Nephritic bs nephrotic
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Nephritic vs. Nephrotic Syndrome
These are two distinct glomerular syndromes with different mechanisms, features, and causes - though overlap exists.
Core Mechanism
| Nephritic | Nephrotic | |
|---|---|---|
| Pathology | Glomerular inflammation - proliferation of cells + leukocyte infiltration damage the capillary wall | Disruption of the filtration barrier - structural/physicochemical changes increase permeability to protein |
| Histology | Mesangial cell proliferation, leukocyte infiltration; crescents in severe disease | GBM thickening or podocyte foot process fusion/effacement (podocytopathy) |
| Key insult | Inflammatory injury → capillary wall disrupts → blood leaks into urine | Protein leaks across damaged filtration barrier → massive proteinuria |
- Comprehensive Clinical Nephrology, 7th Ed. - Robbins & Cotran Pathologic Basis of Disease
Clinical Features Side-by-Side
| Feature | Nephrotic | Nephritic |
|---|---|---|
| Onset | Insidious | Abrupt |
| Edema | ++++ (massive, periorbital, dependent) | ++ (mild-moderate) |
| Blood pressure | Normal | Raised |
| JVP | Normal / low | Raised |
| Proteinuria | ++++ (>3.5 g/day) | ++ (subnephrotic range) |
| Hematuria | May or may not occur | +++ (brown/tea-colored urine) |
| RBC casts | Absent | Present (pathognomonic) |
| Serum albumin | Low (<3 g/dL) | Normal / slightly reduced |
| GFR / azotemia | Usually preserved early | Reduced - oliguria, azotemia |
| Lipids | Hyperlipidemia + lipiduria | Usually normal |
- Comprehensive Clinical Nephrology, 7th Ed., Table 16.4
Pathophysiology Details
Nephrotic
The cascade follows a logical sequence:
- Glomerular barrier damaged → massive proteinuria (>3.5 g/day)
- Liver cannot compensate → hypoalbuminemia (<3 g/dL)
- Reduced plasma oncotic pressure → generalized edema (periorbital, dependent, ascites, pleural effusion)
- Hypovolemia → aldosterone + sympathetic activation → sodium/water retention (worsens edema)
- Liver upregulates lipoprotein synthesis (compensatory) → hyperlipidemia and lipiduria
Key complications:
- Thromboembolism (10-40% of cases) - urinary loss of antithrombotics (antithrombin III, protein C/S) + increased clotting factor synthesis. Deep vein thrombosis and renal vein thrombosis are classic. Prophylactic anticoagulation is considered when albumin <2.0-2.5 g/dL with additional risk factors.
- Increased infection risk (loss of immunoglobulins)
- Cardiovascular disease from hyperlipidemia
Nephritic
The inflammatory glomerular injury leads to:
- Capillary wall damage → hematuria with RBC casts
- Reduced GFR → oliguria, azotemia, fluid retention
- Fluid retention + renin from ischemic kidneys → hypertension
- Some protein leak → mild proteinuria (rarely nephrotic range, so albumin stays near normal)
- Robbins & Cotran Pathologic Basis of Disease
Classic Causes
Nephrotic Syndrome (primary causes = podocytopathies)
| Disease | Key feature | Age group |
|---|---|---|
| Minimal Change Disease (MCD) | Foot process effacement on EM only; responds to steroids | Children (most common) |
| Focal Segmental Glomerulosclerosis (FSGS) | Focal/segmental scarring; often steroid-resistant | Adults, HIV |
| Membranous Nephropathy | Subepithelial deposits, GBM thickening; anti-PLA2R Ab | Adults (most common primary cause in adults) |
| Diabetic nephropathy | Nodular glomerulosclerosis (Kimmelstiel-Wilson) | Adults with DM |
| Amyloidosis | Congo red positive deposits | Older adults |
| Lupus nephritis | Can cause either syndrome | Young women |
Nephritic Syndrome (immune complex/inflammatory GN)
| Disease | Key feature |
|---|---|
| Poststreptococcal GN | 1-4 weeks post Group A strep pharyngitis or impetigo; subepithelial "humps"; low C3; children 6-10 yrs |
| IgA Nephropathy | Most common worldwide; IgA mesangial deposits; normal complement |
| Lupus Nephritis | Low C3/C4; ANA+, anti-dsDNA+ |
| ANCA-associated vasculitis | Pauci-immune, ANCA+; normal complement |
| Anti-GBM disease (Goodpasture) | Linear IgG on IF; pulmonary hemorrhage |
| MPGN | Can present as either syndrome; low C3 |
| RPGN (crescentic GN) | Severe nephritic picture with rapid loss of kidney function over days-weeks |
Workup Tips
Suspected nephrotic:
- ANA, C3/C4, cryoglobulins, viral serologies (HIV, HBV, HCV, CMV, EBV)
- Review medications; rule out malignancy
- SPEP + urine immunofixation (for monoclonal gammopathy if large protein-albumin gap)
- Renal biopsy in all adults
Suspected nephritic:
-
Anti-GBM antibodies, ANCA, ASO titer
-
ANA, C3/C4, cryoglobulins, viral serologies
-
Complement levels key:
- Low C3: postinfectious GN, lupus, MPGN, C3 glomerulopathy, SBE
- Normal complement: IgA nephropathy, ANCA vasculitis, anti-GBM disease
-
Washington Manual of Medical Therapeutics
Glomerular Histology - Nephrotic Foot Process Effacement
Below is a scanning electron micrograph comparing normal podocytes (left) with the extensive foot process loss seen in nephrotic syndrome (right - puromycin aminonucleoside model):
General Management Principles
Both syndromes:
- ACEi/ARBs to reduce intraglomerular pressure and proteinuria
- Diuretics + sodium restriction for edema
- Aggressive BP control
Nephrotic-specific:
- Statins for hyperlipidemia (HMG-CoA reductase inhibitors)
- Anticoagulation for thromboembolic complications (heparin → oral anticoagulant)
- Prophylactic anticoagulation if albumin <2.0-2.5 g/dL + risk factors
- Treat underlying cause (steroids for MCD, etc.)
Nephritic-specific:
- Treat underlying cause (immunosuppression for lupus, ANCA; antibiotics for postinfectious)
- RPGN is a uremic emergency - requires urgent evaluation and usually pulse steroids ± cyclophosphamide ± plasmapheresis
One important caveat: the two syndromes are not always mutually exclusive. Diseases like MPGN and lupus nephritis can present with a mixed picture, and the same disease can shift from one presentation to the other. - Comprehensive Clinical Nephrology, 7th Ed.
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