The glomerular filtration barrier is traditionally thought of as being comprised of 3 layers: (1) the fenestrated endothelium, (2) the glomerular basement membrane, and (3) the podocyte foot processes.
Focusing on (2) the glomerular basement membrane (GBM), this structure is typically 330-460 nm in thickness and can be further subdivided into 3 additional layers: (a) the lamina densa (LD, in figure, the middle lyaer), (b) lamina rara interna (LRI, in figure, the “subendothelial layer” closest to endothelium), and (c) lamina rara externa (LRE, in figure, the “subepithelial layer” closest to the podocytes.). In terms of molecular components, the GBM is comprised of type IV collagen, heparin sulfate proteoglycan, and laminin.
Important diseases of the GBM specifically include Alport’s Syndrome, thin basement membrane disease, and anti-GBM (e.g., Goodpasture’s) Disease to name a few.
That's a very interesting question, and one to which there is little convincing data.
As you may know, anti-GBM disease is pretty rare. It is typically thought of as an autoimmune disease (that is, the body making antibodies which attack itself) rather than an infectious complication. However there are many other examples of kidney diseases which develop as a result of autoantibodies induced by infection. One prominent example is post-streptococcal glomerulonephritis, in which a simple Strep infection can result in kidney failure.
Hope your husband & his transplant are doing well.
My husband suffered from diverticulits, was hospitalized in December 2006 with a micro perforation, his kidneys started to fail and he was diagnosed with anti-GBM with complete kidney failure. He had a living donor transplant (our son)March 2008. Any information on anti-GBM being triggered by a massive infection?