An 8-year-old girl presents to the emergency room with severe headache and tea-colored urine of 2 days duration (Figure 68-1). She has just completed a 10-day course of amoxicillin for streptococcal pharyngitis. Her blood pressure upon arrival is 132/88. She is diagnosed with probable post-streptococcal glomerulonephritis and treated with salt restriction and a diuretic, and recovers.
Post-streptococcal glomerulonephritis is the most common cause of nephritic syndrome in children. It follows a pharyngeal or skin infection involving a nephritogenic strain of group A beta-hemolytic streptococci.
Streptococcal antigens form immune complexes that activate a complement mediated cascade of inflammatory glomerular injury.2
Less common etiologies for nephritic syndrome include: membranoproliferative glomerulonephritis, lupus nephritis, IgA nephropathy, Henoch-Schonlein purpura, infectious glomerulonephritis (commonly associated with endocarditis), and post-infectious glomerulonephritis due to other bacterial, viral, or parasitic etiologies.
Rapidly progressive glomerulonephritis is a syndrome characterized by rapid loss of renal function (over a period of days to weeks) and the presence of glomerular crescents on renal biopsy (Figure 68-2). It represents the most severe presentation of any form of acute nephritis.3
Nephritic syndrome classically presents with an abrupt onset of gross hematuria (tea-colored urine; Figure 68-1), oliguria, elevated blood pressure, and/or generalized edema.
Onset of gross hematuria is 1 to 2 weeks following streptococcal pharyngitis and 3 to 6 weeks following streptococcal skin infection. In contrast, gross hematuria associated with IgA nephropathy commonly occurs concurrently with an upper respiratory infection.
Mild (subclinical) cases of nephritis may be reflected by microscopic hematuria detected on urinalysis.4
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