Nephrotic vs Nephritic Syndrome
Published on
January 5, 2025
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Nephrotic vs. Nephritic Syndrome Comparison
1. Definition
- Nephrotic Syndrome
- Heavy proteinuria >3.5 g/day
- Hypoalbuminemia
- Hyperlipidemia (often elevated cholesterol & triglycerides)
- Edema (frequently significant)
- Pathophysiology: Primarily affects the podocytes, causing increased glomerular permeability
- Nephritic Syndrome
- Hematuria (often with RBC casts)
- Hypertension
- Mild to moderate proteinuria (<3.5 g/day)
- Azotemia (elevated BUN & creatinine)
- Pathophysiology: Primarily inflammatory process affecting the glomerular capillaries/endothelium
2. Clinical Presentation
- Nephrotic Syndrome
- Significant edema (periorbital, peripheral)
- Weight gain (due to fluid retention)
- Hyperlipidemia (fatty casts on urinalysis possible)
- Hypoalbuminemia (leading to fatigue, muscle wasting over time if severe)
- Nephritic Syndrome
- Hematuria (cola-colored urine), often with RBC casts
- Hypertension (fluid retention, altered renal function)
- Mild edema (less pronounced than in nephrotic syndrome)
- Mild to moderate proteinuria (<3.5 g/day)
3. Diagnostic Tests
- Nephrotic Syndrome
- Serum albumin (low)
- Urine protein-to-creatinine ratio (>3.5 g/day)
- Urinalysis: Heavy proteinuria, fatty casts
- Lipid profile: Elevated cholesterol and triglycerides
- Nephritic Syndrome
- Urinalysis: Hematuria, RBC casts, often mild proteinuria
- Blood pressure: Typically elevated
- Serum creatinine & BUN: Often elevated (reflecting reduced GFR)
- Urine protein-to-creatinine ratio (<3.5 g/day)
- Serum complement levels: May be decreased (e.g., C3 in post-streptococcal GN)
4. Treatment Approaches
- Nephrotic Syndrome
- Immunosuppressive therapy:
- Corticosteroids (e.g., for minimal change)
- Other agents (e.g., calcineurin inhibitors, cyclophosphamide) for FSGS or membranous nephropathy
- Diuretics (loop diuretics) to control edema
- RAAS blockade (ACE inhibitors or ARBs) to reduce proteinuria and protect renal function
- Lipid-lowering agents (statins) for hyperlipidemia
- Dietary modifications: Salt restriction to help manage edema
- Immunosuppressive therapy:
- Nephritic Syndrome
- Address underlying cause:
- If post-streptococcal GN is active, consider appropriate antibiotics
- For autoimmune processes, use immunosuppressants (e.g., corticosteroids)
- Blood pressure management: ACE inhibitors, ARBs, or other antihypertensives
- Diuretics if fluid overload is present
- Close monitoring: Watch for progression to RPGN or chronic kidney disease (CKD)
- Address underlying cause:
5. Long-Term Implications
- Nephrotic Syndrome
- Risk of CKD with prolonged heavy proteinuria (especially FSGS, membranous nephropathy)
- Cardiovascular risk elevated due to hyperlipidemia and possible accelerated atherosclerosis
- Thromboembolic complications (loss of antithrombin III and other anticoagulant factors in urine)
- Nephritic Syndrome
- Variable course: Some patients recover fully; others may progress to CKD
- High risk of progression to RPGN (crescentic glomerulonephritis) if severe, especially if untreated
- Ongoing need for regular renal function monitoring (creatinine, eGFR)
6. Underlying Causes
- Nephrotic Syndrome
- Minimal Change Disease (common in children)
- Membranous Nephropathy
- Focal Segmental Glomerulosclerosis (FSGS)
- Diabetic Nephropathy (common in adults)
- Systemic Lupus Erythematosus (can present with nephrotic features)
- Nephritic Syndrome
- Post-Streptococcal Glomerulonephritis (often follows strep infection)
- IgA Nephropathy (Berger’s Disease)
- Rapidly Progressive Glomerulonephritis (RPGN): some text
- Includes anti-GBM disease (Goodpasture’s)
- ANCA-associated vasculitis (e.g., granulomatosis with polyangiitis)
- Systemic Lupus Erythematosus (can present with nephritic features)
- Membranoproliferative GN (MPGN) (mixed nephrotic-nephritic picture)
7. Prognosis
- Nephrotic Syndrome
- Often chronic, with potential relapses (especially minimal change in children)
- Long-term risks: CKD, cardiovascular events, and thromboembolic complications
- Nephritic Syndrome
- Variable; may resolve spontaneously or progress to CKD
- Prognosis depends on underlying cause and responsiveness to treatment
- Rapid intervention in severe or rapidly progressive cases can prevent permanent renal damage
Tip: Both syndromes can overlap in certain conditions (e.g., Membranoproliferative GN), and careful clinical and laboratory evaluation is crucial for accurate diagnosis and targeted management. Regular monitoring of renal function, blood pressure, proteinuria, and electrolytes is essential to detect and mitigate progression to chronic kidney disease.