What's on this Page
What are the major causes of acute glomerulonephritis?
The patient’s history and a physical examination can provide clues to the diagnosis of acute glomerulonephritis.
Looking for skin lesions and disease in other organ systems can help determine if the cause of the acute glomerulonephritis syndrome is a result of kidney-limited or systemic disease.
What approaches should be used to develop an appropriate differential diagnosis?
A focused laboratory examination, including serologic studies, directed by the findings in the patient’s history and physical examination, can also be useful in establishing a diagnosis.
Hematuria with dysmorphic red cell morphology and red cell casts are usually detected on urinalysis. Moderate proteinuria, usually in the non-nephrotic range, is typical. Nephrotic-range proteinuria occurs in <30% of patients. Mild to severe azotemia is universally present.
Here is the table which presents major causes of acute glomerulonephritis stratified by their association with serum complement levels (low vs. normal or high).
Complement levels can help a clinician focus on a differential diagnosis on the most likely causes of the acute glomerulonephritis syndrome. Measuring serum complement levels (C3, C4) and/or activity (CH50) is a somewhat arbitrary choice of initial tests, but they provide a practical approach to further testing and management of the patient with presumptive glomerulonephritis. A kidney biopsy is almost always indicated to establish a definitive diagnosis and direct treatment.
The extent of acute inflammation and fibrosis present in the biopsy can provide important data on prognosis and can be used to project responsiveness to therapy. In order to optimize patient care, a standardized kidney biopsy classification system based on current concepts of glomerulonephritis etiology/pathogenesis has been proposed.
Major Causes of Acute Glomerulonephritis (Serologic and Other Tests that Provide Diagnostic Clues)
Low Serum Complement Level | Normal Serum Complement Level | |
|---|---|---|
| Systemic diseases | Systemic lupus erythematosus (ANA + , anti-DNA antibody + ) Cryoglobulinemia (cryoglobulin + ) Henoch-Schönlein purpura Infectious endocarditis (positive blood cultures) “Shunt” nephritis (positive blood cultures) Infection-associated glomerulonephritis | Microscopic polyangiitis (ANCA + ) Granulomatosis with polyangiitis (ANCA + ) Goodpasture syndrome (anti-GBM Ab + ) Hypersensitivity vasculitis Visceral abscess (positive blood cultures) |
| Primary kidney diseases | Post-infection glomerulonephritis (β-hemolytic streptococci) C3 glomerulopathy Dense deposit disease Membranoproliferative glomerulonephritis | IgA nephropathy Idiopathic RPGN Type I: Anti-GBM disease (Goodpasture disease; anti-GBM Ab + ) Type II: Immune complex/immune deposit disease Type III: Pauci-immune (ANCA + ) |
ANA , Antinuclear antibody; ANCA , anti-neutrophil cytoplasmic antibodies; GBM , glomerular basement membrane; IgA , immunoglobulin-A; RPGN , rapidly progressive glomerulonephritis.
Modified from Manoharon, A., Schelling, J. R., Diamond, M., Chung-Park, M., Madaio, M., & Sedor, J. R. (2013). Immune and inflammatory glomerular diseases. In R. J. Alpern, M. J. Caplan, & O. W. Moe (Eds.), Seldin and Giebisch’s the kidney: Physiology and pathophysiology (pp. 2763–2816). Amsterdam: Elsevier.
