Glomerular inflammation with hematuria, RBC casts, hypertension, and mild-to-moderate proteinuria.
Also known as: nephritic syndrome, glomerulonephritis, GN, RPGN
Overview
Clinical syndrome resulting from glomerular inflammation, characterized by hematuria (often with dysmorphic RBCs and RBC casts), variable proteinuria (typically <3.5 g/day), hypertension, edema, and azotemia. Spans a spectrum from indolent to rapidly progressive glomerulonephritis (RPGN).
Epidemiology
Incidence varies by etiology. Post-streptococcal GN is the most common cause worldwide in children. IgA nephropathy is the most common primary glomerulonephritis globally. ANCA-associated vasculitis and lupus nephritis dominate adult RPGN.
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Question 1RenalMedium
A 7-year-old boy is brought in for 2 days of tea-colored urine and puffy eyes. Three weeks ago he was treated for streptococcal pharyngitis. On exam his blood pressure is 138/90 mmHg and he has periorbital edema. Urinalysis shows 3+ blood with dysmorphic red cells and red cell casts, and 1+ protein. Serum creatinine is mildly elevated. Which of the following findings best supports the suspected diagnosis?
APositive anti-GBM antibody on serology
BPositive c-ANCA targeting proteinase 3
CLow serum C3 with a preserved C4 level
DElevated total serum IgA antibody level
Reveal answer & full explanation
Correct answer: C — Low serum C3 with a preserved C4 level
APositive anti-GBM antibody on serology
BPositive c-ANCA targeting proteinase 3
CLow serum C3 with a preserved C4 level✓
DElevated total serum IgA antibody level
Why Low serum C3 with a preserved C4 level is correct
The vignette (tea-colored urine, periorbital edema, hypertension, RBC casts 1-3 weeks after strep pharyngitis) is classic post-streptococcal glomerulonephritis.
Post-strep GN activates the alternative complement pathway, producing a depressed C3 with a preserved C4; positive ASO/anti-DNase B titers confirm recent streptococcal infection.
Complement classification of GN: LOW C3 = post-strep, MPGN, lupus, cryoglobulinemia; NORMAL C3 = IgA nephropathy, anti-GBM, ANCA-associated vasculitis.
Why the others are wrong
Positive anti-GBM antibody on serology — defines anti-GBM (Goodpasture) disease, a pulmonary-renal RPGN with linear IgG on biopsy and a normal C3; it does not follow strep pharyngitis.
Positive c-ANCA targeting proteinase 3 — points to granulomatosis with polyangiitis (pauci-immune crescentic GN with sinopulmonary disease and normal complement), not a post-infectious GN in a child.
Elevated total serum IgA antibody level — suggests IgA nephropathy, which causes synpharyngitic hematuria within days of a URI and has a normal C3, not the 1-3 week post-strep latent period seen here.
Question 2RenalMedium
A 7-year-old boy is brought in for 2 days of cola-colored urine and puffy eyes. Three weeks ago he was treated for a skin infection on his legs. On exam his blood pressure is 138/90 mm Hg and he has periorbital and pedal edema. Urinalysis shows 3+ blood with dysmorphic red cells and red cell casts; serum creatinine is mildly elevated. Serum C3 is low with a normal C4, and the anti-DNase B titer is elevated. Which of the following best explains the findings?
BLinear deposition of anti-basement-membrane antibody
CGlomerular deposition of circulating immune complexes✓
DMesangial deposition of IgA-containing immune complexes
Why Glomerular deposition of circulating immune complexes is correct
Nephritic syndrome 1-3 weeks after a streptococcal skin infection, with low C3, a normal C4, and a positive anti-DNase B, is classic post-streptococcal glomerulonephritis.
Streptococcal antigens form immune complexes that deposit in the subepithelial glomerular space, activate complement (driving the low C3), and provoke proliferative, inflammatory injury.
The resulting endothelial and mesangial inflammation breaches the filtration barrier, letting RBCs into Bowman space and producing dysmorphic RBCs and RBC casts.
Why the others are wrong
Linear deposition of anti-basement-membrane antibody is the mechanism of anti-GBM (Goodpasture) disease, which causes a pulmonary-renal syndrome with a normal C3, not low C3 after strep.
Pauci-immune neutrophil-mediated glomerular necrosis describes ANCA-associated vasculitis, which is ANCA-positive with normal complement and few immune deposits.
Mesangial deposition of IgA-containing immune complexes is IgA nephropathy, in which hematuria is synpharyngitic (within days of a URI, not 1-3 weeks later) and C3 is normal.
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Autoimmune disease: SLE, ANCA vasculitis, anti-GBM (Goodpasture)
Family history: Alport syndrome, IgA nephropathy
Cryoglobulinemia (often hep C-related)
Recent URI (synpharyngitic hematuria of IgA nephropathy)
Pathophysiology
Immune-mediated glomerular injury — immune complex deposition, in situ antibody formation, or pauci-immune inflammation — disrupts the filtration barrier and triggers proliferative changes. Endothelial and mesangial inflammation allow RBC passage into Bowman space, generating dysmorphic RBCs and RBC casts. Loss of nephron mass causes azotemia and sodium retention → hypertension and edema.
Clinical presentation
Symptoms
Cola-colored, tea-colored, or smoky urine (gross hematuria)
Periorbital and peripheral edema
Headache, malaise (from hypertension)
Oliguria in severe or rapidly progressive cases
Constitutional symptoms (fever, weight loss, arthralgia) in systemic vasculitis or SLE
Membranoproliferative GN (MPGN) — Mixed nephritic/nephrotic; low C3; hepatitis C with cryoglobulinemia, monoclonal gammopathy
Alport syndrome — Hereditary X-linked; hematuria, sensorineural hearing loss, lenticonus; type IV collagen mutation
Thin basement membrane disease — Benign familial hematuria; isolated microhematuria; thin GBM on EM; preserved function
Diagnostic workup
Diagnostic criteria
Nephritic syndrome = hematuria (often gross) with RBC casts and dysmorphic RBCs + variable proteinuria + hypertension + azotemia. Kidney biopsy is the definitive test for adults and complicated pediatric cases to determine pattern and guide immunosuppression.
Labs
Urinalysis with microscopy — dysmorphic RBCs, RBC casts (diagnostic of glomerular bleed)
Spot UPCR or 24-h urine protein
BMP, CBC, creatinine trend
Complement: C3 and C4 (low in post-strep, lupus, MPGN, cryoglobulinemia; normal in IgA, anti-GBM, ANCA)
ANA, anti-dsDNA (lupus); ANCA with PR3/MPO; anti-GBM antibody
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