Poststreptococcal glomerulonephritis or PSGN is where the kidneys’ glomeruli, which is
the location where small molecules are first filtered out of blood and into the urine,
become inflamed after an infection by streptococcal bacteria.
Most commonly, PSGN starts with an infection by strains of group A beta-hemolytic streptococci
bacteria, and this particular group of streptococcus has a specific antigen on its surface that
lumps it into a group called “group A”.
This group A streptococci also produces an enzyme called streptolysin, and when the bacteria
is grown on a petri dish of blood, the enzyme completely lyses red blood cells that are
near the bacterial colony—called beta-hemolysis.
Beta-hemolysis is where they’re completely destroyed—as opposed to alpha-hemolysis,
where cells aren’t actually destroyed, but they’re just damaged or bruised.
Additionally, these strains are considered nephritogenic strains because they carry the
M-protein virulence factor, a protein that essentially helps them get around host defenses.
An infection by a nephritogenic strain of group A beta-hemolytic streptococcus bacteria
initiates a type III hypersensitivity reaction, where immune complexes are formed, composed
of antigens and antibodies, often IgG or IgM, that end up being carried in the bloodstream
to the glomerulus and become trapped.
Specifically these deposits end up in the glomerular basement membrane or GBM, and most
of the time they’re subepithelial, meaning between the epithelial cells, or podocytes,
and the basement membrane.
It’s also possible the antigens from the bacteria are first trapped in the glomeruli,
and then antibodies bind in the glomerulus itself.
Either way, these complexes initiate an inflammatory reaction in the glomerulus, which involves
activation and deposition of C3 complement, inflammatory cytokines, oxidants, and proteases
that all damage the podocytes.
This damage ends up allowing larger molecules to filter into the urine, like red blood cells
and proteins, which then get into the urine and cause hematuria and proteinuria.
Those red blood cells in the urine actually often make it darker or cola-colored; also
there tends to be less urine produced than normal, called oliguria.
These, along with inflammation, are several of the characteristic features making PSGN
a nephritic syndrome.
Not only that, as less fluid is excreted into the urine, more’s retained by the body,
causing peripheral edema as well as periorbital edema, fluid buildup around the orbit of the
eye.
Typically PSGN affects children and follows about 6 weeks after infections of the skin,
called impetigo, or about 1-2 weeks after infections of the throat, or pharyngitis.
Generally the disease is usually generally mild, and runs its course and spontaneously
resolves within a month.
Under light microscopy, the glomerulus looks enlarged and hypercellular, and a closer look
on electron microscopy shows subepithelial deposits, which appear as “humps”.
On immunofluorescence, the immune deposits cause a “starry sky” granular appearance
along the basement membrane and mesangium, which includes the mesangial cells and other
supporting tissue.
Blood tests may show antibodies against group A streptococcus—called anti-DNase B, as
well as decreased complement levels.
Since it’s generally a mild illness, treatment is usually supportive.
A few children, though, progress to renal failure, and about a quarter of adults with
PSGN develop rapidly progressive glomerulonephritis, which can quickly lead to renal failure as
well.
Alright, so as a quick recap: Poststreptococcal glomerulonephritis is a nephritic syndrome
involving a group A beta-hemolytic streptococcus infection of the skin or throat that causes
immune complex-mediated inflammation of the glomeruli 1-6 weeks after infection.
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