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Renal tubular acidosis
Minimal change disease
Focal segmental glomerulosclerosis (NORD)
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Acute tubular necrosis
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Nephroblastoma (Wilms tumor)
Posterior urethral valves
Hypospadias and epispadias
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
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Tanner Marshall, MS
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.
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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