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Health condition · Clinically reviewed

Glomerulonephritis, the biopsy, the bloods and modern kidney-protective care.

Inflammation of the kidney's filters can quietly progress to end-stage renal failure. A structured work-up and targeted treatment protect what matters.

Jump to treatment
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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 practice including sparsentan, budesonide (Nefecon) and avacopan for ANCA-associated disease.

Key facts

Glomerulonephritis at a glance.

The essentials, in plain English - what it is, the two clinical patterns and how it is treated in the UK today.

  • What it is

    Inflammation of the glomeruli - the filtering units of the kidney - producing haematuria, proteinuria and reduced kidney function.

  • Two clinical patterns

    Nephritic (haematuria, hypertension, reduced GFR) and nephrotic (heavy proteinuria, low albumin, oedema, high lipids).

  • Why it matters

    A leading cause of chronic kidney disease and end-stage renal failure in the UK if left unrecognised.

  • Diagnosis

    Blood and urine tests plus a renal biopsy - the gold standard for typing the disease and guiding treatment.

  • Treatment principles

    Treat the underlying cause, protect the kidney with ACE inhibitors and SGLT2 inhibitors, and use targeted immunosuppression.

  • Newer options

    Sparsentan, budesonide (Nefecon), rituximab and avacopan have transformed care for IgA, membranous and ANCA-associated disease.

Why this guide matters

The kidney rewards early, decisive care.

Glomerulonephritis is often silent until proteinuria, hypertension or a falling eGFR turn up on routine tests. The three points below shape everything else on this page.

  • Nephritic and nephrotic patterns

    Two clinical fingerprints - blood-and-hypertension nephritic disease, and heavy-protein nephrotic disease - narrow the differential and speed up biopsy.

  • The renal biopsy is central

    Light microscopy, immunofluorescence and electron microscopy together give the diagnosis - see our renal biopsy guide for what to expect.

  • Modern targeted therapy

    Sparsentan, budesonide, rituximab and avacopan have transformed outcomes for IgA nephropathy, membranous disease and ANCA-associated vasculitis.

How the diagnosis is made

From dipstick to a defined pattern.

The KDIGO-aligned steps a UK nephrology team will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    Urinalysis and microscopy

    Dipstick blood and protein plus microscopy for red-cell casts and dysmorphic cells - the earliest clue to a glomerular process.

  2. 02

    Assessing

    Bloods and eGFR

    FBC, U&Es, LFTs, eGFR, albumin, lipids and urinary protein-to-creatinine ratio to gauge severity.

  3. 03

    Assessing

    Blood pressure and oedema check

    Hypertension and peripheral or facial oedema help place the picture on the nephritic-nephrotic spectrum.

  4. 04

    Confirming

    Immunology and infection screen

    Complement (C3, C4), ANA, ANCA, anti-GBM, anti-PLA2R, anti-dsDNA, immunoglobulins, cryoglobulins, electrophoresis, free light chains, HIV, HBV, HCV and syphilis.

  5. 05

    Confirming

    Urgent ANCA and anti-GBM

    In rapidly progressive glomerulonephritis these results are needed within hours to prevent irreversible kidney injury.

  6. 06

    Defining

    Renal biopsy

    The gold-standard test - light microscopy, immunofluorescence and electron microscopy define the histological pattern and drive treatment.

  7. 07

    Defining

    Specialist nephrology review

    A commissioned nephrology (and, where relevant, rheumatology) team plans immunosuppression and monitoring.

Typical timeline: first bloods to biopsy report in one to three weeks, faster where the disease is progressing quickly.

Symptoms

What glomerulonephritis actually looks like.

The classic mix of haematuria, proteinuria, hypertension and oedema - and the systemic features that reshape the diagnosis.

  • Visible or microscopic haematuria

    Cola-coloured urine or a persistent dipstick positive for blood - see our guide to haematuria for the wider work-up.

  • Proteinuria

    Frothy urine or a raised protein-to-creatinine ratio - heavy proteinuria points towards a nephrotic pattern.

  • Hypertension

    New or worsening high blood pressure, often the first sign of a nephritic process.

  • Oedema

    Puffy eyes in the morning, swollen ankles, or generalised fluid overload from low albumin.

  • Reduced kidney function

    A falling eGFR on routine bloods - the trigger for urgent nephrology review.

  • Haemoptysis

    Coughing up blood alongside kidney disease raises the flag for anti-GBM disease or ANCA-associated vasculitis.

  • Rash and joint pain

    Palpable purpura, arthralgia or a butterfly rash suggest Henoch-Schonlein purpura, lupus nephritis or systemic vasculitis.

  • Red flag - rapid decline

    A doubling of creatinine over days to weeks is rapidly progressive glomerulonephritis and needs same-day nephrology input.

Treatment

How glomerulonephritis is treated in the UK.

Kidney-protective foundations first - ACE inhibitors, ARBs and SGLT2 inhibitors - then targeted immunosuppression matched to the biopsy pattern.

  • ACE inhibitor or ARB

    The backbone of kidney protection - lowers blood pressure and proteinuria in almost every type of glomerulonephritis.

  • SGLT2 inhibitor

    Now standard for chronic proteinuric kidney disease - see our SGLT2 inhibitor clinic for how it is started and monitored.

  • Corticosteroids

    Prednisolone is central to minimal change disease and induction in several other patterns - tapered carefully.

  • Rituximab

    A specialist-commissioned option for membranous nephropathy, minimal change and ANCA-associated disease - given by infusion.

  • Budesonide (Nefecon)

    Gut-targeted steroid approved for IgA nephropathy - reduces proteinuria and slows progression in selected patients.

  • Sparsentan (Filspari)

    A dual angiotensin and endothelin receptor antagonist approved by NICE in 2024 for IgA nephropathy - specialist commissioned.

  • Avacopan (Tavneos)

    An oral complement C5a inhibitor for ANCA-associated vasculitis - allows lower steroid exposure alongside rituximab or cyclophosphamide.

  • Dialysis and transplantation

    Where the disease progresses to end-stage renal failure - offered through commissioned renal services.

What this guide is based on

The sources behind every claim on this page.

International and UK national 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, your biopsy and your history, and can tell you which parts apply to you. If in doubt, get seen.

  • KDIGO 2021 and 2024 Clinical Practice Guideline for the Management of Glomerular Diseases.

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

  • NICE TA. Sparsentan for treating IgA nephropathy; Avacopan for ANCA-associated vasculitis.

  • MHRA and EMA. Budesonide (Nefecon) marketing authorisation for primary IgA nephropathy.

  • UK Kidney Association. Clinical Practice Guidelines on Glomerulonephritis.

Red flags

When glomerulonephritis needs urgent attention.

Some patterns of kidney inflammation can cause irreversible damage in days. These are the situations that warrant same-day nephrology contact.

  • Rapidly progressive glomerulonephritis

    A rise in creatinine over days to weeks with active urinary sediment - a nephrology emergency needing same-day assessment.

  • Pulmonary-renal syndrome

    Haemoptysis with kidney injury raises anti-GBM disease and ANCA-associated vasculitis - both can progress within hours.

  • Nephrotic syndrome with clots

    Heavy proteinuria carries a real risk of venous thromboembolism - unexplained leg swelling or breathlessness needs urgent review.

  • Uncontrolled hypertension

    Very high blood pressure with kidney injury may need admission for controlled reduction and workup.

  • Severe hyperkalaemia or acidosis

    Metabolic derangement from acute kidney injury is a hospital-level problem, not a primary-care one.

  • Systemic features

    Fever, weight loss, palpable purpura, mono-neuritis multiplex or scleritis point to systemic vasculitis needing urgent rheumatology-nephrology input.

  • Pregnancy with glomerular disease

    Requires joint obstetric and nephrology care - some drugs are contraindicated and blood pressure targets differ.

  • Failed response to first-line therapy

    Ongoing proteinuria or falling eGFR despite treatment triggers reassessment - a repeat biopsy is sometimes needed.

  • End-stage renal failure

    Advanced kidney failure needs early planning for dialysis or transplantation and honest conversations about choices.

Living with it

A long-term condition, with a clear plan.

Four things that make the biggest difference day to day - monitoring, lifestyle, medicines and support from the right charities alongside your NHS or private team.

A quiet reminder

Consistency beats intensity, every time.

Steady blood pressure, steady medication and steady follow-up do more than a heroic week that does not last.

  1. 01 Monitor

    Keep an eye on the numbers

    Blood pressure at home, regular urine dipsticks and scheduled bloods let your team spot flares early.

  2. 02 Lifestyle

    Salt, weight and smoking

    Salt restriction, a healthy weight and stopping smoking all lower proteinuria and protect the kidneys.

  3. 03 Medicines

    Take kidney-protective drugs on time

    ACE inhibitors, ARBs and SGLT2 inhibitors work best when taken consistently and monitored for side effects.

  4. 04 Support

    Use patient charities

    Kidney Care UK, Vasculitis UK and Lupus UK offer real practical and emotional support alongside your NHS or private team.

Frequently asked

Everything we get asked about glomerulonephritis.

Quick answers on nephritic versus nephrotic disease, biopsy, and the newer targeted therapies.

  • What is glomerulonephritis?

    Glomerulonephritis is inflammation of the tiny filters in the kidney called glomeruli. Depending on the type, it can cause blood in the urine, protein in the urine, high blood pressure, swelling and a fall in kidney function. It is one of the leading causes of chronic kidney disease and end-stage renal failure in the UK.

  • What is the difference between nephritic and nephrotic syndrome?

    Nephritic syndrome is a pattern of blood in the urine, high blood pressure and reduced kidney function - classically seen in IgA nephropathy and post-infectious disease. Nephrotic syndrome is heavy protein loss in the urine with a low blood albumin, swelling and high cholesterol - classically seen in minimal change disease, focal segmental glomerulosclerosis (FSGS) and membranous nephropathy.

  • Why do I need a kidney biopsy?

    A renal biopsy is the gold-standard test for glomerulonephritis. Light microscopy, immunofluorescence and electron microscopy together identify the exact pattern of disease - for example IgA nephropathy, membranous nephropathy or lupus nephritis - which then guides treatment. Without a biopsy, immunosuppression is rarely justified.

  • What treatments are available for IgA nephropathy?

    Treatment starts with an ACE inhibitor or ARB, an SGLT2 inhibitor and blood pressure control. For patients at risk of progression, gut-targeted budesonide (Nefecon) and the dual receptor antagonist sparsentan (Filspari) are now available on a specialist-commissioned basis. Corticosteroids and rituximab are used in selected cases.

  • How is ANCA-associated vasculitis treated?

    Induction is with rituximab or cyclophosphamide alongside corticosteroids. Avacopan (Tavneos), an oral complement C5a inhibitor approved by NICE in 2022, is used alongside these agents to reduce steroid exposure. Care is coordinated between nephrology and rheumatology.

  • Will my kidneys recover?

    It depends on the type of glomerulonephritis, how advanced the damage is at diagnosis and how well the disease responds to treatment. Many people stabilise or improve with modern therapy. A minority progress to end-stage renal failure and will need dialysis or a transplant - both of which can offer good quality of life with the right support.

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