Membranoproliferative glomerulonephritis risk factors: Difference between revisions
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==== Autoimmune ==== | ==== Autoimmune ==== | ||
* Systemic lupus erythematosus (SLE), | * [[Systemic lupus erythematosus]] (SLE), | ||
* Sjögren syndrome | * [[Sjögren syndrome]] | ||
* Rheumatoid arthritis | * [[Rheumatoid arthritis]] | ||
* Inherited complement deficiencies (in particular, C2 deficiency) | * Inherited [[complement]] deficiencies (in particular, C2 deficiency) | ||
* Scleroderma | * [[Scleroderma]] | ||
* Celiac | * [[Celiac disease]] | ||
==== Chronic infections ==== | ==== Chronic infections ==== | ||
* Viral – Hepatitis B, hepatitis C, cryoglobulinemia type II | * Viral – [[Hepatitis B]], [[hepatitis C]], [[cryoglobulinemia]] type II | ||
* Bacterial – Endocarditis, infected ventriculoatrial (or jugular) shunt, multiple visceral abscesses, leprosy | * Bacterial – [[Endocarditis]], infected ventriculoatrial (or jugular) shunt, multiple visceral [[abscesses]], [[leprosy]] | ||
* Protozoal – Malaria, schistosomiasis | * Protozoal – Malaria, schistosomiasis | ||
! | ! | ||
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!thrombotic microangiopathies | !thrombotic microangiopathies | ||
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* Healing phase of hemolytic uremic syndrome (HUS) and/or thrombotic thrombocytopenic purpura (TTP) | * Healing phase of [[hemolytic uremic syndrome]] (HUS) and/or [[thrombotic thrombocytopenic purpura]] (TTP) | ||
* Syndromes of circulating antiphospholipid (anticardiolipin) antibodies | * Syndromes of circulating [[antiphospholipid (anticardiolipin) antibodies]] | ||
* Radiation nephritis | * [[Radiation nephritis]] | ||
* Nephropathy associated with bone marrow transplantation | * [[Nephropathy]] associated with [[bone marrow transplantation]] | ||
* Sickle cell anemia and polycythemia | * [[Sickle cell anemia]] and [[polycythemia]] | ||
* Transplant glomerulopathy | * Transplant [[glomerulopathy]] | ||
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!Paraprotein deposition diseases | !Paraprotein deposition diseases | ||
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* Glomerulonephropathies associated with cryoglobulinemia type I | * [[Glomerulonephropathies]] associated with [[cryoglobulinemia]] type I | ||
* Waldenström macroglobulinemia | * [[Waldenström macroglobulinemia]] | ||
* Immunotactoid glomerulopathy | * Immunotactoid [[glomerulopathy]] | ||
* Immunoglobulin light-chain or heavy-chain deposition diseases | * [[Immunoglobulin]] light-chain or heavy-chain deposition diseases | ||
* Fibrillary glomerulonephritis | * [[Fibrillary glomerulonephritis]] | ||
* Monoclonal gammopathy of unknown significance | * [[Monoclonal gammopathy]] of unknown significance | ||
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|- | |- | ||
!Malignant neoplasms | !Malignant [[neoplasms]] | ||
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* Lymphoma | * [[Lymphoma]] | ||
* Leukemia, and carcinoma are associated with a membranoproliferative pattern of renal injury. | * [[Leukemia]], and carcinoma are associated with a membranoproliferative pattern of renal injury. | ||
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:*:* MPGN type III | :*:* MPGN type III | ||
:* Autoimmune diseases<ref>{{Cite journal|last=H. Terence Cook and Matthew C. Pickering|first=|date=2014|title=Histopathology of MPGN and C3 glomerulopathies|url=|journal=NATURE REVIEWS NEPHROLOGY|volume=|pages=|via=}}</ref><ref>{{Cite journal|last=MICHELINE LEVY, MARIE-CLAIRE GUBLER, MIREILLE SICH, AGNES BEZIAU, AND RENE HABIB|first=|date=1978|title=lmmunopathology Glomerulonephritis of Membranoproliferative with Subendothelial Deposits|url=|journal=clinical immunology and immunopathology|volume=|pages=|via=}}</ref><ref>{{Cite journal|last=Mårten Segelmark, Thomas Hellmark|first=|date=2010|title=Autoimmune kidney diseases|url=|journal=Elsevier|volume=|pages=|via=}}</ref> | :* Autoimmune diseases<ref>{{Cite journal|last=H. Terence Cook and Matthew C. Pickering|first=|date=2014|title=Histopathology of MPGN and C3 glomerulopathies|url=|journal=NATURE REVIEWS NEPHROLOGY|volume=|pages=|via=}}</ref><ref>{{Cite journal|last=MICHELINE LEVY, MARIE-CLAIRE GUBLER, MIREILLE SICH, AGNES BEZIAU, AND RENE HABIB|first=|date=1978|title=lmmunopathology Glomerulonephritis of Membranoproliferative with Subendothelial Deposits|url=|journal=clinical immunology and immunopathology|volume=|pages=|via=}}</ref><ref>{{Cite journal|last=Mårten Segelmark, Thomas Hellmark|first=|date=2010|title=Autoimmune kidney diseases|url=|journal=Elsevier|volume=|pages=|via=}}</ref> | ||
:*:* Systemic lupus erythematosus (SLE) | :*:* [[Systemic lupus erythematosus]] (SLE) | ||
:*:* Sjögren syndrome | :*:* [[Sjögren syndrome]] | ||
:*:* Rheumatoid arthritis | :*:* [[Rheumatoid arthritis]] | ||
:*:* Inherited complement deficiencies, in particular, C2 deficiency | :*:* Inherited [[complement deficiencies]], in particular, C2 deficiency | ||
:*:* Scleroderma | :*:* [[Scleroderma]] | ||
:*:* Celiac disease | :*:* [[Celiac disease]] | ||
:* Chronic infections<ref>{{Cite journal|last=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|first=|date=2006|title=Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II)|url=|journal=International Society of Nephrology|volume=|pages=|via=}}</ref> | :* Chronic infections<ref>{{Cite journal|last=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|first=|date=2006|title=Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II)|url=|journal=International Society of Nephrology|volume=|pages=|via=}}</ref> | ||
:*:* Viral - Hepatitis B, hepatitis C, and cryoglobulinemia type II | :*:* Viral - [[Hepatitis B]], [[hepatitis C]], and [[cryoglobulinemia]] type II | ||
:*:* Bacterial - Endocarditis, infected ventriculoatrial (or jugular) shunt, multiple visceral abscesses, leprosy | :*:* Bacterial - [[Endocarditis]], [[infected ventriculoatrial (or jugular) shunt]], multiple [[visceral abscesses]], [[leprosy]] | ||
:*:* Protozoal - Malaria, schistosomiasis | :*:* Protozoal - [[Malaria]], [[schistosomiasis]] | ||
:*:* Other infections - Mycoplasma, Lyme Disease<ref>{{Cite journal|last=Dimitrios Kirmizis, MD, Georgios Efstratiadis, MD, Dominiki Economidou, MD, Evdoxia Diza-Mataftsi, MD, Maria Leontsini, MD, and Dimitrios Memmos, MD|first=|date=2004|title=MPGN Secondary to Lyme Disease|url=|journal=American Journal of Kidney Diseases|volume=43|pages=|via=}}</ref> | :*:* Other infections - [[Mycoplasma]], [[Lyme Disease]]<ref>{{Cite journal|last=Dimitrios Kirmizis, MD, Georgios Efstratiadis, MD, Dominiki Economidou, MD, Evdoxia Diza-Mataftsi, MD, Maria Leontsini, MD, and Dimitrios Memmos, MD|first=|date=2004|title=MPGN Secondary to Lyme Disease|url=|journal=American Journal of Kidney Diseases|volume=43|pages=|via=}}</ref> | ||
:* Miscellaneous - Chronic liver disease (cirrhosis and alpha1-antitrypsin deficiency) | :* Miscellaneous - [[Chronic liver disease]] ([[cirrhosis]] and [[alpha1-antitrypsin deficiency]]) | ||
* Chronic and recovered thrombotic microangiopathies | * Chronic and recovered thrombotic [[microangiopathies]] | ||
:* Healing phase of hemolytic uremic syndrome and/or thrombotic thrombocytopenic purpura | :* Healing phase of [[hemolytic uremic syndrome]] and/or [[thrombotic thrombocytopenic purpura]] | ||
:* Syndromes of circulating antiphospholipid (anticardiolipin) antibodies | :* Syndromes of circulating [[antiphospholipid (anticardiolipin) antibodies]] | ||
:* Radiation nephritis | :* Radiation [[nephritis]] | ||
:* Nephropathy associated with bone marrow transplantation | :* [[Nephropathy]] associated with [[bone marrow transplantation]] | ||
:* Sickle cell anemia and polycythemia | :* [[Sickle cell anemia]] and [[polycythemia]] | ||
:* Transplant glomerulopathy | :* Transplant [[glomerulopathy]] | ||
* Paraprotein deposition diseases | * [[Paraprotein]] deposition diseases | ||
:* Glomerulonephropathies associated with cryoglobulinemia type I | :* Glomerulonephropathies associated with [[cryoglobulinemia]] type I | ||
:* Waldenström macroglobulinemia | :* [[Waldenström macroglobulinemia]] | ||
:* Immunotactoid glomerulopathy | :* [[Immunotactoid glomerulopathy]] | ||
:* Immunoglobulin light chain or heavy chain deposition diseases | :* [[Immunoglobulin]] light chain or heavy chain deposition diseases | ||
:* Fibrillary glomerulonephritis | :* [[Fibrillary glomerulonephritis]] | ||
* Genetic mutation | * Genetic mutation | ||
** Deletion of Lys224 in regulatory domain 4 of Factor H | ** 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. | *** 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. | ||
* Malignant neoplasms | * Malignant neoplasms | ||
:* Lymphoma | :* [[Lymphoma]] | ||
:* Leukemia | :* [[Leukemia]] | ||
:* Carcinoma | :* [[Carcinoma]] | ||
==References== | ==References== | ||
Revision as of 19:22, 25 July 2018
Overview
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Membranoproliferative glomerulonephritis is associated with several disease that can be categorize 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 this disease 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 |
|
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| 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.