Poststreptococcal glomerulonephritis (Postinfectious glomerulonephritis)

Poststreptococcal (or postinfectious) glomerulonephritis (PSGN) refers to acute glomerular inflammation that results from a preceding infection with nephritogenic strains of streptococci. Although most commonly seen in children following group A streptococcal tonsillopharyngitis, skin infections such as impetigo may trigger PSGN as well. Deposition of immune complexes containing the streptococcal antigen within the glomerular basement membrane results in complement activation and subsequent damage to the glomeruli. PSGN typically presents as a nephritic syndrome with hematuria, mild proteinuria, edema, and hypertension. Elevated antistreptolysin O titers (ASO), low complement levels, and elevated creatinine support the diagnosis. In children, close monitoring and supportive therapy facilitate the recovery process. While most children recover fully, the prognosis in adults is typically less favorable.

• Mostly affects children (between the ages of 3–12 years); and patients > 60 years of age
• The incidence has decreased in developed countries due to the systematic use of antibiotics and improved hygienic standards.

References:^[1][2][3]

Epidemiological data refers to the US, unless otherwise specified.

• Occurs approximately 10–30 days following an acute infection
  • The most common cause is a prior infection with group A beta-hemolytic streptococci
    • Infection of the mouth and pharynx (tonsillitis, pharyngitis)
    • Soft tissue infections (erysipelas, impetigo)
    • Osteomyelitis
  • It occurs less frequently following other bacterial, viral infections, or malaria.
• Immune complex glomerulonephritis can also manifest during an acute infection (e.g., in endocarditis or soft tissue abscesses)!

References:^[1][4]

• Infection with nephritogenic strains of group A beta-hemolytic streptococci → immune complexes containing the streptococcal antigen deposit within the glomerular basement membrane; (likely involves molecular mimicry) → complement activation → destruction of the glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome (see glomerular diseases for more information)

References:^[2]

• Approx. 50% of cases remain asymptomatic
• Nephritic syndrome
  • Hematuria: tea- or cola-colored urine
  • Hypertension: can lead to headaches
  • Edema; may be associated with dyspnea and neurologic symptoms (e.g., seizures)
  • Oliguria
• Influenza-like symptoms
• Flank pain

References:^[1][4]

• Laboratory tests
  • Normocytic, normochromic anemia
  • Possibly elevated BUN and creatinine (often transient)
  • ↑ Antistreptolysin-O titer (ASO) (particularly following streptococcal infection of the pharynx)
  • ↑ Anti-DNase B antibody (ADB) titer (particularly following streptococcal infection of the soft tissue)
  • ↓ C3 complement
  • Urinalysis: nephritic sediment (e.g., hematuria and RBC casts, mild proteinuria)

• Ultrasound: enlarged kidneys
• Renal biopsy (not performed in most cases)
  • Indication: suspected rapidly progressive glomerulonephritis
  • Findings
    • Light microscopy: glomeruli appear enlarged and hypercellular (infiltration of monocytes and polymorphonuclear cells)
    • Immunofluorescent microscopy: granular deposits (IgG, IgM, C3 complement), which create a "lumpy-bumpy" appearance (starry sky pattern)
    • Electron microscopy: "humps" = subepithelial immune complexes (between epithelial cells and the glomerular basement membrane)

References:^[1][2][4]

• IgA nephropathy
• Thin basement membrane disease
• See “Etiology” of nephritic syndrome

The differential diagnoses listed here are not exhaustive.

In most cases the disease is self-limiting and only supportive treatment focused on the complications of volume overload is necessary.

• Monitor electrolytes, renal function parameters, and blood pressure
• For edema: low-sodium and low-protein diet, loop diuretics
• For hypertension: ACE-inhibitors/ARBs, calcium channel blockers (see "Treatment" in the article on hypertension)
• If persisting streptococcal infection: antibiotic therapy (penicillin G benzathine)
• If severe course/complications: glucocorticoids, temporary need for dialysis

References:^[2][4][3]

• Recovery usually occurs within 6–8 weeks.
  • In children: restitution of kidney function in > 90% of cases
  • In some cases, urinalysis may remain abnormal for extended periods. Follow-ups are therefore important!
• In adults, about 50% of patients suffer from persistently reduced renal function.

References:^[1][3]