Acute Glomerulonephritis (AGN)


Acute Glomerulonephritis (AGN)

Acute Glomerulonephritis (AGN)

Epidemiology:

  • AGN is more common during winter and spring, often associated with pharyngitis.
  • In summer, AGN can be linked to skin infections.

Pathogenesis:

  • AGN is caused by group A beta-hemolytic streptococcus (GAS) or other bacteria.
  • The bacteria do not directly attack the kidneys but trigger a cross-reactive immune response against components of the glomerular basement membrane.
  • This immune response leads to the formation of immune complexes, activating the complement system and attacking the glomerular basement membrane.
  • This results in:
  • Reduced normal blood C3 and C4 levels.
  • Increased IgG deposition and leukocyte recruitment to the kidneys, causing cell damage.
  • Immune complex deposition in the kidney parenchyma, causing acute glomerulonephritis.
  • In severe cases, the inflammatory process can activate coagulation, leading to increased growth factors and damage to the glomeruli and renal tubules.

Pathology:

  • Glomerular basement membrane inflammation: thickens the glomerular basement membrane, leading to:
  • Reduced glomerular filtration rate.
  • Water and salt retention, causing edema, affecting the heart and nerves.
  • Red blood cell leakage, causing hematuria.

Clinical Manifestations:

  • Age of onset: 5-12 years old.
  • Male-to-female ratio: 2:1.
  • Classic triad: edema, gross hematuria, and hypertension (HTN) (approximately 40% of cases).
  • 100% of patients have microscopic hematuria.

Diagnosis:

  • History and physical examination: based on epidemiology and clinical manifestations of nephritis.
  • Disease progression:
  • The disease usually subsides after 10-14 days.
  • No recurrence.
  • Exclusion: Other conditions causing glomerulonephritis need to be ruled out.

Prognosis:

  • 90-95% of patients recover spontaneously after one week.
  • The acute phase is critical during the first 7-10 days.
  • 10-25% of cases have a poor outcome.

Paraclinical Investigations:

  • Reduced complement CH50 and C3 (70-94%).
  • X-ray: increased pulmonary circulation, pulmonary edema. Note for Mycoplasma in case of pneumonia.
  • Anti-GAS antibody test: ASO.

Treatment:

Renal function rehabilitation:

  • Furosemide (diuretic).
  • Antihypertensive drugs.
  • Note: Digitalis and Morphine are ineffective.

Hypertension management:

  • Always combined with diuretics.
  • Maintain normal blood pressure within 48 hours.
  • Calcium channel blockers:
  • Nifedipine orally.
  • Nicardipine intravenously.
  • Avoid ACE inhibitors due to the risk of hyperkalemia.

Edema reduction:

  • Low-salt diet.
  • Fluid restriction.
  • Furosemide.
  • Do not use Spironolactone as it is ineffective.

Antibiotic treatment:

  • Only used if pharyngitis or skin infection progresses.
  • Penicillin V: 100,000 IU/kg.
  • Erythromycin: 75 mg/kg/day for 10 days.

Referral Indications:

  • Anuria for > 2 days.
  • No decrease in serum creatinine for > 2 weeks.
  • Hypertension for > 4 weeks.
  • Nephrotic syndrome for > 4 weeks.
  • Gross hematuria for > 3-4 weeks.
  • Proteinuria for > 6 weeks.
  • Decreased C3 for > 8 weeks.
  • Recurrence.
  • Extrarenal complications.



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