Membranoproliferative glomerulonephritis risk factors: Difference between revisions
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== Overview == | == Overview == | ||
{{Membranoproliferative glomerulonephritis}} | {{Membranoproliferative glomerulonephritis}} | ||
Membranoproliferative glomerulonephritis is associated with several | Membranoproliferative glomerulonephritis is associated with several diseases that can be categorized in to several groups. The most relevant conditions are :<ref name=":0">{{Cite journal|last=Fernando C. Fervenza, Sanjeev Sethi and Richard J. Glassock|first=|date=2012|title=Idiopathic membranoproliferative glomerulonephritis: does it exist?|url=|journal=Nephrology Dialysis Transplantation|volume=|pages=|via=}}</ref> | ||
* Chronic infections | * Chronic infections | ||
* [[Autoimmune diseases]] | * [[Autoimmune diseases]] | ||
* Chronic liver disease ([[cirrhosis]] and [[alpha1-antitrypsin deficiency]]) | * Chronic liver disease ([[cirrhosis]] and [[alpha1-antitrypsin deficiency]]) | ||
* Chronic and recovered thrombotic | * Chronic and recovered thrombotic microangiopathies | ||
* [[Paraprotein]] deposition diseases | * [[Paraprotein]] deposition diseases | ||
* Malignant [[neoplasms]] | * Malignant [[neoplasms]] | ||
| Line 13: | Line 13: | ||
== [[Membranoproliferative glomerulonephritis risk factors|Risk Factors]] == | == [[Membranoproliferative glomerulonephritis risk factors|Risk Factors]] == | ||
There are too many conditions that are associated with MPGN and each of | There are too many conditions that are associated with MPGN and each of them have their own potential to increase the risk of MPGN. | ||
{| class="wikitable" | {| class="wikitable" | ||
Revision as of 19:25, 25 July 2018
Overview
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Membranoproliferative glomerulonephritis is associated with several diseases that can be categorized in to several groups. The most relevant conditions are :[1]
- Chronic infections
- Autoimmune diseases
- Chronic liver disease (cirrhosis and alpha1-antitrypsin deficiency)
- Chronic and recovered thrombotic microangiopathies
- Paraprotein deposition diseases
- Malignant neoplasms
- Genetic mutations
Risk Factors
There are too many conditions that are associated with MPGN and each of them have their own potential to increase the risk of MPGN.
| Risk Factor | |||
|---|---|---|---|
| Immune complex–mediated disease |
Autoimmune
Chronic infections
|
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| thrombotic microangiopathies |
|
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| Paraprotein deposition diseases |
|
||
| Malignant neoplasms |
Conditions associated with a membranoproliferative pattern of injury are listed as follows:
- Immune complex–mediated disease
- Idiopathic forms of MPGN or of unknown association[1]
- MPGN type I
- MPGN type II or dense deposit disease and PLD
- MPGN type III
- Autoimmune diseases[2][3][4]
- Systemic lupus erythematosus (SLE)
- Sjögren syndrome
- Rheumatoid arthritis
- Inherited complement deficiencies, in particular, C2 deficiency
- Scleroderma
- Celiac disease
- Chronic infections[5]
- Viral - Hepatitis B, hepatitis C, and cryoglobulinemia type II
- Bacterial - Endocarditis, infected ventriculoatrial (or jugular) shunt, multiple visceral abscesses, leprosy
- Protozoal - Malaria, schistosomiasis
- Other infections - Mycoplasma, Lyme Disease[6]
- Miscellaneous - Chronic liver disease (cirrhosis and alpha1-antitrypsin deficiency)
- Idiopathic forms of MPGN or of unknown association[1]
- Chronic and recovered thrombotic microangiopathies
- Healing phase of hemolytic uremic syndrome and/or thrombotic thrombocytopenic purpura
- Syndromes of circulating antiphospholipid (anticardiolipin) antibodies
- Radiation nephritis
- Nephropathy associated with bone marrow transplantation
- Sickle cell anemia and polycythemia
- Transplant glomerulopathy
- Paraprotein deposition diseases
- Glomerulonephropathies associated with cryoglobulinemia type I
- Waldenström macroglobulinemia
- Immunotactoid glomerulopathy
- Immunoglobulin light chain or heavy chain deposition diseases
- Fibrillary glomerulonephritis
- Genetic mutation
- Deletion of Lys224 in regulatory domain 4 of Factor H
- A study demonstrated that a delegation of a single Lys residue (K224) located within the complement regulatory region in domain 4 of Factor H will resulted in defected complement control . Mutant protein purified from the plasma of patients, so on laboratories test they showed severely reduced cofactor and decay-accelerating activity, as well as diminished attachment to the core complement component C3b. Albeit, cell-binding activity of the mutant protein was normal and comparable to wild-type Factor H.
- Deletion of Lys224 in regulatory domain 4 of Factor H
- Malignant neoplasms
References
- ↑ 1.0 1.1 Fernando C. Fervenza, Sanjeev Sethi and Richard J. Glassock (2012). "Idiopathic membranoproliferative glomerulonephritis: does it exist?". Nephrology Dialysis Transplantation.
- ↑ H. Terence Cook and Matthew C. Pickering (2014). "Histopathology of MPGN and C3 glomerulopathies". NATURE REVIEWS NEPHROLOGY.
- ↑ MICHELINE LEVY, MARIE-CLAIRE GUBLER, MIREILLE SICH, AGNES BEZIAU, AND RENE HABIB (1978). "lmmunopathology Glomerulonephritis of Membranoproliferative with Subendothelial Deposits". clinical immunology and immunopathology.
- ↑ Mårten Segelmark, Thomas Hellmark (2010). "Autoimmune kidney diseases". Elsevier.
- ↑ C Licht, S Heinen, M Jo ́zsi, I Lo ̈schmann, RE Saunders, SJ Perkins, R Waldherr, C Skerka, M Kirschfink, B Hoppe and PF Zipfel (2006). "Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II)". International Society of Nephrology.
- ↑ Dimitrios Kirmizis, MD, Georgios Efstratiadis, MD, Dominiki Economidou, MD, Evdoxia Diza-Mataftsi, MD, Maria Leontsini, MD, and Dimitrios Memmos, MD (2004). "MPGN Secondary to Lyme Disease". American Journal of Kidney Diseases. 43.