• Mini Michael, Arvind Bagga, Sarah E Sartain, and SmithRichard J HRJHDepartment of Otolaryngology, Pediatrics and Molecular Physiology & Biophysics, The University of Iowa, Iowa City, IA, USA..
• Division of Pediatric Nephrology, Baylor College of Medicine, Texas Children's Hospital, Houston, TX, USA. Electronic address: mmichael@bcm.edu.
• Lancet. 2022 Nov 12; 400 (10364): 172217401722-1740.

AbstractHaemolytic uraemic syndrome (HUS) is a heterogeneous group of diseases that result in a common pathology, thrombotic microangiopathy, which is classically characterised by the triad of non-immune microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury. In this Seminar, different causes of HUS are discussed, the most common being Shiga toxin-producing Escherichia coli HUS. Identifying the underlying thrombotic microangiopathy trigger can be challenging but is imperative if patients are to receive personalised disease-specific treatment. The quintessential example is complement-mediated HUS, which once carried an extremely high mortality but is now treated with anti-complement therapies with excellent long-term outcomes. Unfortunately, the high cost of anti-complement therapies all but precludes their use in low-income countries. For many other forms of HUS, targeted therapies are yet to be identified.Copyright © 2022 Elsevier Ltd. All rights reserved.

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