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FSGS — the scarring of kidney filters that causes heavy proteinuria. Primary vs secondary forms, diagnosis, and the treatment ladder from steroids to SGLT2 inhibitors.
Evidence reviewed & updated: 2026-08 — reflects the latest published trials and guidelines.
FSGS is a pattern of kidney injury where patches of the glomeruli (filters) scar — it's a leading cause of nephrotic syndrome and kidney failure in adults, and increasingly common (partly from obesity-related and genetic forms). Treatment depends on whether it's primary (immune-mediated, steroid-responsive) or secondary (caused by obesity, genetics, infections, drugs).
FSGS describes the biopsy pattern: some glomeruli are scarred, and in those, only a segment of the filter is affected. The scarring is driven by injury to podocytes — the cells that wrap the filter and keep protein in the blood. When podocytes are lost, protein pours into the urine and the filter collapses into scar.
It's a leading cause of nephrotic syndrome in adults, and one of the most common causes of kidney failure from primary kidney disease.
Primary FSGS is caused by an immune 'circulating factor' that attacks podocytes — it can recur after transplant, and it's potentially steroid-responsive. Secondary FSGS comes from causes that overload or injure podocytes: obesity (the most common driver of the rising incidence), HIV, heroin, some drugs, vesicoureteral reflux, and genetic variants — most notably APOL1 (strongly enriched in people of West African ancestry).
The distinction drives treatment: primary FSGS gets immunosuppression; secondary FSGS gets cause management (weight, BP, glucose, discontinuing the offending drug) — steroids don't help secondary forms.
For everyone: ACEi/ARB, SGLT2 inhibitors, blood pressure control, and sodium restriction — these slow progression regardless of type. For primary FSGS: high-dose steroids for 4-6 months, with calcineurin inhibitors (tacrolimus/cyclosporine) or other agents if steroid-resistant or to reduce steroid exposure.
Obesity-related secondary FSGS responds to weight loss (including GLP-1 therapy now), BP control, and RAAS blockade. Genetic FSGS is managed with kidney-protective therapy rather than immunosuppression. Advanced disease: dialysis/transplant — though primary FSGS can recur in the graft.
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