Causes of Nephritic Syndrome in Adults
The main causes of nephritic syndrome in adults include infection-related glomerulonephritis, IgA nephropathy, lupus nephritis, membranoproliferative glomerulonephritis, and ANCA-associated vasculitis. 1
Primary Causes
IgA Nephropathy (IgAN)
- Most common primary glomerulonephritis worldwide
- Characterized by IgA deposits in the mesangium
- Presents with hematuria, proteinuria, and variable degrees of renal dysfunction
- May be associated with IgA vasculitis (Henoch-Schönlein purpura) 2
Membranoproliferative Glomerulonephritis (MPGN)
- Characterized by mesangial cell proliferation and thickening of capillary walls
- Can be immunoglobulin-mediated or complement-mediated
- Often presents with nephritic-nephrotic features 2
Anti-Glomerular Basement Membrane (Anti-GBM) Disease
- Autoantibodies target the glomerular basement membrane
- Can present as rapidly progressive glomerulonephritis
- May be associated with pulmonary hemorrhage (Goodpasture syndrome) 2
ANCA-Associated Vasculitis
- Includes granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA)
- Characterized by pauci-immune crescentic glomerulonephritis
- Often presents with rapidly progressive renal failure 2
Secondary Causes
Infection-Related Glomerulonephritis
- Post-streptococcal glomerulonephritis (following streptococcal pharyngitis or skin infection)
- Other bacterial infections (endocarditis, pneumococcal, staphylococcal)
- Viral infections (hepatitis B, hepatitis C, HIV)
- Parasitic infections 3, 1
Systemic Lupus Erythematosus (SLE)
- Lupus nephritis is a common manifestation of SLE
- Can present with various patterns of glomerular injury
- Often associated with other systemic manifestations of lupus 1
Systemic Vasculitides
- Polyarteritis nodosa
- Henoch-Schönlein purpura (IgA vasculitis)
- Cryoglobulinemic vasculitis (often associated with hepatitis C) 2
Other Systemic Conditions
- Amyloidosis
- Diabetic nephropathy (can sometimes present with nephritic features)
- Malignancy-associated glomerulonephritis
- Drug-induced glomerulonephritis 4
Complement-Mediated Glomerular Diseases
- C3 glomerulopathy (C3 glomerulonephritis and dense deposit disease)
- Characterized by predominant C3 deposition with minimal or absent immunoglobulin deposits
- May be associated with genetic or acquired dysregulation of the alternative complement pathway 2
Clinical Presentation and Diagnosis
Nephritic syndrome typically presents with:
- Hematuria (microscopic or macroscopic)
- Proteinuria (usually non-nephrotic range)
- Hypertension
- Reduced glomerular filtration rate
- Edema (less prominent than in nephrotic syndrome) 1
Diagnostic evaluation should include:
- Urinalysis and urine microscopy
- Quantification of proteinuria
- Serum creatinine and estimated glomerular filtration rate
- Serological tests (ANA, ANCA, anti-GBM antibodies, complement levels)
- Renal biopsy (often necessary for definitive diagnosis) 2, 4
Key Distinctions
It's important to differentiate nephritic syndrome from nephrotic syndrome:
- Nephritic syndrome: predominant hematuria, variable proteinuria, hypertension, and impaired kidney function
- Nephrotic syndrome: heavy proteinuria (>3.5g/day), hypoalbuminemia, edema, and often hyperlipidemia 5, 6
However, some conditions can present with features of both syndromes (nephritic-nephrotic overlap), particularly membranoproliferative glomerulonephritis and lupus nephritis 2.
Treatment Considerations
Treatment depends on the underlying cause and may include:
- Immunosuppressive therapy for autoimmune causes
- Antimicrobial therapy for infection-related causes
- Supportive care including blood pressure control and management of fluid overload
- Specific therapies targeted at the underlying disease mechanism 2, 1
Early diagnosis and appropriate management are crucial to prevent progression to chronic kidney disease and end-stage renal disease.