Focal segmental glomerulosclerosis causes
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Differentiating Focal segmental glomerulosclerosis from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief:’’’ Cafer Zorkun, M.D., Ph.D. [2]
Overview
Causes
According to D'Agati and colleagues[1], FSGS may be primary of secondary. Primary FSGS is defined as idiopathic FSGS, whereas secondary FSGS is defined as FSGS due to the adaptive structural-functional response mediated by glomerular hypertrophy or hyperfiltration.[1]
- Primary (idiopathic) FSGS
- C1q nephropathy
- HIV-associated nephropathy
- Heroin nephropathy
- Familial FSGS
- Autosomal dominant mutation in alpha-actinin 4
- Autosomal recessive mutation in podocin
- Mitochondrial cytopathies
- Drug toxicities
- Pamidronate
- Lithium
- Interferon-alpha
- Secondary FSGS
- Reduced renal mass
- Oligomeganephronia
- Unilateral renal agenesis
- Renal dysplasia
- Reflux nephropathy
- Sequela to cortical necrosis
- Surgical renal ablation
- Any advanced renal disease with reduction in functioning nephrons
- Chronic allograft nephropathy
- Initial normal renal mass
- Diabetes mellitus
- Hypertension
- Obesity
- Cyanotic congenital heart disease
- Sickle cell anemia
- Reduced renal mass
- Non-specific pattern of FSGS caused by renal scarring
- Focal proliferative glomerulonephritis
- IgA nephropathy
- Lupus nephritis
- Pauci-immune focal necrotizing and crescentic glomerulonephritis
- Hereditary nephritis
- Diabetic nephropathy
- Hypertensive arterionephrosclerosis
- Membranous glomerulopathy
- Thrombotic microangiopathies
- Focal proliferative glomerulonephritis
References
- ↑ 1.0 1.1 D'Agati V (2003). "Pathologic classification of focal segmental glomerulosclerosis". Semin Nephrol. 23 (2): 117–34. doi:10.1053/snep.2003.50012. PMID 12704572.