Abstract
As water and solutes are filtered through the slit membrane, it is an a priori concept that a slit membrane is an essential filtration barrier for proteins, including albumin. However, in cases of minimal change nephrotic syndrome, the number of slit membranes is reduced by the foot process effacement and tight junction-like cell adhesion. Furthermore, albumin endocytosis is enhanced in the podocytes under condition of minimal change disease, and albumin is selectively transported by the albumin receptor FcRn. Suppressing the endocytosis of albumin with anti-FcRn antibody decreases the urinary protein level. The expression of motor molecules, such as cytoplasmic dynein 1 and myosin IX, is increased in the podocytes under conditions of minimal change nephrotic syndrome, suggesting the enhanced transport of vesicles containing albumin. Podocyte vesicle transport may play an important role in the pathology of selective albuminuria in cases of nephrotic syndrome.
Highlights
It is important to understand the mechanism underlying proteinuria and albuminuria because they are early detection markers of renal diseases
Tubular proteinuria caused by tubular dysfunction of protein reabsorption in Fanconi syndrome [3, 4], Dent’s disease [5], or tubulointerstitial nephritis is characterized by the presence of low-molecular-weight proteins (LMWPs), including β2-microglobulin, light chain, α1-microglobulin, and retinol binding proteins [1, 6]
It is difficult to find the filtration pathway of proteins when a patient with minimal change nephrotic syndrome (MCNS) shows selective albuminuria because Transmission electron microscopy (TEM) shows that the podocyte cell body and primary process with foot process effacement cover the glomerular basement membrane (GBM) wall in MCNS, the slit pore density is reduced by a maximum of 80%, and half of the slit membrane between the foot processes becomes a tight junction-like structure [18]
Summary
It is important to understand the mechanism underlying proteinuria and albuminuria because they are early detection markers of renal diseases. E mechanism underlying selective proteinuria used to be ascribed to dysfunction of the slit membrane due to a reduction in nephrin or reduced negative charge at the glomerular basement membrane (GBM) in patients with minimal change nephrotic syndrome (MCNS) [10,11,12]. It is difficult to determine the morphological pathway of albumin filtration when the cell body or primary process of the podocyte covers the GBM with tight junctionlike cell adhesion in cases of MCNS, even if the reduction in nephrin of the slit membrane and negative charge at the GBM play important roles in selective albuminuria.
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