Membranoproliferative glomerulonephritis: Difference between revisions

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== [[Membranoproliferative glomerulonephritis historical perspective|Historical Perspective]] ==
== [[Membranoproliferative glomerulonephritis historical perspective|Historical Perspective]] ==
* The term membranous glomerulonephritis was used first by Bell in 1946 to describe a category of glomerular renal disease classified within the spectrum of Ellis type II glomerulonephritis. This category also included lipoid nephrosis, lobular glomerulonephritis, and chronic glomerulonephritis .


The term membranous glomerulonephritis was used first by Bell in 1946 to describe a category of glomerular renal disease classified within the spectrum of Ellis type II glomerulonephritis. This category also included lipoid nephrosis, lobular glomerulonephritis, and chronic glomerulonephritis .
* In 1957, David Jones, a renal pathologist from Syracuse University in New York, separated membranous glomerulonephritis as a distinct morphologic entity using the special stain periodic acid–silver methenamine (now known as Jones stain). Jones fully illustrated the special features of this lesion such as lobular glomerulonephritis (now known as membranoproliferative glomerulonephritis), lipoid nephrosis (now known as minimal change disease), and chronic glomerulonephritis (now known as focal and segmental glomerulosclerosis). The thickening of the capillary wall and alteration in basement membrane structure, so characteristic of the membranous lesion, were convincingly shown . 


In 1957, David Jones, a renal pathologist from Syracuse University in New York, separated membranous glomerulonephritis as a distinct morphologic entity using the special stain periodic acid–silver methenamine (now known as Jones stain). Jones fully illustrated the special features of this lesion such as lobular glomerulonephritis (now known as membranoproliferative glomerulonephritis), lipoid nephrosis (now known as minimal change disease), and chronic glomerulonephritis (now known as focal and segmental glomerulosclerosis). The thickening of the capillary wall and alteration in basement membrane structure, so characteristic of the membranous lesion, were convincingly shown . 
* The electron-dense subepithelial location of the were also subsequently identified by Movat and McGregor in 1959 using electron microscopic methods applied to renal biopsy specimens in 1957. Mellors  in 1957 had identified the third component of the unique lesion of membranous glomerulonephritis; namely, the presence of immunoglobulin in the deposits, using the immunofluorescence technique. Thus, over the span of just 2 years, the triad of essential features of membranous glomerulonephritis were delineated. These are still the fundamental features used today to identify membranous glomerulonephritis, now called Membranoproliferative glomerulonephritis.
 
The electron-dense subepithelial location of the were also subsequently identified by Movat and McGregor in 1959 using electron microscopic methods applied to renal biopsy specimens in 1957. Mellors  in 1957 had identified the third component of the unique lesion of membranous glomerulonephritis; namely, the presence of immunoglobulin in the deposits, using the immunofluorescence technique. Thus, over the span of just 2 years, the triad of essential features of membranous glomerulonephritis were delineated. These are still the fundamental features used today to identify membranous glomerulonephritis, now called Membranoproliferative glomerulonephritis.


== [[Membranoproliferative glomerulonephritis classification|Classification]] ==
== [[Membranoproliferative glomerulonephritis classification|Classification]] ==

Revision as of 13:06, 25 June 2018

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Membranoproliferative glomerulonephritis
ICD-10 N00-N08 with .2 suffix
ICD-9 581.2, 582.2, 583.2
MeSH D015432

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Overview

Membranoproliferative Glomerulonephritis (MPGN) is a relatively uncommon inflammatory glomerulopathy that can cause chronic nephritis. Based on the histological pattern of glomerular injury it has been described as a chronic kidney disease found mostly in children and young adults. Like many forms of glomerulopathies, membranoproliferative glomerulonephritis (glomerulopathy) has been a diagnosis of tissue pathology rather the diagnosis of a specific disease entity. Therefore, the term membranoploriferative glomerulonephritis (MPGN) relates to a pattern of glomerular injury characterized by mesangial proliferation and expansion, lobularization of the glomerular tufts and double contours which can be caused by many disease states [1]. Glomerular injury occurs due to deposition of immune complexes on the glomerular mesangium or on the glomerular basement membrane. MPGN has been categorized into 3 types based on the histological pattern of glomerular damage. Clinically, MPGN often present with hematuria, varying degrees of proteinuria, with or without Glomerular filtration rate impairment depending on the severity of glomerular injury, and the underlying etiology.

Historical Perspective

  • The term membranous glomerulonephritis was used first by Bell in 1946 to describe a category of glomerular renal disease classified within the spectrum of Ellis type II glomerulonephritis. This category also included lipoid nephrosis, lobular glomerulonephritis, and chronic glomerulonephritis .
  • In 1957, David Jones, a renal pathologist from Syracuse University in New York, separated membranous glomerulonephritis as a distinct morphologic entity using the special stain periodic acid–silver methenamine (now known as Jones stain). Jones fully illustrated the special features of this lesion such as lobular glomerulonephritis (now known as membranoproliferative glomerulonephritis), lipoid nephrosis (now known as minimal change disease), and chronic glomerulonephritis (now known as focal and segmental glomerulosclerosis). The thickening of the capillary wall and alteration in basement membrane structure, so characteristic of the membranous lesion, were convincingly shown . 
  • The electron-dense subepithelial location of the were also subsequently identified by Movat and McGregor in 1959 using electron microscopic methods applied to renal biopsy specimens in 1957. Mellors  in 1957 had identified the third component of the unique lesion of membranous glomerulonephritis; namely, the presence of immunoglobulin in the deposits, using the immunofluorescence technique. Thus, over the span of just 2 years, the triad of essential features of membranous glomerulonephritis were delineated. These are still the fundamental features used today to identify membranous glomerulonephritis, now called Membranoproliferative glomerulonephritis.

Classification

Classification of MPGN based on immunofluorescence microscopy is a result of all advances in the understanding of the pathogenesis of the disease. Based on this advanced techniques, there are three types of MPGN [2];

  • Immune-complex-mediated MPGN (Type I)
  • Complement-mediated MPGN (Type II)
  • Non-Ig/complement-mediated MPGN (Type III)

Pathophysiology

Causes

Differentiating Membranoproliferative glomerulonephritis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or 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


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  1. Lionaki S, Gakiopoulou H, Boletis JN (2016). "Understanding the complement-mediated glomerular diseases: focus on membranoproliferative glomerulonephritis and C3 glomerulopathies". APMIS. 124 (9): 725–35. doi:10.1111/apm.12566. PMID 27356907.
  2. Sethi S, Fervenza FC (2011). "Membranoproliferative glomerulonephritis: pathogenetic heterogeneity and proposal for a new classification". Semin Nephrol. 31 (4): 341–8. doi:10.1016/j.semnephrol.2011.06.005. PMID 21839367.