrane of the kidneys. Podocytes regularly interlock with the foot projections of adjacent podocytes. The slit membrane stretched between the foot processes is an albumin barrier [9], [10]. Furthermore, leaked albumin is reabsorbed in the renal tubules and very little is excreted in the urine. CKD is often associated with proteinuria and/or hematuria due to injury to the glomerular endothelial cells, basement membrane, or podocytes. The major difference between PE and CKD, is that albumin excretion, disappears promptly after delivery in PE.

Here, we hypothesized that the increase in urinary albumin leakage in patients with PE is related to the dysfunction of the glomerular endothelial glycocalyx and podocytes and associated with tubular dysfunction. This study aimed to assess the relationship between urinary albumin leakage and damage to the glomerular endothelial glycocalyx, podocytes, and renal tubules in patients with PE.