Membranoproliferative glomerulonephritis risk factors
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Membranoproliferative glomerulonephritis is associated with several disease than can categorize in to several groups. The most relevant conditions that have strong evidence behind them to prove the correlation of them with MPGN are included:[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 those are associated with MPGN and each of this disease have their own potential to increase the risk of occurring MPGN.
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
- Lymphoma
- Leukemia
- Carcinoma
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.