Nephrotic syndrome vs nephritic syndrome
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Nephrotic Syndrome vs. Nephritic Syndrome
These two syndromes reflect fundamentally different patterns of glomerular injury, and distinguishing them is one of the most important skills in clinical nephrology.
Core Pathophysiology
Nephrotic Syndrome
The glomerular injury is primarily a loss of the filtration barrier's permeability, allowing massive protein leak. The glomerular capillary wall (endothelium + GBM + podocytes) normally acts as both a size and charge barrier. When this barrier is disrupted - structurally or physicochemically - plasma proteins escape into the urine.
Nephritic Syndrome
The injury is primarily glomerular inflammation. Proliferation of glomerular cells and infiltration by leukocytes severely injures capillary walls, allowing blood into the urine and causing hemodynamic changes that reduce GFR. The reduced GFR leads to oliguria, fluid retention, and azotemia. Hypertension results from both fluid retention and renin release from ischemic kidneys.
- Robbins, Cotran & Kumar Pathologic Basis of Disease, pp. 843-844
Comparison Table
| Feature | Nephrotic | Nephritic |
|---|---|---|
| Onset | Insidious | Abrupt |
| Proteinuria | Massive (>3.5 g/day) | Mild-moderate (<3.5 g/day) |
| Hematuria | Absent or mild | +++ (hallmark) |
| RBC casts | Absent | Present |
| Edema | ++++ (soft, pitting, periorbital) | ++ |
| Blood pressure | Normal | Raised (hypertension) |
| Serum albumin | Low (<3 g/dL) | Normal or slightly reduced |
| JVP | Normal/low | Raised |
| GFR | Usually preserved initially | Reduced (oliguria, azotemia) |
| Complement | Usually normal | Often low (e.g., C3 low in post-strep GN, MPGN) |
- Comprehensive Clinical Nephrology, 7th Edition, Table 16.4
Nephrotic Syndrome - Key Features
Pathophysiology Chain
- Increased glomerular permeability → massive proteinuria
- Hypoalbuminemia (liver synthesis overwhelmed; renal catabolism of filtered albumin also contributes)
- Low plasma oncotic pressure → fluid shifts into interstitium → pitting edema (periorbital, dependent areas, pleural effusions, ascites)
- Hyperlipidemia: increased hepatic lipoprotein synthesis, abnormal lipid transport, decreased catabolism → elevated cholesterol, TG, VLDL, LDL, Lp(a); decreased HDL in some
- Lipiduria: lipoproteins leak across the GBM, appear as oval fat bodies or free fat in urine
Complications
- Infections - especially staphylococcal and pneumococcal, due to loss of immunoglobulins in urine
- Thromboembolism - loss of antithrombin III and other endogenous anticoagulants creates a hypercoagulable state; renal vein thrombosis is a consequence (not a cause), especially in membranous nephropathy
- Hyperlipidemia-related cardiovascular risk
Causes by Age (Approximate Prevalence)
| Cause | Children | Adults |
|---|---|---|
| Minimal change disease | 75% | 8% |
| Focal segmental glomerulosclerosis (FSGS) | 10% | 35% |
| Membranous nephropathy | 3% | 30% |
| MPGN / dense deposit disease | 10% | 10% |
| Systemic causes | Rare | Common |
Systemic causes in adults include: diabetes mellitus (most common worldwide), amyloidosis, SLE, drugs (NSAIDs, penicillamine, heroin).
- Robbins, Cotran & Kumar, Table 20.7
Nephritic Syndrome - Key Features
Core Clinical Features
- Hematuria - red blood cells and RBC casts in urine (pathognomonic of glomerular origin)
- Proteinuria - subnephrotic range, with or without edema
- Azotemia - elevated BUN/creatinine from reduced GFR
- Hypertension - from sodium/water retention + renin release
- Oliguria
The classic presentation is post-streptococcal GN in children: brown urine (hematuria without clots), rapid onset edema over days, hypertension, RBC casts. Serum albumin is usually normal. Low C3 (complement consumed by immune complex activation) with normal C4 is characteristic.
Causes (Primary Glomerular Diseases)
- Acute proliferative (post-infectious) GN - most common; nephritogenic strains of Group A β-hemolytic streptococcus (M types 1, 4, 12); latent period 1-4 weeks after pharyngitis or impetigo
- Rapidly Progressive GN (RPGN) / Crescentic GN - nephritic syndrome + rapid decline in function over days to weeks; histologically shows "crescents" in Bowman's space
- Type 1: Anti-GBM antibodies (Goodpasture syndrome)
- Type 2: Immune complex deposition (lupus, post-infectious)
- Type 3: Pauci-immune / ANCA-associated vasculitis (GPA, MPA)
- IgA nephropathy (Berger's disease) - most common GN worldwide; episodic hematuria with upper respiratory infections
- Lupus nephritis (proliferative forms)
Overlap and Mixed Presentations
The classification is not absolute. Some diseases can present with either or both patterns:
- MPGN (membranoproliferative GN) - can present as nephrotic, nephritic, or both
- Lupus nephritis - various classes span both spectra
- Severe nephrotic syndrome can develop RBC casts in advanced disease
The syndromes serve as clinical starting points to narrow the differential, not as rigid diagnostic boxes.
- Comprehensive Clinical Nephrology, 7th Edition, p. 243
Memory Aid
| NephrOTic | NephrITic | |
|---|---|---|
| Key word | O = Oedema (massive) | IT = InflamITis, hemaTuria |
| Mechanism | Leak (protein out) | Inflammation (blood leaks in) |
| Urine | Protein, fat, oval fat bodies | RBCs, RBC casts |
| Albumin | Low | Normal |
| BP | Normal | High |
| Complement | Usually normal | Often low |
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