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Understand the genetic and environmental factors causing FSGS, including mutations and virus associations, with a focus on renal pathologies and disease management.
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Primary (idiopathic) FSGS 4. Mediated by adaptive structural-functional responses Secondary FSGS A. Reduced renal mass 1. Familial/genetic Oligomeganephronia Unilateral renal agenesis A. Mutations in -actinin 4 B. Mutations in podocin Renal dysplasia C. Mutations in WT-1 Reflux nephropathy D. Mutations in integrin Sequela to cortical necrosis Surgical renal ablation 2. Virus-associated Chronic allograft nephropathy A. HIV-1 (HIV-associated nephropathy) Renal disease with reduction in functioning nephrons B. Parvovirus B19 B. Initially normal renal mass 3. Drug-induced Hypertension A. Heroin (heroin nephropathy) Atheroemboli or other acute vaso-occlusive B. Interferon- Obesity C. Lithium Cyanotic congenital heart disease D. Pamidronate Sickle cell anemia Classificação etiológica de GESF – AJKD, 2004
Grupo I- membranosa sem GESF Grupo II- membranosa com GESF
Grupo I- membranosa sem GESF Grupo II- membranosa com GESF
Grupo I- membranosa sem GESF Grupo II- membranosa com GESF