Focal segmental glomerulosclerosis causes
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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, 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.
- 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