Nephritis: Glomerulonephritis - The Causes

Nephritis is defined as a condition of inflammation of the nephrons in the kidneys.
Glomerulonephritis is defined as the condition of inflammation of the tiny filters in  kidneys (glomeruli), which filter blood by removing excess fluid, electrolytes and waste and pass them through urination.  

B.1. Causes
1. Infections
In the study of Glomerulonephritis causing acute renal failure during the course of bacterial infections of of four male patients, aged 53-71 years, who developed GN and ARF following bacterial infections, showed that
a. The first two patients developed GN with immunoglobulin A (IgA) deposits after infections with hospital-acquired methicillin resistant Staphylococcus aureus (MRSA). Clinical, serologic and histological features, classification of GN and treatment differed between the two patients.
b. The third patient developed simultaneous acute rheumatic fever and post-streptococcal GN causing severe ARF requiring hemodialysis. Complete recovery of ARF and migratory polyarthritis followed initiation of corticosteroids.
c. The fourth patient developed ARF and cerebral vasculitis following a prolonged course of Streptococcus mutans endocarditis with delayed diagnosis. He also developed multiple serological abnormalities including elevated titers of antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), anti-phospholipid antibodies, rheumatoid factor, and modest hypocomplementemia(6).

2. Lupus
In the study of Distinct roles for complement in glomerulonephritis and atherosclerosis revealed in mice with a combination of lupus and hyperlipidemia by Dr. Lewis MJ and the research team at the Imperial College London showed that accelerated atherosclerosis and renal inflammation in SLE are closely linked via immune complex formation and systemic complement depletion. However, whereas hyperlipidemia will enhance renal immune complex-mediated complement activation and the development of nephritis, accelerated atherosclerosis is, instead, related to complement depletion and a reduction in the uptake of apoptotic/necrotic debris(7).

3. Goodpasture's disease
In the study of the Progression from Goodpasture's disease to membranous glomerulonephritis, according to the research team at the Department of Renal Medicine, Concord Hospital, Sydney, thwew is report of an unusual case of a patient with Goodpasture's disease presenting with hemoptysis, severe iron deficiency anemia and microscopic hematuria and proteinuria.... Nine months after presentation he developed nephrotic range proteinuria and a repeat renal biopsy revealed membranous glomerulonephritis with no evidence of his original disease(8).

4.  IgA nephropathy
IgA nephropathy is an autoimmune disease, affecting the kidneys
IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23(9).

5. Polyarteritis nodosa (PAN)
Polyarteritis nodosa (PAN) is defined as a vasculitis of medium & small-sized arteries
There is a report of a 53-year-old man with hepatitis C virus (HCV) infection underwent cholecystectomy for presumed cholecystitis. Gallstones were not present, and histological examination demonstrated medium-sized arteritis, consistent with polyarteritis nodosa (PAN). The patient later developed rapidly progressive glomerulonephritis. Kidney biopsy demonstrated cryoglobulinemic glomerulonephritis(10).

6. Polyangiitis (Wegener's granulomatosis)
Polyangiitis is defined as a vasculitis of small-sized blood vessels. Granulomatosis with polyangiitis (GPA), is the recently proposed, new alternative name for Wegener's granulomatosis. It defines a systemic small-vessels vasculitis, characterized by frequent involvement of upper and lower respiratory tract. According to Dr. Karras A, and the research team at hôpital Européen Georges-Pompidou, service de néphrologie(11).

7. Other causes
a. Homozygous C1q deficiency
According to the study of in mice, Dr. Botto M and the research team at the Imperial College School of Medicine, indicated that among mice without glomerulonephritis, there were significantly greater numbers of glomerular apoptotic bodies in C1q-deficient mice compared with controls. The phenotype associated with C1q deficiency was modified by background genes. These findings are compatible with the hypothesis that C1q deficiency causes autoimmunity by impairment of the clearance of apoptotic cells(12).

b.  Deficiency of factor H
Factor H is a member of the regulators of complement activation family, a complement control protein. Factor H, the main regulator of this activation, prevents formation and promotes dissociation of the C3 convertase enzyme, and, together with factor I, mediates the proteolytic inactivation of C3b. Factor H deficiency, described in 29 individuals from 12 families and in pigs, allows unhindered activation of fluid-phase C3 and severe depletion of plasma C3 (ref. 11). Membranoproliferative glomerulonephritis (MPGN) occurs in factor H-deficient humans and pigs(13). 
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Sources
(6) http://www.ncbi.nlm.nih.gov/pubmed/18247152
(7) http://www.ncbi.nlm.nih.gov/pubmed/22392450
(8) http://www.ncbi.nlm.nih.gov/pubmed/8532389
(9) http://www.ncbi.nlm.nih.gov/pubmed/11062479
(10) http://www.ncbi.nlm.nih.gov/pubmed/16775442
(11) http://www.ncbi.nlm.nih.gov/pubmed/22902722
(12) http://www.ncbi.nlm.nih.gov/pubmed/9590289 
(13) http://www.ncbi.nlm.nih.gov/pubmed/12091909