Acute Glomerulonephritis
Sudden kidney inflammation causing dark urine, swelling, and high blood pressure, often occurring a few weeks after a strep throat or skin infection.
Emergency Management: Hypertensive emergency causing encephalopathy or acute left ventricular failure.
Acute Glomerulonephritis (AGN) is an immunological inflammation of the kidney glomeruli characterized by the abrupt onset of hematuria, proteinuria, hypertension, edema, and impaired renal function (acute nephritic syndrome). The classic and most common prototype in children is post-streptococcal glomerulonephritis (PSGN), which occurs after infection with nephritogenic strains of Group A beta-hemolytic Streptococcus.
Detailed Overview
AGN is an immune complex-mediated disease. When antibodies bind to circulating antigens (or antigens planted in the glomerulus), they form complexes that deposit in the glomerular basement membrane. This triggers complement activation and inflammatory cell recruitment, which damages the filtration barrier. Clinically, this results in the classic nephritic triad of hematuria (often 'cola-colored'), edema, and hypertension. While most pediatric PSGN cases resolve completely, adult cases and other variants (like IgA nephropathy) may progress to chronic kidney disease.
Epidemiology & Demographics
PSGN primarily affects children aged 5-12 years. It is twice as common in males. Incidence is highest in developing countries (up to 25 per 100,000). In developed nations, IgA nephropathy is the most common cause of acute glomerulonephritis overall.
Etiological Mechanism
Typically post-infectious: Group A Streptococcus (PSGN). Other causes: IgA nephropathy, Lupus nephritis, Anti-GBM disease (Goodpasture's), and ANCA-associated vasculitis.
Primary Causes
Immune complex deposition in the glomeruli leading to complement activation and structural damage to the filtration barrier.
In PSGN, streptococcal antigens (such as SPE-B) localize to the glomerular basement membrane (GBM). Host IgG antibodies bind these antigens, forming immune complexes. These complexes deposit in the subepithelial space (forming 'humps' on electron microscopy). This activates the alternative complement pathway, resulting in neutrophil infiltration, mesangial cell proliferation, and GBM damage. This damage leads to red blood cells and protein leaking into the urine, while reduced GFR causes fluid retention, edema, and hypertension.
Diagnostic Criteria & Guidelines
Clinical presentation of nephritic syndrome plus evidence of recent streptococcal infection (positive ASO titer or Anti-DNAse B) and low C3 complement levels. Kidney biopsy is rarely needed in classic pediatric PSGN but is required for rapidly progressive cases or atypical presentations.
Supportive care. Loop diuretics (e.g., Furosemide 1-2 mg/kg/dose PO or IV) for fluid overload and edema. Antihypertensives (e.g., Nifedipine or Amlodipine) to control blood pressure.
Second-Line & Adjunctive Therapy
Antibiotics (e.g., Penicillin V 250 mg PO BID for 10 days) to eradicate residual streptococcal carriage, though this does not change the course of the kidney disease.
Surgical & Procedural Management
None.
Patient Counseling & Advice
Reassure parents that the prognosis for childhood PSGN is excellent and gross hematuria usually resolves in a few weeks. However, microscopic hematuria can take over a year to clear.
Follow-Up & Monitoring Schedule
Weekly blood pressure and urinalysis until normalization. Check serum C3 at 8 weeks to ensure it has returned to normal (failure to normalize suggests MPGN or lupus).
Preventive Strategies
Prompt treatment of streptococcal pharyngitis and impetigo (prevents rheumatic fever but not necessarily PSGN).
In children, >95% have a complete recovery. In adults, 30-40% may progress to chronic kidney disease or persistent hypertension.