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Health condition · Clinically reviewed

Haemolytic uraemic syndrome, the triad, its types and specialist commissioned care.

Rare, serious and treatable. Knowing STEC-HUS from atypical HUS shapes everything that follows, from antibiotics to complement inhibition.

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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 BSH, NHS England commissioning policies and peer-reviewed sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK guidance including complement inhibition with eculizumab and ravulizumab for atypical HUS.

Key facts

HUS at a glance.

The essentials, in plain English. What HUS is, the types, and how it is treated in the UK today.

  • What it is

    A thrombotic microangiopathy defined by the triad of microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury.

  • STEC-HUS

    Around 90 per cent of cases. Shiga toxin-producing E. coli, often O157:H7, usually preceded by bloody diarrhoea. Notifiable to UKHSA.

  • Atypical HUS

    Complement dysregulation, often driven by CFH, CFI, CFB, C3 or MCP variants. Relapsing and severe. Specialist commissioned care.

  • Secondary HUS

    Triggered by drugs, pregnancy, malignancy, transplantation, autoimmune disease or infections such as pneumococcal disease and HIV.

  • Rule out TTP

    ADAMTS13 activity below 10 per cent indicates thrombotic thrombocytopenic purpura, not HUS. Management differs.

  • Specialist care

    Managed by commissioned haematology and nephrology teams, with intensive care support when needed.

Why this guide matters

The right label unlocks the right treatment.

HUS is uncommon, but the differences between its types shape everything from antibiotics to complement inhibition. These three anchors run through the rest of the page.

  • Triad first, cause second

    Recognise microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury together, then work out which type of HUS is driving it.

  • Distinguish HUS from TTP

    ADAMTS13 activity is the fork in the road. Below 10 per cent points to TTP and urgent plasma exchange, above that HUS pathways apply.

  • Complement changes outcomes

    Eculizumab and ravulizumab transformed atypical HUS. They are delivered through specialist commissioned centres with strict vaccination and antibiotic cover.

How the diagnosis is made

From first bloods to a clear plan.

The steps a UK acute team, haematologist or nephrologist will normally follow, in order, so you know what to expect and why.

  1. 01

    Assessing

    History and exposure

    A careful history of diarrhoea, undercooked beef, unpasteurised dairy, petting farms, travel and family kidney disease.

  2. 02

    Assessing

    Bedside assessment

    Pallor, petechiae, purpura, oliguria, blood pressure and neurological signs such as confusion or seizures.

  3. 03

    Assessing

    Bloods and film

    FBC showing haemolytic anaemia and thrombocytopenia, blood film for schistocytes, raised LDH, low haptoglobin and a negative Coombs.

  4. 04

    Confirming

    Renal and coagulation panel

    U and Es to quantify AKI, LFTs, coagulation studies and lactate to guide fluid, transfusion and dialysis decisions.

  5. 05

    Confirming

    Stool microbiology

    Stool PCR and culture for Shiga toxin-producing E. coli, with UKHSA notification and public health follow-up.

  6. 06

    Confirming

    Complement and ADAMTS13

    C3, C4, CH50 and AH50 screening, plus ADAMTS13 activity to distinguish atypical HUS from TTP.

  7. 07

    Preparing

    Genetics and renal biopsy

    Genetic testing for aHUS variants, cascade family screening and selective renal biopsy at specialist commissioned centres.

Typical timeline: from admission to a working diagnosis in hours to days, with specialist commissioned input.

Symptoms

What HUS actually looks like.

A classic mix of prodromal diarrhoea, pallor, bruising and reduced urine output. And the features that mean it is time to escalate.

  • Diarrhoea prodrome

    Often bloody, typically five to seven days before HUS in the STEC form. A key clue in children.

  • Pallor and fatigue

    Rapid onset anaemia from microangiopathic haemolysis. Breathlessness, weakness and pale conjunctivae.

  • Petechiae and purpura

    Small bruises and pinpoint spots reflect the drop in platelet count.

  • Oliguria and AKI

    Reduced urine output, rising creatinine and fluid overload. Some patients need short-term dialysis.

  • Hypertension

    Common during the acute phase and after recovery. Needs careful, sustained control.

  • Neurological features

    Confusion, seizures, focal deficits or stroke. A signal of severe disease that needs specialist commissioned care.

  • Relapsing pattern

    Atypical HUS may recur, especially after infection, pregnancy or transplantation. Long-term follow up matters.

  • Red flag - rapid deterioration

    Anuria, seizures, chest pain or falling consciousness needs urgent hospital and intensive care assessment.

Treatment

How HUS is treated in the UK.

Careful supportive care for STEC-HUS. Specialist commissioned complement inhibition for atypical HUS. Multidisciplinary follow up for everyone.

  • Supportive care

    Careful fluid and electrolyte balance, blood pressure control and red cell transfusion when needed. The foundation of every HUS admission.

  • Renal replacement therapy

    Short-term haemodialysis or haemofiltration for severe AKI, hyperkalaemia or fluid overload. Most STEC-HUS patients recover kidney function.

  • STEC-HUS approach

    Supportive management with cautious avoidance of antibiotics for confirmed STEC, which may worsen toxin release. Public health notification is mandatory.

  • Eculizumab

    Anti-C5 monoclonal antibody for atypical HUS. Delivered through specialist commissioned aHUS centres with meningococcal vaccination and antibiotic cover.

  • Ravulizumab

    Long-acting complement inhibitor alternative to eculizumab. Fewer infusions, same specialist commissioned pathway.

  • Plasma exchange

    Reserved for suspected TTP or selected secondary microangiopathies. Not first-line for STEC-HUS or aHUS in modern UK practice.

  • Kidney transplantation

    Selective option for end-stage kidney disease after HUS. Peri-operative eculizumab prophylaxis reduces recurrence in aHUS.

  • Multidisciplinary follow up

    Long-term nephrology, haematology, cardiovascular and genetics review. Family cascade screening for inherited complement variants.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society 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 acute team, nephrologist or haematologist knows your history and can tell you which parts apply to you. If in doubt, seek urgent review.

  • British Society for Haematology (BSH). Guidelines on the diagnosis and management of thrombotic microangiopathies.

  • NHS England. Clinical commissioning policy for eculizumab and ravulizumab in atypical HUS.

  • UK Health Security Agency (UKHSA). Guidance on Shiga toxin-producing E. coli and HUS surveillance.

  • Kidney Research UK and the aHUS Registry. Long-term outcomes and patient information.

Red flags

When HUS needs urgent attention.

HUS is always a hospital condition. These are the features that push care to intensive care, dialysis or specialist commissioned centres.

  • Anuria or severe AKI

    No urine output, rapidly rising creatinine or life-threatening hyperkalaemia needs urgent nephrology and dialysis review.

  • Neurological deterioration

    Seizures, stroke, drowsiness or focal weakness need immediate hospital admission and specialist commissioned input.

  • Suspected TTP

    Fever, marked thrombocytopenia and neurological signs with a normal or minimally impaired kidney raise the suspicion of TTP. Plasma exchange must not be delayed.

  • Pregnancy-related HUS

    HUS in late pregnancy or the postpartum period overlaps with pre-eclampsia and HELLP. See the pre-eclampsia guide and involve maternal medicine.

  • Bloody diarrhoea in children

    Bloody stools with reduced urine output and pallor need same-day paediatric assessment for possible STEC-HUS.

  • Cardiac features

    Chest pain, arrhythmia or breathlessness may reflect complement-mediated cardiac involvement in aHUS.

  • Post-transplant microangiopathy

    New thrombocytopenia and rising creatinine after transplantation, especially on calcineurin inhibitors, may indicate recurrent or secondary HUS.

  • Pneumococcal HUS

    Invasive pneumococcal infection, often after shellfish exposure, can trigger neuraminidase-related HUS with severe haemolysis.

  • Rapid haemolysis

    Fall in haemoglobin with rising LDH and jaundice needs urgent transfusion planning and specialist review.

Living with it

A treatable condition, with lifelong follow up.

Four things that make the biggest difference after HUS. Regular kidney checks, vigilance for relapse, careful vaccination and family screening in atypical disease.

A quiet reminder

Consistency of follow up matters most.

Steady, planned reviews with your kidney and haematology teams catch problems early and keep long-term outcomes strong.

  1. 01 Recovery

    Kidney recovery takes months

    Most STEC-HUS patients regain kidney function within weeks, but blood pressure and proteinuria need long-term follow up.

  2. 02 Vigilance

    Watch for relapse in aHUS

    Report new bruising, dark urine, headache or reduced urine output early. Complement inhibition greatly reduces relapse but does not eliminate it.

  3. 03 Vaccines

    Vaccinate before complement therapy

    Meningococcal, pneumococcal and Haemophilus influenzae type b vaccination is essential before eculizumab or ravulizumab, with antibiotic cover for the first two weeks.

  4. 04 Family

    Cascade screening for aHUS

    Genetic variants can affect siblings and children. Specialist commissioned genetics teams support families through counselling and testing.

Frequently asked

Everything we get asked about HUS.

Quick answers on causes, TTP overlap, antibiotics, eculizumab and long-term outlook.

  • What is haemolytic uraemic syndrome?

    HUS is a rare but severe thrombotic microangiopathy. Small blood vessels are damaged, red cells fragment as they pass through them, platelets are consumed and the kidneys are injured. The classic triad is microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury.

  • What causes HUS?

    Most cases in the UK follow gut infection with Shiga toxin-producing E. coli, especially O157:H7, contracted from undercooked beef, unpasteurised dairy, petting farms or person-to-person spread. Atypical HUS is driven by inherited or acquired complement dysregulation. Secondary HUS can follow certain drugs, pregnancy, cancer, transplantation, autoimmune disease or infections such as invasive pneumococcal disease and HIV.

  • How is HUS different from TTP?

    Both are thrombotic microangiopathies, but TTP is driven by very low ADAMTS13 activity and needs plasma exchange, steroids and often caplacizumab. HUS has near-normal ADAMTS13 and management centres on supportive care and, in atypical HUS, complement inhibition.

  • Why are antibiotics avoided in STEC-HUS?

    Antibiotics may increase Shiga toxin release from dying bacteria and worsen outcomes in confirmed STEC infection. Management is supportive, with careful fluid, electrolyte and transfusion care, and dialysis when needed.

  • What is eculizumab and who needs it?

    Eculizumab is a monoclonal antibody that blocks complement C5. It transformed outcomes for atypical HUS and is prescribed through specialist commissioned aHUS centres in the UK, including Newcastle, Cambridge and Great Ormond Street. Ravulizumab is a long-acting alternative with less frequent dosing.

  • Do children fully recover from STEC-HUS?

    Most children recover kidney function over weeks to months with supportive care and short-term dialysis when needed. A minority develop long-term hypertension, proteinuria or chronic kidney disease, so life-long follow up is important.

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