Glomerulonephritis
Videos
Glomerulonephritis with Dr. Caster
What is Glomerulonephritis? (Acute Kidney Inflammation)
Membranous glomerulonephritis (membranous nephropathy) - causes & symptoms
Kidney Failure Disorder Glomerulonephritis (GN) Explained
Acute Glomerulonephritis: What Are the Common Symptoms and How Is It Diagnosed?
Its typically found in kids, who pee out dark cocoa colored urine and display edema, a swollen appearance, after having had a recent strep throat infection.
There are various autoimmune causes of glomerulonephritis:
•IgG antibodies against the Goodpasture antigen of the basement membrane cause an inflammation reaction that is mediated by antibodies. The Goodpasture antigen is also found in the alveolar basement membrane.
- Immune complexes that are formed due to an infection or an autoimmune disease attach to the capillary walls.
- Anti-neutrophil cytoplasmic antibodies (ANCA) interact with components of the neutrophil granules and thereby produce glomerular damage.
All immune mechanisms start a pro-inflammatory immune cascade with a subsequent inflammatory reaction. This inflammatory reaction eventually leads to a damage of the glomerular capillary wall. This causes bleeding into the Bowman’s capsule and thus into the primary urine. The renal corpuscle then becomes necrotic and loses functionality. The more glomeruli are affected the more overall kidney function is lost with a decreasing glomerular filtration rate.Note :The urinary sediment is typically notable for a mild, unselective proteinuria, a microhematuria with dysmorphic RBCs (acanthocytes), and red blood cell casts. This constellation is referred to as nephritic sediment.
Discovery
In 1827, Dr. Richard Bright noticed that many cases of kidney involvement are accompanied by a typical set of signs, cloudy urine, blood in urine, fever, marble drawing of skin, edema, etc. He collected these as a separate disease, named after him as Bright's disease. Anatomic pathophysiologists took a look at kidneys and saw how they were involved with inflammation. But it was not clear what the reason was.
The next step was made by a clinician, Bela Schick (1877-1967), who suspected an immunopathological mechanism because his pediatric patients sometimes developed a pattern similar to Bright's disease after anti-diptheria serotherapy (vaccination) (1900). While he hypothesized that the immune system was involved, the mechanism was unknown.
The next step was made by pathophysiology pathologists;
Lindeman (1901) -
by means of rabbit immunization with a homogenate of homologous kidney tissue obtained homologous antirenal cytotoxic antisera, proving that this is the immune system attacking kidneys.
But many more steps were needed to come to a model understanding of glomerulonephritis.
Masugi (1911);
succeeded transforming this model in heterologous (rabbit treatment with duck antisera to their glomerular basement membrane), a model of anti-GBM-nephritis of humans.
It was still unclear, which was the target antigen?
P.S. & E.S. Cavelty (1945), in a try to reflect real epidemiological conditions of clinical human post-streptococcal glomerulonephritis (link to scarlet fever) started to immunize with kidney antigen admixed with Streptococci toxin and adjuvant.
Finally, W. Heyman et. al (1959) immunized rats with proximal tubule brush border.
Later there was located a subepithelial antigen 330kD which later (in 1985) proved to be a protein of clatrin-coated endocytotic vesicles, a target antigen for common membranous glomerulonephritis of humans – 330gp megalin-fusion protein.
But nature is always much more clever than the naturalists are.
A considerable part of real human cases of acute, subacute and chronic glomerular diseases results from antibody-mediated attacks against absolutely different antigens, of not relation with Heymann’s factor. These are collagen of GBM, collagen-associated minor proteins, endothelial cell antigens, like certain selectins, etc. The disease is versatile with many facets.