Poststreptococcal glomerulonephritis

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Poststreptococcal glomerulonephritis

Renal system


Poststreptococcal glomerulonephritis


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Poststreptococcal glomerulonephritis

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A 10-year-old boy is brought to the emergency department because of generalized body swelling. The swelling started 2 days ago when his parent noticed swelling around the patient’s eyes. Review of systems reveals mild shortness of breath after climbing a flight of stairs. The patient experienced an episode of flu-like symptoms and throat pain 2 weeks ago that responded to over-the-counter medications. Temperature is 37.0°C (98.6°F), pulse is 96/min, respirations are 20/min, and blood pressure is 155/92 mmHg. Physical examination shows periorbital pitting edema and 1+ generalized pitting edema. Pulmonary exam reveals bilateral fine expiratory crackles in the lower lobes. Complete blood count is normal. Serum chemistries and urinalysis findings are as follows:

Which of the following is the most likely cause of this patient’s condition?

External References

First Aid



Acute glomerulonephritis p. 571


Content Reviewers

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.


Poststreptococcal glomerulonephritis (PSGN) is a type of glomerulonephritis that is caused by a reaction to group A Streptococcus bacterial infection. PSGN is usually a complication of skin bacterial infections, typically by Streptococcus, but can also occur after streptococcal pharyngitis. Symptoms of PSGN may include swelling of the face, hands, and feet; dark, and foamy urine. Treatment for PSGN may include antibiotics to treat the underlying infection, steroids to reduce inflammation, and dialysis to manage kidney failure.


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