Diagnosis: Acute Post-Streptococcal Glomerulonephritis (APSGN)

Connecting the Clues

Every detail in this case points directly to APSGN:

Clinical Finding	Significance
8-year-old boy	Classic demographic (ages 2-18, male:female = 2:1)
Tea/Coca-Cola colored urine	Gross hematuria - hallmark of nephritic syndrome
Periorbital puffiness ("puffy eyes")	Edema from sodium/water retention
Tight shoes (ankle edema)	Bilateral pitting edema at extremities
BP 135/92 mmHg	Hypertension - a defining feature of nephritic syndrome
Oliguria (urinated only twice)	Reduced GFR causing decreased urine output
Crusted skin lesions / bug bite scars on shins ~3 weeks ago	The trigger: skin infection (impetigo) with Group A Streptococcus (GAS)

The timing is perfect: APSGN appears 2-4 weeks after skin infection (impetigo/pyoderma) - and here it was exactly 3 weeks ago.

What Is APSGN?

APSGN is a postinfectious, immune complex-mediated glomerulonephritis triggered by prior skin or throat infection with Group A Streptococcus (Streptococcus pyogenes), and occasionally groups C or G streptococcus.

Goldman-Cecil Medicine describes it as: "a postinfectious, immune complex-mediated glomerulonephritis associated with prior skin or throat infection by group A streptococcus."

Pathophysiology

The sequence of events:

GAS skin infection (impetigo from bug bites) infects the skin ~3 weeks prior
Certain "nephritogenic" strains of GAS release antigens (notably nephritis-associated plasmin receptor / NAPIr and streptococcal pyrogenic exotoxin B / SpeB)
These antigens deposit in the glomerular basement membrane and mesangium
The immune system forms antibody-antigen immune complexes that lodge in the glomeruli
Complement activation occurs - C3 levels drop (the complement is consumed)
Neutrophils and macrophages are recruited, causing glomerular inflammation
The inflamed, leaky glomeruli allow RBCs and protein to spill into urine (hematuria, proteinuria)
Reduced GFR causes sodium and water retention → edema + hypertension
Low urine output with concentrated blood-tinted urine = oliguria with gross hematuria → the "tea-colored urine"

Classic Presentation (Nephritic Syndrome)

APSGN most commonly presents as nephritic syndrome, which includes:

Hematuria - smoky, tea-colored, or Coca-Cola colored urine (RBC casts on microscopy)
Edema - especially periorbital (puffy eyes in the morning) and dependent (ankle/pedal edema)
Hypertension - from salt/water retention (this child: 135/92 mmHg)
Oliguria - reduced kidney filtration
Proteinuria - usually sub-nephrotic range

Key Investigations to Order

Test	Expected Finding
Urinalysis	Hematuria, RBC casts, granular casts, proteinuria
Serum C3	LOW (complement consumed by immune complexes)
ASO titer (Anti-streptolysin O)	Elevated (rises 7-14 days after infection, peaks 3-4 weeks)
Anti-DNase B	Elevated - especially useful after skin infections (ASO may be less reliable for impetigo)
BMP/Chem	Elevated creatinine/BUN (azotemia), hyperkalemia possible
Throat/skin culture	May still show GAS
Renal biopsy	Rarely needed; shows "lumpy-bumpy" immune complex deposits on IF

Note: ASO is most reliable after pharyngitis. For skin infections (as in this case), anti-DNase B is the preferred streptococcal antibody test.

Treatment

Treatment is supportive (there is no specific cure):

Loop diuretics (furosemide) - for fluid overload and edema
Antihypertensives - if BP remains elevated
Salt and fluid restriction
Antibiotics (benzathine penicillin G 1.2 million units IM, or oral amoxicillin) - if active streptococcal infection is still present, to eradicate the organism and prevent spread of nephritogenic strains
Dialysis - only if severe acute kidney injury develops

Prognosis

The prognosis in children is excellent:

Symptoms typically resolve within 2-7 days
Hematuria and proteinuria clear over weeks to months
Long-term end-stage renal disease is uncommon in children
Recurrence is rare (immunity develops against the nephritogenic strain)

Summary

This 8-year-old boy has Acute Post-Streptococcal Glomerulonephritis following impetigo (skin infection with GAS) 3 weeks ago. His immune system formed complexes that damaged the glomeruli, resulting in classic nephritic syndrome: tea-colored urine (hematuria), periorbital and pedal edema, hypertension, and oliguria. Immediate workup should include urinalysis with microscopy, serum C3, and anti-DNase B. Supportive treatment with diuretics and antihypertensives is the mainstay, and the outlook for full recovery is excellent.

Goldman-Cecil Medicine International Edition, block 44
Symptom to Diagnosis: An Evidence-Based Guide, 4th Edition, block 5

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