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Management of Focal Segmental Glomerulosclerosis (FSGS)

Appropriate treatment matters for patients living with FSGS

Without effective disease control, patients living with focal segmental glomerulosclerosis (FSGS) face poor long-term outcomes.1-4 Real-world and registry data show that elevated proteinuria is closely linked to progressive kidney function decline, kidney failure, dialysis and transplantation, and increased cardiovascular risk.1-3,5 The burden of FSGS also extends beyond clinical outcomes with patients and care-partners reporting impaired quality of life, emotional distress, and reduced work or daily activity.4

Given these risks, early treatment is important in FSGS.6 The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) guideline emphasizes that FSGS is a histopathologic pattern of injury rather than a single disease.7

Primary, genetic, and secondary FSGS and FSGS of undetermined cause converge on a pattern of podocyte injury.7,8 Biopsy and histological findings should be evaluated alongside clinical presentation7,8

  • Light microscopy shows the defining lesion of FSGS, segmental sclerosis involving part of the glomerular tuft.8 Patterns on light microscopy may provide clues to subtype and prognosis8
  • Electron microscopy provides additional information about the pattern of podocyte injury, particularly the extent of foot process effacement.7-9
Primary FSGS

Primary FSGS

Defined clinically by nephrotic syndrome (>3.5 g/day) and diffuse foot process effacement on electron microscopy, without an identifiable secondary or genetic cause.7,8 It may present with sudden onset7,8

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Genetic FSGS

Genetic FSGS

Associated with pathogenic variants affecting podocyte biology, the glomerular basement membrane, or other components of the glomerular filtration barrier, and may present as renal-limited or syndromic disease7,8

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Secondary FSGS

Secondary FSGS

Diagnosed when the lesion occurs in the setting of an established process known to cause FSGS.7,8 It generally presents without nephrotic syndrome and may occur with normal or reduced nephron mass7,8

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FSGS of undetermined cause

FSGS of undetermined cause

Determined when patients have lesions without a primary, genetic, or secondary cause.7,8 These patients generally do not have nephrotic syndrome with diffuse foot process effacement7

Distinguishing FSGS from other proteinuric kidney diseases

Because FSGS is a histologic lesion with diverse causes, biopsy evaluation should also distinguish an FSGS lesion from other lesions that can appear similar but require different management strategies, including but not limited to8:

  • Focal global glomerulosclerosis (FGGS) associated with aging or hypertensive nephropathy
  • Post-inflammatory focal segmental scarring in immune-mediated glomerulonephritides, such as IgA nephropathy

Management strategies by FSGS etiology

Across FSGS etiologies, management is anchored by reduction of proteinuria, preservation of kidney function, and slowing progression to kidney failure.7 
Supportive care forms the foundation of treatment for patients with persistent proteinuria and generally includes7: 


Immunosuppressive therapy may be provided for certain patients, particularly those with primary FSGS.7 The 2021 KDIGO guideline recommends high-dose oral glucocorticoids as first-line therapy for primary FSGS, with calcineurin inhibitors used in adults who cannot tolerate glucocorticoids or who have contraindications.7 
In steroid-resistant primary FSGS, cyclosporine or tacrolimus is recommended.7

For secondary, genetic, and undetermined cause FSGS, management is centered on supportive care rather than immunosuppression.7 Treatment for secondary FSGS may also be directed at the underlying driver of disease when one is identified, such as maladaptive stress, viral infection, or drug exposure.7

On April 13, 2026, sparsentan was also approved to reduce proteinuria in adult and pediatric patients aged 8 years and older with focal segmental glomerulosclerosis (FSGS) without nephrotic syndrome10

Nephrotic syndrome includes the presence of three concurrent criteria: proteinuria greater than 3.5 g/24h (adults) or UPCR >2.0 g/g (pediatric patients <18 years of age), serum albumin <3.0 g/dL, and edema10

Limitations of conventional therapies

Therapies described in the 2021 KDIGO guideline are largely nonspecific to the pathophysiology of FSGS, tolerability can be challenging, and sustained remission is uncommon.8,11

Because proteinuria is both a marker and mediator of disease progression, sustained reduction in proteinuria remains a key therapeutic goal and an important endpoint in ongoing research evaluating emerging therapies for FSGS.2,12

Sparsentan Clinical Trials in FSGS Sparsentan Clinical Trials in FSGS
Nephrology FSGS

Sparsentan Clinical Trials in FSGS

Learn more about sparsentan clinical trials in adults and children aged 8 years and older with FSGS

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Footnotes

*Observational survey data from the HONUS study (adults with FSGS, n=78; caregivers, n=77).4
†Retrospective data from a Veteran Affairs cohort of patients with FSGS (N=2,515).5

††Retrospective data from the UK National Registry of Kidney Diseases (RaDaR; N=4,066).2
§Major adverse kidney event defined as ≥40% eGFR decline, kidney failure, dialysis/transplant, or death.1

||Retrospective data from the Providence and University of California (UCLA) Health Systems’ records within the CURE-CKD registry (2016-2022; N=629).1

Retrospective, observational data from from Optum Market Clarity on a real-world US cohort of patients with FSGS.3

FSGS, focal segmental glomerulosclerosis; KDIGO, Kidney Disease: Improving Global Outcomes; RASi, renin–angiotensin system inhibition.

  1. Nicholas SB et al. BMC Nephrology. 2025;26(1):403.
  2. Pitcher D et al. Journal of the American Society of Nephrology. 2025;36(7):1398-1413.
  3. Velez JCQ et al. Kidney360. 2024;5(8).
  4. Szklarzewicz J et al. Quality of Life Research. 2025;34(7):1925-1937.
  5. Goldschmidt D et al. PLOS ONE. 2024;19(12):e0315302.
  6. Aldhouse NVJ et al. Adv Ther. 2023;40(12):5155-5167.
  7. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. Kidney Int. 2021;100(4S):S1-S276.
  8. De Vriese AS et al. J Am Soc Nephrol. 2018;29(3):759-774.
  9. Hommos MS et al. Mayo Clin Proc. 2017;92(12):1772-1781.
  10. FILSPARI® (sparsentan) Prescribing Information. San Diego, CA: Travere Therapeutics, Inc.
  11. Zhu Y et al. Drug Des Devel Ther. 2025;19:857-875.
  12. Trachtman H et al. Future Rare Diseases. 2025;5(1):2461966.

MA-DS-26-0036 | May 2026