Renal · Glomerulonephritis
The facts most likely to be tested
Press 1–5 to rate · ↑↓ to navigate
The clinical hallmark of nephritic syndrome is hematuria presenting as dysmorphic RBCs or RBC casts on urinalysis.
Patients with nephritic syndrome typically present with the classic triad of hypertension, edema, and azotemia.
Post-streptococcal glomerulonephritis is characterized by low C3 complement levels and occurs 1–3 weeks after a group A beta-hemolytic streptococcal pharyngitis, or 3–6 weeks after impetigo.
IgA nephropathy (Berger disease) is the most common primary glomerulonephritis worldwide and typically presents as recurrent gross hematuria occurring synpharyngitically (concurrent with, or within 1-2 days of, an upper respiratory infection).
Rapidly progressive glomerulonephritis (RPGN) is defined by a rapid decline in glomerular filtration rate and is histologically characterized by crescent formation on biopsy.
Goodpasture syndrome involves anti-glomerular basement membrane (anti-GBM) antibodies and presents with nephritic syndrome and pulmonary hemorrhage, which often occur together.
Alport syndrome is a genetic defect in type IV collagen (classically X-linked, COL4A5; autosomal COL4A3/COL4A4 forms also occur) that manifests as a triad of hematuria, sensorineural hearing loss, and anterior lenticonus.
Vignette unlocked
A 10-year-old boy is brought to the clinic by his mother due to dark, cola-colored urine noted over the past two days. Two weeks ago, he had a sore throat that resolved without treatment. Physical examination reveals periorbital edema and a blood pressure of 135/85 mmHg. Urinalysis demonstrates hematuria and RBC casts. Serum studies show low C3 complement levels and an elevated antistreptolysin O (ASO) titer.
What is the most likely diagnosis?
Post-streptococcal glomerulonephritis
The patient presents with the classic nephritic triad and low C3 levels following a recent streptococcal infection, which is the hallmark of post-streptococcal glomerulonephritis as described in Bet 3.
Full handout
High yield triage
Etiology / Epidemiology
Post-infectious (GABHS) is the most common cause in children; IgA nephropathy is the most common cause in adults.
Clinical Manifestations
Classic triad: hematuria (cola-colored urine), hypertension, and edema. Look for RBC casts.
Diagnosis
Renal biopsy is the reference standard. Urinalysis shows dysmorphic RBCs and proteinuria < 3.5g/day.
Treatment
Management depends on the cause: supportive care (loop diuretics for fluid overload, antihypertensives, and ACE inhibitors/ARBs for persistent proteinuria/HTN) for post-infectious GN, with immunosuppression for RPGN (e.g., ANCA vasculitis, anti-GBM disease, lupus nephritis).
Prognosis
Most children recover fully; adults with crescentic glomerulonephritis have a high risk of progression to ESRD.
Full handout
Epidemiology & Etiology
Post-streptococcal glomerulonephritis typically follows a Group A Beta-Hemolytic Streptococcus pharyngitis or impetigo. IgA nephropathy (Berger disease) often presents concurrently with (within 1–2 days of) a viral URI. Other causes include Goodpasture syndrome and granulomatosis with polyangiitis (formerly Wegener granulomatosis).
Pertinent Anatomy
The primary site of injury is the glomerular basement membrane and mesangium. Inflammation disrupts the filtration barrier, allowing leakage of blood cells into the urinary space.
Pathophysiology
Immune complex deposition or anti-GBM antibodies trigger a pro-inflammatory cascade. This leads to glomerular capillary wall damage, resulting in decreased GFR and sodium retention. The resulting hypervolemia manifests as systemic hypertension.
Clinical Manifestations
Patients present with cola-colored urine (hematuria) and periorbital edema. Hypertensive emergency and pulmonary edema are critical complications. Microscopic examination reveals RBC casts, which are highly specific for glomerulonephritis.
Diagnosis
Renal biopsy is the reference standard for tissue diagnosis. Urinalysis demonstrates dysmorphic RBCs and mild-to-moderate proteinuria. Serum C3 levels are typically low in post-infectious cases.
Treatment
Initial management focuses on salt and water restriction. ACE inhibitors or ARBs are the first-line agents to reduce proteinuria. Avoid NSAIDs due to risk of worsening renal perfusion. Severe cases (e.g., RPGN) may require glucocorticoids plus cyclophosphamide or rituximab (KDIGO 2024, ANCA vasculitis), with plasma exchange added for anti-GBM disease (KDIGO 2021).
Prognosis
Monitor for ESRD via serial creatinine and urine protein-to-creatinine ratios. Crescentic glomerulonephritis is a medical emergency requiring urgent immunosuppression to prevent permanent renal failure.
Differential Diagnosis
Nephrotic Syndrome: massive proteinuria > 3.5g/day and hypoalbuminemia
IgA Nephropathy: hematuria occurring concurrently with URI
Post-streptococcal GN: hematuria 1-3 weeks after pharyngitis
Alport Syndrome: sensorineural hearing loss and family history
Goodpasture Syndrome: hemoptysis and anti-GBM antibodies