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Health condition · Clinically reviewed

FSGS, a shared pattern of glomerular scarring - four distinct types, one clear ladder.

Focal segmental glomerulosclerosis is one of the commonest causes of adult nephrotic syndrome. A biopsy-led plan and a modern renoprotective toolkit protect long-term kidney function.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against KDIGO, NICE and peer-reviewed nephrology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK nephrology practice including SGLT2 inhibitors, sparsentan and rituximab-based regimens.

Key facts

FSGS at a glance.

The essentials, in plain English - what the pattern means, the four types and how it is treated in the UK today.

  • What it is

    A histopathological pattern of glomerular scarring - focal (some glomeruli) and segmental (parts of each) - not a single disease but a shared endpoint.

  • Why it matters

    One of the commonest causes of nephrotic syndrome in adults and a frequent route to progressive chronic kidney disease.

  • The four types

    Primary (immune-driven), secondary (HIV, obesity, drugs, reflux), genetic (podocyte gene variants) and adaptive (hyperfiltration).

  • Gold-standard test

    Renal biopsy - light microscopy, immunohistochemistry and electron microscopy together classify the Columbia variant.

  • Foundation therapy

    ACE inhibitor or ARB, blood-pressure control, statin, diuretic and, where appropriate, an SGLT2 inhibitor.

  • Immunosuppression

    Reserved for biopsy-proven primary FSGS - high-dose prednisolone, calcineurin inhibitors, MMF or rituximab.

Why this guide matters

A pattern, not a single disease.

The three points below shape everything else on this page - and explain why two people with the same biopsy report can need very different treatment.

  • Type drives treatment

    Primary, secondary, genetic and adaptive FSGS look similar under the microscope but call for very different plans.

  • Renoprotection is universal

    ACE inhibitors or ARBs, blood-pressure control and, increasingly, SGLT2 inhibitors are used in every FSGS phenotype.

  • Immunosuppression is selective

    Reserved for biopsy-proven primary disease - steroids, calcineurin inhibitors, MMF and rituximab, not for everyone.

How the diagnosis is made

From frothy urine to a biopsy-led plan.

The steps a UK GP and nephrologist will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    Urinalysis and protein quantification

    Dipstick plus a urine protein-creatinine ratio and, where needed, a 24-hour urinary protein confirm the nephrotic-range picture.

  2. 02

    Assessing

    Bloods and secondary work-up

    FBC, U&Es, LFTs, albumin, lipids, complement, autoimmune screen, HIV, hepatitis B, hepatitis C and syphilis serology.

  3. 03

    Assessing

    Renal ultrasound

    Confirms two kidneys of normal size and rules out obstruction before proceeding to biopsy.

  4. 04

    Confirming

    Renal biopsy - the gold standard

    Light microscopy, immunohistochemistry and electron microscopy identify focal segmental sclerosis and the Columbia variant. See our /treatments/renal-biopsy/ guide.

  5. 05

    Confirming

    Columbia variant classification

    Collapsing (worst prognosis), tip lesion (best), cellular, perihilar and not-otherwise-specified (NOS).

  6. 06

    Planning

    Genetic panel where indicated

    NPHS1 (nephrin), NPHS2 (podocin), APOL1, ACTN4, TRPC6, INF2 and others - selective and specialist commissioned.

  7. 07

    Planning

    Specialist nephrology review

    A consultant nephrologist decides on primary versus secondary causation and shapes the treatment ladder - specialist commissioned.

Typical timeline: first bloods to a biopsy-led plan in a few weeks.

Symptoms

What FSGS actually looks like.

The full nephrotic picture - heavy proteinuria, low albumin, oedema and dyslipidaemia - with hypertension, haematuria and thrombotic risk in the wings.

  • Heavy proteinuria

    Frothy urine and a protein-creatinine ratio in the nephrotic range - the defining laboratory feature.

  • Hypoalbuminaemia

    Low serum albumin drives fluid shift into the tissues - the biochemical partner to the oedema you can see.

  • Peripheral and periorbital oedema

    Swelling around the eyes in the morning and in the ankles by evening - the classic nephrotic pattern.

  • Hyperlipidaemia

    The liver ramps up lipoprotein production in response to low albumin - a marker of active nephrotic syndrome.

  • Hypertension

    Common at presentation and a driver of further nephron loss if left uncontrolled.

  • Microscopic haematuria

    Present in a minority - not the dominant feature but part of the picture on urinalysis.

  • Progressive renal impairment

    A rising creatinine and falling eGFR track the underlying glomerular scarring over months to years.

  • Red flag - thromboembolism

    Nephrotic syndrome is a hypercoagulable state - deep-vein thrombosis, pulmonary embolus and renal-vein thrombosis all occur.

Treatment

How FSGS is treated in the UK.

Renoprotection for every phenotype, immunosuppression for biopsy-proven primary disease, and cause-directed care for the rest. Dialysis and transplantation for end-stage disease, all specialist commissioned.

  • Treat the underlying cause

    Antiretroviral therapy in HIV-associated FSGS, withdrawal of causative drugs, weight loss for obesity-related disease and treatment of reflux.

  • ACE inhibitor or ARB

    First-line in every FSGS phenotype - reduces proteinuria and slows progression through renoprotective haemodynamics.

  • SGLT2 inhibitor

    Dapagliflozin - NICE-approved for chronic kidney disease after the DAPA-CKD trial. See our /treatments/sglt2-inhibitor-clinic/ guide.

  • Blood-pressure control

    Target under 130/80 mmHg with a low-salt diet and combination therapy where needed.

  • Diuretics and statin

    Furosemide (often with spironolactone) for oedema, plus a statin to address nephrotic-range dyslipidaemia.

  • Anticoagulation

    Prophylactic anticoagulation is considered when the serum albumin falls below 20 g/L, given the thrombotic risk.

  • Immunosuppression (primary)

    High-dose prednisolone (1 mg/kg for 8 to 16 weeks with a taper), calcineurin inhibitors (ciclosporin, tacrolimus), mycophenolate mofetil or rituximab. See /treatments/rituximab-infusion-clinic/.

  • Sparsentan and end-stage care

    Sparsentan (dual angiotensin and endothelin receptor antagonist - see /treatments/sparsentan-clinic/) is an emerging option. Dialysis and transplantation are specialist commissioned, with recurrence risk on the table.

What this guide is based on

The sources behind every claim on this page.

International and UK nephrology guidance, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or nephrologist knows your bloods, biopsy and history and can tell you which parts apply to you. If in doubt, get seen.

  • KDIGO. Clinical Practice Guideline for the Management of Glomerular Diseases (2021, and updates).

  • NICE. Chronic kidney disease: assessment and management (NG203).

  • NICE Technology Appraisal. Dapagliflozin for treating chronic kidney disease (TA775).

  • MHRA and NICE. Sparsentan for treating primary IgA nephropathy and FSGS (current guidance).

  • The Renal Association / UK Kidney Association. Clinical practice guideline on glomerulonephritis.

Red flags

When FSGS needs urgent attention.

Most day-to-day FSGS is managed steadily. These are the situations that need same-day or specialist review.

  • Acute kidney injury

    A rapidly rising creatinine or falling urine output on top of FSGS deserves same-day nephrology assessment.

  • Renal-vein thrombosis

    Sudden flank pain, worsening proteinuria or a rising creatinine in a nephrotic patient - imaging and anticoagulation are urgent.

  • Pulmonary embolus

    Nephrotic syndrome is prothrombotic - new pleuritic pain, breathlessness or hypoxia needs immediate assessment.

  • Severe hypoalbuminaemia

    A serum albumin below 20 g/L raises thromboembolic risk and often prompts prophylactic anticoagulation.

  • Collapsing variant on biopsy

    The most aggressive Columbia variant - rapid progression is common and specialist commissioned care is essential.

  • Suspected HIV-associated nephropathy

    Any new nephrotic syndrome in an at-risk patient warrants urgent HIV testing and early antiretroviral therapy.

  • Post-transplant recurrence

    Primary FSGS recurs in roughly 30 to 50 per cent of transplants - specialist immunosuppression and plasma exchange are used.

  • Infective decompensation

    Loss of immunoglobulins in the urine and immunosuppression together raise infection risk - fever needs early review.

  • Uncontrolled hypertension

    Persistent readings above target accelerate scarring - escalate therapy rather than watch and wait.

Living with it

A treatable condition, with a clear ladder.

Four things that make the biggest difference day to day - a low-salt diet, daily renoprotective tablets, self-monitoring at home, and knowing when to escalate.

A quiet reminder

Slow progression is a real win.

Modern nephrology is about preserving nephrons - years of stable eGFR add up to years off dialysis.

  1. 01 Salt

    Keep sodium down

    A low-salt diet makes every antihypertensive and diuretic work harder. Aim for under 6 g of salt a day.

  2. 02 Adherence

    Take the ACE inhibitor or ARB

    It is the single most important daily tablet in FSGS - protective of proteinuria and long-term kidney function.

  3. 03 Monitor

    Watch weight and blood pressure

    A home blood-pressure monitor and daily weights catch fluid retention early and guide diuretic changes.

  4. 04 Escalate

    Speak up about new swelling or clots

    Sudden leg swelling, chest pain or breathlessness in nephrotic syndrome needs same-day medical review.

Frequently asked

Everything we get asked about FSGS.

Quick answers on biopsy, causes, ACE inhibitors, immunosuppression and sparsentan.

  • What is FSGS?

    Focal segmental glomerulosclerosis is a pattern of scarring in some (focal) glomeruli and in parts (segmental) of those glomeruli. It is not a single disease - it is the shared histological endpoint of several primary, secondary, genetic and adaptive processes, and one of the commonest causes of nephrotic syndrome in adults.

  • What causes FSGS?

    The causes fall into four groups. Primary (idiopathic) FSGS is thought to be driven by a circulating permeability factor that damages podocytes. Secondary FSGS follows HIV, heroin use, obesity, vesico-ureteric reflux, a single kidney, sickle cell disease, viral infections or medications such as pamidronate, lithium, interferon, sirolimus and anabolic steroids. Genetic FSGS involves podocyte genes (NPHS1, NPHS2, APOL1, ACTN4, TRPC6, INF2 and others). Adaptive FSGS is a response to hyperfiltration.

  • How is FSGS diagnosed?

    Diagnosis starts with urinalysis, a urine protein-creatinine ratio and a broad blood work-up (including HIV, hepatitis B and C, autoimmune serology and complement). A renal biopsy is the gold standard - light microscopy shows focal segmental sclerosis, and immunohistochemistry and electron microscopy classify the Columbia variant (collapsing, tip lesion, cellular, perihilar or not-otherwise-specified).

  • What is the difference between primary and secondary FSGS?

    Primary FSGS is immune-driven, tends to present with heavy nephrotic-range proteinuria and diffuse foot-process effacement on electron microscopy, and often responds to immunosuppression. Secondary FSGS reflects an identifiable insult (HIV, obesity, reflux, drugs) - proteinuria is often lower, effacement is patchy, and treatment focuses on the underlying cause plus renin-angiotensin blockade rather than immunosuppression.

  • Do I need immunosuppression?

    Not everyone. Immunosuppression is reserved for biopsy-proven primary FSGS. High-dose prednisolone (typically 1 mg/kg for 8 to 16 weeks with a taper) is first-line. Calcineurin inhibitors (ciclosporin or tacrolimus), mycophenolate mofetil and rituximab are used in relapsing, steroid-dependent or steroid-resistant disease. Secondary and genetic forms are managed with cause-directed and supportive therapy.

  • What is sparsentan and where does it fit?

    Sparsentan is a dual angiotensin and endothelin receptor antagonist. It reduces proteinuria more than an ARB alone and is NICE-approved for IgA nephropathy in the UK, with a role in FSGS under active review. Your nephrologist will discuss whether you are a candidate. See our /treatments/sparsentan-clinic/ guide for more.

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