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):

Podocyte foot process effacement in nephrotic syndrome - normal (left) vs effaced (right)

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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