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 | The term membranous glomerulonephritis was used first by Bell in1946 to describe a category of glomerular renal disease classified within the spectrum of Ellis type II glomerulonephritis, characterized clinically by a more insidious onset and marked proteinuria and edema. This category also included lipoid nephrosis, lobular glomerulonephritis, and chronic glomerulonephritis (not otherwise specified). Thus, membranous glomerulonephritis (later to morph into MN) was “lumped” together with other histologic lesions subsumed by the Ellis classification of glomerulonephritis.[null 6] In 1957, David Jones,[null 1] 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), applied to human renal biopsy specimens. In this seminal study, Jones[null 1] fully illustrated the special features of this lesion not shared by other lesions, 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 (Fig 1). The electron-dense subepithelial location of the deposits occupying the spaces between the altered glomerular basement membrane (GBM) also subsequently were identified by Movat and McGregor[null 7] in 1959 using electron microscopic methods applied to renal biopsy specimens pioneered by Farquhar et al[null 8] in 1957. Mellors et al[null 9] 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 described by Coons and Kaplan[null 10] in 1950. Thus, in a burst of morphologic investigations using newly developed technology, over the span of just 2 years, the triad of essential (diagnostic) features of the lesion of membranous glomerulonephritis were delineated; namely, alteration in basement membrane structure, subepithelial electron-dense deposits, the latter containing immunoglobulin G (IgG). These are still the fundamental features used today to identify membranous glomerulonephritis (called extramembranous glomerulonephritis or epimembranous nephropathy by some Europeans), henceforth called MN in this essay. | ||
== [[Membranoproliferative glomerulonephritis classification|Classification]] == | == [[Membranoproliferative glomerulonephritis classification|Classification]] == | ||
Revision as of 19:59, 10 June 2018
| https://https://www.youtube.com/watch?v=uriIHhO5kVQ%7C350}} |
| Membranoproliferative glomerulonephritis | |
| ICD-10 | N00-N08 with .2 suffix |
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| ICD-9 | 581.2, 582.2, 583.2 |
| MeSH | D015432 |
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Membranoproliferative glomerulonephritis Microchapters |
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Differentiating Membranoproliferative glomerulonephritis from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Membranoproliferative glomerulonephritis On the Web |
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American Roentgen Ray Society Images of Membranoproliferative glomerulonephritis |
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Directions to Hospitals Treating Membranoproliferative glomerulonephritis |
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Risk calculators and risk factors for Membranoproliferative glomerulonephritis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ali Poyan Mehr, M.D. [2]; Associate Editor-In-Chief: Olufunmilola Olubukola M.D.[3]Cafer Zorkun, M.D., Ph.D. [4]
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 in1946 to describe a category of glomerular renal disease classified within the spectrum of Ellis type II glomerulonephritis, characterized clinically by a more insidious onset and marked proteinuria and edema. This category also included lipoid nephrosis, lobular glomerulonephritis, and chronic glomerulonephritis (not otherwise specified). Thus, membranous glomerulonephritis (later to morph into MN) was “lumped” together with other histologic lesions subsumed by the Ellis classification of glomerulonephritis.[null 6] In 1957, David Jones,[null 1] 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), applied to human renal biopsy specimens. In this seminal study, Jones[null 1] fully illustrated the special features of this lesion not shared by other lesions, 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 (Fig 1). The electron-dense subepithelial location of the deposits occupying the spaces between the altered glomerular basement membrane (GBM) also subsequently were identified by Movat and McGregor[null 7] in 1959 using electron microscopic methods applied to renal biopsy specimens pioneered by Farquhar et al[null 8] in 1957. Mellors et al[null 9] 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 described by Coons and Kaplan[null 10] in 1950. Thus, in a burst of morphologic investigations using newly developed technology, over the span of just 2 years, the triad of essential (diagnostic) features of the lesion of membranous glomerulonephritis were delineated; namely, alteration in basement membrane structure, subepithelial electron-dense deposits, the latter containing immunoglobulin G (IgG). These are still the fundamental features used today to identify membranous glomerulonephritis (called extramembranous glomerulonephritis or epimembranous nephropathy by some Europeans), henceforth called MN in this essay.
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
et:Membranoproliferatiivne glomerulonefriit
- ↑ 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.
- ↑ 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.