Abstract
Nephrotic syndrome is characterized by heavy proteinuria followed by hypoproteinemia, hypercholestrolemia, lipiduria, and edema. The glomerular filtration barrier (GFB) consists of glomerular endothelial cells covered with glycocalyx, the basement membrane, subpodocyte space and podocytes with foot processes and slit membranes between them.
The coordinated function of GFB has been considered to be the major barrier against filtration of plasma proteins to urine. However, new hypothesis suggesting more permeable GFB has emerged.
According to this, proteinuria might be prevented by tubular protein reabsorbtion. Experments and human studies have revealed numerous putative permeability factors in idiopathic nephrotic syndrome (minimal change disease/focal segmental glomerulosclerosis).
New antigens and antibodies have been suggested in "idiopathic" membranous nephropathy as well. Formation of nephrotic edema, the role of oncotic pressure and of different sodium and water retaining hormones have been subject of intensive study.
These findings should pave the way to new therapeutic modalities targeted more precisely to the pathogenic mechanisms.