Concept:
Post-Streptococcal Glomerulonephritis (PSGN) is the classic prototype of acute post-infectious glomerulonephritis in children.
It occurs following infection with nephritogenic strains of Group A $\beta$-hemolytic Streptococcus (GAS) and is mediated by immune complex deposition activating the alternative complement pathway.
Explanation:
• PSGN develops $1\text{--}3$ weeks after streptococcal pharyngitis (or $3\text{--}6$ weeks after streptococcal impetigo/pyoderma) and presents with acute nephritic syndrome: hematuria (tea- or cola-colored urine), oliguria, hypertension, and periorbital edema.
• Immune complex deposition (involving streptococcal antigens like SpeB/NAPlr) triggers intense activation of the alternative complement pathway, causing marked consumption of serum complement C3.
• Consequently, serum C3 levels are significantly decreased/depressed in $>90\%$ of patients during the acute phase (typically normalizing within $6\text{--}8$ weeks). Therefore, stating that C3 levels are elevated is incorrect.
• Serum Antistreptolysin O (ASO) titers are elevated in approximately $70\text{--}80\%$ of cases following streptococcal pharyngitis (anti-DNase B is elevated after skin infections).
• Electron microscopy characteristically demonstrates large, discrete subepithelial electron-dense "humps" ("dome-shaped humps") along the glomerular basement membrane.
• Because the disease is self-limiting with an excellent long-term prognosis ($>95\%$ complete recovery), management is supportive, focusing on salt and water restriction, loop diuretics (furosemide) for hypervolemia/hypertension, and antihypertensives.
Final Answer:
The incorrect statement is that C3 levels are elevated; in acute PSGN, serum C3 levels are characteristically low due to alternative complement pathway activation.