Table 1.
Main causes of secondary FSGS (adapted from KDIGO guidelines 2012 for glomerulonephritis [4])
| Causes of secondary FSGS | |
|---|---|
| Genetic | Mutations in the genes coding for crucial podocyte proteins: |
| Mutations in ACTN4 (α-actinin 4), mutations in NPHS1 (nephrin), mutations in NPHS2 (podocin), mutations in WT-1 (Wilms tumor 1), mutations in TRPC6 (transient receptor potential cation channel subfamily C member 6), mutations in SCARB2 (lysosomal integral membrane protein 2), mutations in INF2 (formin), mutations in CD2-associated protein, others: PAX-2 (paired box protein Pax-2), MYO1E (unconventional myosin-Ie), among others [11] | |
| Mitochondrial cytopathies | |
| Apolipoprotein L1 risk variants: associated to APOL1(apolipoprotein L1) polymorphisms | |
| Associated with infectious diseases | Secondary to viral infections: human immunodeficiency virus, parvovirus B19, hepatitis virus B and C, cytomegalovirus, Epstein–Barr virus, varicella zoster |
| Secondary to parasite or bacterial infections: malaria, syphilis, toxoplasmosis | |
| Medication | Medication or drug consumption induced: heroin, interferon-α, lithium, pamidronate/alendronate, anabolic steroids |
| Adaptive structural–functional responses likely due to hypertrophy or hyperfiltration | Reduced kidney mass: oligomeganephronia, unilateral kidney agenesis, kidney dysplasia,cortical necrosis, reflux nephropathy, surgical kidney ablation, chronic allograft nephropathy, any advanced kidney disease with reduction in functioning nephrons |
| Initially normal kidney mass: diabetes mellitus, hypertension, obesity, cyanotic congenital heart disease, sickle cell anaemia | |
| Malignancy | Associated mainly with lymphoma |
| Non-specific pattern of FSGS | Produced secondary to the scarring due to the presence of other glomerulopathies: focal proliferative glomerulonephritis (immunoglobulin A nephropathy, lupus nephritis, pauci-immune focal necrotizing and crescentic glomerulonephritis), hereditary nephritis (Alport syndrome), membranous glomerulopathy, thrombotic microangiopathy, associated with apolipoprotein L1 (ApoL1) polymorphisms |