Glomerular basement membrane



The glomerular basement membrane (GBM) lies  between the glomerular capillaries and the podocytes. 


The glomerular basement membrane is 250–400 nm thick.


It is thicker than basement membranes of other tissues. 


The GBM is a barrier to blood proteins such as albumin and globulin.


Abnormalities in the GBM are associated with albuminuria.


Mutations in GBM are associated with albuminuria.

The glomerular basement membrane of the kidney is the basal lamina layer of the glomerulus. 

The glomerular endothelial cells, the glomeular basement membrane, and the filtration slits between the podocytes perform the filtration function of the glomerulus.


The interdigitating podocyte foot processes serve as buttresses against physical forces of hydrostatic pressure in the glomerular capillaries, compressing GBM‘s gel like structure.

The altered GBM acts as selective filter and restricts the permeability to macromolecules transported by diffusion and bulk flow.

The podocyte foot process architecture maximizes the area available for filtration of water and small solutes and provides mechanical resistance against blood pressure that compresses the GBM, preserving selectivity and preventing loss of albumin and other macromolecules.

These components of the glomerulus separate the blood in the capillaries from the filtrate that forms in Bowman’s capsule.

The GBM is a fusion of the endothelial cell and podocyte basal laminas.

The GBM is the main site of restriction of water flow in the kidney.

Podocyte cells secrete and maintain the GBM.

The glomular basement membrane has three layers:

lamina rara externa adjacent to podocyte processes

lamina densa dark central zone

lamina rara interna adjacent to endothelial cells

The glomerular basement membrane consists of mesangial cells, modified pericytes.

The podocytes adjoining MRSA goal cells have filtration slits of diameter 25 nm that are formed by the pseudopodia arising from them. 

The podocyte filtration slits are covered by a diaphragm that includes the transmembrane protein nephrin.

There is a glomular basement membrane spike formation in membranous nephropathy. 

((Goodpasture syndrome)) is also known as anti-glomerular basement membrane disease. 

Capillaries become inflamed as a result of damage to the basement membrane by antibodies to alpha 3 NC1 domain of type IV collagen.

Nephrotic syndrome is due to a change in the structure of the glomerular filtration mechanism usually in the glomerular basement membrane: associated proteinuria, hypoalbuminaemia, edema, and hyperlipidemia.

In diabetic glomerulosclerosis is a thickening of the basement membrane, which can become up to 4-5 times thicker than normal. 

Alport syndrome is a X-linked hereditary nephritis caused by mutations in type IV collagen, leading to a split lamina densa of the glomerular basement membrane: It also affects the eye and inner ear as well.


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