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Health condition · Clinically reviewed

IgA nephropathy, renoprotection, targeted therapies and modern nephrology.

The commonest primary glomerulonephritis worldwide - and treatable. A stepped plan from urine dip to biopsy to Nefecon or sparsentan under specialist care.

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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 practice including targeted-release budesonide, sparsentan and SGLT2 inhibitors.

Key facts

IgA nephropathy at a glance.

The essentials, in plain English - what it is, how it presents, how it is diagnosed, and how it is treated in UK nephrology today.

  • What it is

    Mesangial deposition of galactose-deficient IgA1 immune complexes causing mesangioproliferative glomerulonephritis - the commonest primary glomerulonephritis worldwide.

  • How it shows up

    Episodic visible haematuria after upper respiratory infections (synpharyngitic), or silent microscopic haematuria with proteinuria found on a routine dip.

  • Who it affects

    A genetic predisposition sits behind most cases - young adults, more men than women, and a well-recognised familial cluster.

  • How it is diagnosed

    Renal biopsy is definitive. The Oxford MEST-C score grades mesangial, endocapillary, segmental, tubular and crescentic features.

  • Foundation therapy

    Maximally-dosed ACE inhibitor or ARB plus an SGLT2 inhibitor - the renoprotective backbone recommended by KDIGO 2021.

  • Progression

    Up to 30% of people reach end-stage kidney disease over 20 to 30 years - risk is stratified by proteinuria and MEST-C features.

Why this guide matters

The three pillars of modern IgA care.

IgA nephropathy has shifted from a wait-and-watch disease to one with genuinely disease-modifying options. Three ideas shape everything below.

  • Proteinuria is the target

    Every plan aims to get urine protein as low as possible. Proteinuria is the single strongest predictor of kidney survival.

  • Renoprotection first, always

    Maximally-dosed ACE inhibitor or ARB with an SGLT2 inhibitor and tight blood pressure control is the foundation, and it works.

  • Targeted therapies for high risk

    Nefecon and sparsentan are UK-licensed for IgA nephropathy - real options now, on top of renoprotection, under specialist care.

How the diagnosis is made

From a red urine dip to a graded diagnosis.

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

  1. 01

    Suspecting

    History and pattern

    Episodes of visible haematuria during a sore throat or chest infection - synpharyngitic haematuria - are a strong pointer. Family history matters.

  2. 02

    Suspecting

    Urinalysis and microscopy

    Dipstick blood and protein, urine albumin-to-creatinine ratio (ACR) or protein-to-creatinine ratio, and microscopy for red cell casts.

  3. 03

    Suspecting

    Blood tests

    Creatinine, urea, eGFR, full blood count and inflammatory markers. Serum IgA is raised in about half but is not diagnostic.

  4. 04

    Confirming

    Rule out mimics

    Complement (C3, C4), ANA, ANCA, anti-GBM and hepatitis serology to exclude lupus nephritis, vasculitis and secondary IgA deposition.

  5. 05

    Confirming

    Imaging

    Renal ultrasound to confirm two kidneys of normal size and exclude obstruction, cysts or scarring before biopsy.

  6. 06

    Confirming

    Renal biopsy

    The definitive test. Immunofluorescence shows dominant mesangial IgA. Light microscopy and the Oxford MEST-C score guide prognosis.

  7. 07

    Planning

    Specialist nephrology plan

    Risk stratification by proteinuria, blood pressure, eGFR trajectory and biopsy features shapes what happens next.

Typical timeline: from a positive urine dip to a biopsy-confirmed plan in weeks, not months.

Symptoms

How IgA nephropathy actually shows up.

The classic patterns of haematuria and proteinuria - and the presentations that mean urgent nephrology assessment is needed.

  • Visible haematuria

    Brown, tea-coloured or frankly red urine, often triggered by a sore throat or chest infection - the classic synpharyngitic pattern.

  • Microscopic haematuria

    A silent finding on a routine dipstick - persistent, with dysmorphic red cells and red cell casts on microscopy.

  • Proteinuria

    Foamy urine or a raised urine ACR - the single most important predictor of long-term kidney outcome in IgA nephropathy.

  • Hypertension

    New or worsening high blood pressure is common and both a marker and a driver of kidney damage.

  • Nephritic syndrome

    Acute kidney injury with hypertension, oedema and an active urinary sediment - warrants urgent nephrology review.

  • Nephrotic-range proteinuria

    Heavy proteinuria with oedema and low serum albumin - less common in IgA nephropathy but not rare and needs assessment.

  • Rapidly progressive disease

    A fast fall in kidney function with crescents on biopsy - a nephrology emergency needing prompt immunosuppression.

  • Red flag - IgA vasculitis

    Palpable purpura, joint pain and abdominal pain with haematuria points to Henoch-Schönlein purpura, the systemic form of the same disease.

Treatment

How IgA nephropathy is treated in the UK.

Renoprotection first, then Nefecon or sparsentan for high-risk disease under specialist nephrology - with immunosuppression reserved for aggressive presentations.

  • ACE inhibitor or ARB

    Titrated to the maximum tolerated dose to reduce proteinuria and blood pressure. The renoprotective foundation of every IgA nephropathy plan.

  • SGLT2 inhibitor

    Dapagliflozin, following the DAPA-CKD evidence, is now standard alongside RAS blockade for persistent proteinuria - see our SGLT2 inhibitor clinic.

  • Blood pressure and lifestyle

    A target below 130/80 mmHg, reduced dietary salt, weight management, smoking cessation and a Mediterranean pattern of eating.

  • Targeted-release budesonide

    Nefecon, approved in the UK, delivers gut-targeted steroid to the Peyer patches where pathogenic IgA1 is made. Specialist-commissioned.

  • Sparsentan

    A dual endothelin and angiotensin II receptor antagonist licensed for IgA nephropathy since 2023. Specialist-commissioned and selected.

  • Systemic corticosteroids

    Reserved for selected high-risk patients after weighing the TESTING trial data on benefit versus infection and metabolic harm.

  • Other immunosuppression

    Mycophenolate, cyclophosphamide or rituximab for crescentic or steroid-refractory disease - specialist-commissioned only.

  • Dialysis and transplantation

    For end-stage kidney disease. Recurrence of IgA deposition in the graft is common but rarely graft-threatening in the medium term.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and international nephrology standards, 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 kidneys and history and can tell you which parts apply to you. If in doubt, get seen.

  • KDIGO. 2021 Clinical Practice Guideline for the Management of Glomerular Diseases.

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

  • MHRA. Marketing authorisations for Nefecon (targeted-release budesonide) and Filspari (sparsentan).

  • UK Kidney Association. Clinical practice guideline on IgA nephropathy.

Red flags

When IgA nephropathy needs urgent attention.

Most IgA nephropathy is managed in outpatient nephrology. These situations are the ones that need same-day or same-week specialist input.

  • Rapidly progressive glomerulonephritis

    A doubling of creatinine over weeks with crescents on biopsy - urgent nephrology admission and immunosuppression.

  • Nephritic syndrome

    Acute kidney injury with hypertension, oedema and an active sediment - needs same-day nephrology assessment.

  • Malignant hypertension

    Blood pressure at or above 180/120 mmHg with fundal haemorrhages or headache - a hypertensive emergency.

  • Henoch-Schönlein purpura (IgA vasculitis)

    Palpable purpura, arthritis, abdominal pain and haematuria - the systemic form of IgA nephropathy needs joined-up care.

  • Heavy proteinuria

    Urine ACR persistently above 100 mg/mmol despite optimal supportive care - a strong signal to escalate therapy.

  • Falling eGFR trajectory

    A steady decline of more than 5 mL/min per year should prompt an urgent review of therapy and biopsy features.

  • Systemic features

    Fever, weight loss, joint or lung involvement raises the question of a systemic vasculitis rather than isolated IgA nephropathy.

  • Pregnancy planning

    ACE inhibitors, ARBs, sparsentan and SGLT2 inhibitors need review before conception. Preconception counselling is essential.

  • Post-transplant recurrence

    Recurrence of mesangial IgA deposition in the graft can occur in up to 60% of transplants over 10 years - needs ongoing surveillance.

Living with it

A long-term condition, with real levers to pull.

Four things make the biggest difference in day-to-day life with IgA nephropathy - a monitoring routine, sensible lifestyle, respect for infections and a support network.

A quiet reminder

Kidneys reward steady habits, not heroic weeks.

Blood pressure at target, urine protein trending down and a consistent medication routine matter more than any single test result.

  1. 01 Monitoring

    Know your numbers

    Blood pressure, urine ACR and eGFR are the three numbers to track. A home BP monitor is worth its weight in gold.

  2. 02 Lifestyle

    Salt, weight and movement

    Reducing salt, keeping weight in a healthy range and moving daily all lower blood pressure and slow kidney damage.

  3. 03 Infections

    Look after your throat

    Upper respiratory infections can trigger flares of visible haematuria. Prompt review of tonsillitis or persistent sore throats is sensible.

  4. 04 Support

    You are not on your own

    Kidney Care UK and the UK Kidney Association offer patient support, peer contact and clear resources for every stage.

Frequently asked

Everything we get asked about IgA nephropathy.

Quick answers on biopsy, renoprotection, Nefecon, sparsentan and what happens if kidneys eventually fail.

  • What is IgA nephropathy?

    IgA nephropathy, sometimes called Berger disease, is the most common primary glomerulonephritis worldwide. Immune complexes containing galactose-deficient IgA1 lodge in the mesangium of the glomerulus and drive inflammation. It typically shows up as haematuria and proteinuria in young adults and progresses slowly in most, but up to 30% reach end-stage kidney disease over 20 to 30 years.

  • Why did my urine turn red during a sore throat?

    That pattern is called synpharyngitic haematuria and is a classic feature of IgA nephropathy. An upper respiratory or gut infection triggers a surge of IgA production, more of it lands in the mesangium, and the glomerulus bleeds briefly. Any episode of visible haematuria needs assessment even if it settles quickly.

  • Do I really need a kidney biopsy?

    Biopsy is the definitive test. Immunofluorescence showing dominant mesangial IgA confirms the diagnosis, and the Oxford MEST-C score guides how aggressively to treat and how carefully to monitor. Blood tests and urine dips can suggest IgA nephropathy but cannot confirm it or grade it.

  • What treatment will I be offered first?

    Everyone starts on a foundation of renoprotection - a maximally-dosed ACE inhibitor or ARB, an SGLT2 inhibitor such as dapagliflozin, tight blood pressure control and lifestyle changes. If proteinuria stays above target after that, targeted-release budesonide (Nefecon) or sparsentan can be added under specialist care.

  • Are the newer drugs, Nefecon and sparsentan, available in the UK?

    Yes - both are licensed and available through specialist nephrology services on a commissioned basis. Nefecon delivers gut-targeted budesonide to reduce production of the pathogenic IgA1. Sparsentan is a dual endothelin and angiotensin II receptor antagonist that lowers proteinuria more than an ARB alone in the PROTECT trial.

  • What happens if my kidneys eventually fail?

    Dialysis and transplantation are highly effective. Kidney transplantation gives the best outcomes and quality of life. IgA deposition can recur in the transplanted kidney - up to 60% over ten years - but this rarely causes graft loss in the medium term and is monitored with regular urine and blood tests.

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