Nephritic Syndrome

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Basics

Description

  • Acute glomerulonephritis (AGN) is acute inflammatory damage to glomerulus, associated with:
    • Abrupt onset of hematuria with or without RBC casts
    • Acute renal failure manifested by edema, hypertension, azotemia, decline in urine output
    • Variable proteinuria
    • Active urine sediment (RBC casts)
  • Exact mechanism of AGN unclear:
    • Combination of autoimmune reactivity to specific antigens at renal glomeruli
    • Characterized by crescent formation secondary to nonspecific injury at the glomerular wall

Etiology

  • Poststreptococcal glomerulonephritis (PSGN):
    • A postinfectious cause of acute nephritic syndrome, resulting from group A β-hemolytic streptococci
    • Considered a nonsuppurative complication (antibiotic treatment does not prevent this complication)
    • Occurs when immune complexes create hump-shaped subepithelial deposits in renal glomeruli
    • Most commonly affects patients between ages 3–15 yr but can occur at any age
    • Incidence of nephritis is 5–10% after pharyngitis and 25% after skin infections
    • Consider PSGN in the setting of new-onset proteinuria, RBC casts, edema, and any recent infection
    • Latent period between infection and onset of nephritis helps differentiate between PSGN and IgA nephropathy (IgA-N):
      • 1–3 wk in pharyngeal infection
      • 2–4 wk in cutaneous infection
    • Renal biopsy is usually not necessary for diagnosis
    • Low complement (C3) for 6–8 wk
    • Can progress to severe renal failure if underlying infection goes untreated
    • Prognosis:
      • Excellent; >95% recover spontaneously with normalization of renal function within 6–8 wk, even with dialysis
      • Hematuria usually resolves in 3–6 mo
      • Transient nephrotic phase in 20% of patients during resolution of illness
      • End-stage renal disease occurs <5%
      • Rapidly progressive glomerulonephritis (RPGN) is rare, occurring in <1% cases
      • Most cases resolve spontaneously with no long-term sequelae
  • Other infectious sources of glomerulonephritis (GN):
    • Sepsis, pneumonia, endocarditis, viruses, HIV
    • Pulmonary, intra-abdominal, or cutaneous infections
    • Syphilis, leprosy, schistosomiasis, and malaria
    • Goal: Treat underlying infection
  • Hepatitis virus–related glomerular disease:
    • Can present with either nephritic or nephrotic symptoms
    • Causes membranoproliferative GN
    • Complements remain low indefinitely (compared to PSGN)
  • Noninfectious causes of GN (due to immune complex formation):
    • Systematic lupus erythematosus, Henoch–Schönlein purpura, vasculitis, Wegener granulomatosis
    • Goodpasture syndrome
  • IgA-N:
    • Most common cause of AGN (>25%) worldwide
    • Antibody–antigen causes immune complex deposition of IgA and C3
    • Complement levels are usually normal
    • IgA-N has different presentations:
      • Gross hematuria following upper respiratory infection (URI)
      • Microscopic hematuria with proteinuria
      • Hematuria during viral illness or after exercise
      • Prognosis is related to serum creatinine, BP, and proteinuria
      • 50% of patients with proteinuria may develop progressive renal disease
      • ACE inhibitors or angiotensin-receptor blockers (ARBs) may help
  • RPGN:
    • Certain patients with AGN may progress rapidly to renal failure
    • Hallmarks are crescents on renal biopsy
  • Hereditary nephritis:
    • Alport syndrome

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Basics

Description

  • Acute glomerulonephritis (AGN) is acute inflammatory damage to glomerulus, associated with:
    • Abrupt onset of hematuria with or without RBC casts
    • Acute renal failure manifested by edema, hypertension, azotemia, decline in urine output
    • Variable proteinuria
    • Active urine sediment (RBC casts)
  • Exact mechanism of AGN unclear:
    • Combination of autoimmune reactivity to specific antigens at renal glomeruli
    • Characterized by crescent formation secondary to nonspecific injury at the glomerular wall

Etiology

  • Poststreptococcal glomerulonephritis (PSGN):
    • A postinfectious cause of acute nephritic syndrome, resulting from group A β-hemolytic streptococci
    • Considered a nonsuppurative complication (antibiotic treatment does not prevent this complication)
    • Occurs when immune complexes create hump-shaped subepithelial deposits in renal glomeruli
    • Most commonly affects patients between ages 3–15 yr but can occur at any age
    • Incidence of nephritis is 5–10% after pharyngitis and 25% after skin infections
    • Consider PSGN in the setting of new-onset proteinuria, RBC casts, edema, and any recent infection
    • Latent period between infection and onset of nephritis helps differentiate between PSGN and IgA nephropathy (IgA-N):
      • 1–3 wk in pharyngeal infection
      • 2–4 wk in cutaneous infection
    • Renal biopsy is usually not necessary for diagnosis
    • Low complement (C3) for 6–8 wk
    • Can progress to severe renal failure if underlying infection goes untreated
    • Prognosis:
      • Excellent; >95% recover spontaneously with normalization of renal function within 6–8 wk, even with dialysis
      • Hematuria usually resolves in 3–6 mo
      • Transient nephrotic phase in 20% of patients during resolution of illness
      • End-stage renal disease occurs <5%
      • Rapidly progressive glomerulonephritis (RPGN) is rare, occurring in <1% cases
      • Most cases resolve spontaneously with no long-term sequelae
  • Other infectious sources of glomerulonephritis (GN):
    • Sepsis, pneumonia, endocarditis, viruses, HIV
    • Pulmonary, intra-abdominal, or cutaneous infections
    • Syphilis, leprosy, schistosomiasis, and malaria
    • Goal: Treat underlying infection
  • Hepatitis virus–related glomerular disease:
    • Can present with either nephritic or nephrotic symptoms
    • Causes membranoproliferative GN
    • Complements remain low indefinitely (compared to PSGN)
  • Noninfectious causes of GN (due to immune complex formation):
    • Systematic lupus erythematosus, Henoch–Schönlein purpura, vasculitis, Wegener granulomatosis
    • Goodpasture syndrome
  • IgA-N:
    • Most common cause of AGN (>25%) worldwide
    • Antibody–antigen causes immune complex deposition of IgA and C3
    • Complement levels are usually normal
    • IgA-N has different presentations:
      • Gross hematuria following upper respiratory infection (URI)
      • Microscopic hematuria with proteinuria
      • Hematuria during viral illness or after exercise
      • Prognosis is related to serum creatinine, BP, and proteinuria
      • 50% of patients with proteinuria may develop progressive renal disease
      • ACE inhibitors or angiotensin-receptor blockers (ARBs) may help
  • RPGN:
    • Certain patients with AGN may progress rapidly to renal failure
    • Hallmarks are crescents on renal biopsy
  • Hereditary nephritis:
    • Alport syndrome

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