How are primary and secondary FSGS distinguished?

Primary FSGS: nephrotic syndrome, diffuse podocyte foot process effacement (>80%), high recurrence post-transplant (~30-40%). Secondary: incomplete effacement (<80%), non-nephrotic proteinuria, usually from adaptive hyperfiltration, HIV, or drugs.

What genetic variants cause FSGS?

Podocin (NPHS2), nephrin (NPHS1), alpha-actinin-4 (ACTN4), TRPC6, and WT1 are key FSGS genes. Genetic FSGS does not respond to immunosuppression and has low recurrence post-transplant.

Primary FSGS: high-dose prednisone (1 mg/kg/day) for 4-6 months as first line. Calcineurin inhibitors for steroid-resistant cases. Secondary FSGS: treat underlying cause and add RAAS blockade.

FSGS Primary vs Secondary Etiology Score

Differentiate primary FSGS (immune-mediated, nephrotic syndrome) from secondary FSGS (adaptive, HIV, drugs, obesity) using clinical, histological, and genetic features.

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FSGS Primary vs Secondary Etiology Score

Frequently Asked Questions

How are primary and secondary FSGS distinguished?

What genetic variants cause FSGS?

How is FSGS treated?