Rapidly progressive glomerulonephritis classification

Rapidly progressive glomerulonephritis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Rapidly progressive glomerulonephritis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray Findings
CT-scan Findings
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Rapidly progressive glomerulonephritis classification On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Rapidly progressive glomerulonephritis classification All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Rapidly progressive glomerulonephritis classification
CDC on Rapidly progressive glomerulonephritis classification
Rapidly progressive glomerulonephritis classification in the news
Blogs on Rapidly progressive glomerulonephritis classification
Directions to Hospitals Treating Rapidly progressive glomerulonephritis
Risk calculators and risk factors for Rapidly progressive glomerulonephritis classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Classification

RPGN is classified on the basis of the cause of crescent formation resulting from glomerular injury

Type I

• Type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM).
• Type I also known as anti-GBM glomerulonephritis.
• The antibodies formed are known as anticollagen antibodies and react against type IV collagen of GBM.
• The antibodies can be produced by a stimulus such as viral URTI that exposes alveolar collagen membrane or it can be idiopathic.
• The antibodies formed can act against alveolar membrane and lungs get involved in some cases such as in goodpasture syndrome.

Type II

• Type II RPGN is caused by the deposition of immune complexes in the GBM.
• Immune complexes can be formed in certain infections or in connective tissue disorders.
• These immune complexes deposit over the GBM and activate the complement system resulting in crescent formation.
• Examples include:
• Postinfectious (staphylococci/streptococci)
• Connective tissue disorders
• Lupus nephritis
• Henoch-Schönlein purpural)
• Immunoglobulin A nephropathy
• Mixed cryoglobulinemia
• Membranoproliferative glomerulonephritis

Type III

• Type III RPGN is also known as pauci immune RPGN.
• There are no anti GBM antibodies or no immune complexes involved.
• It occurs due to the activation of neutrophils in the GBM which is caused by the presence of ANCA(p-ANCA or c-ANCA).
• Systemic vasculitis is present in most of the cases but some occur without systemic involvement and only renal findings maybe present.
• Examples include
  • Granulomatosis with polyangiitis (Wegener granulomatosis)
  • Microscopic polyangiitis (MPA)
  • Renal-limited necrotizing crescentic glomerulonephritis (NCGN)
  • Eosinophilic granulomatosis with polyangiitis (EGPA; Churg-Strauss syndrome)

.