Hemolytic uremic syndrome: An updated review

Elmukhtar Habas¹ , Amnna Rayani² , Ala Habas³ , Kalifa Farfar⁴ , Eshrak Habas³, Ahmed Elmarghani⁵, Abdel-Naser Elzouki⁶

Keywords: Atypical hemolytic uremic syndrome, Hemolysis, Hemolytic uremic syndrome, Renal impairment, Shiga toxin, Thrombocytopenia, Typical hemolytic uremic syndrome

DOI: 10.32677/yjm.v1i1.3346

DOI URL: https://doi.org/10.32677/yjm.v1i1.3346

Publish Date: 25-03-2025

Pages: 6 - 13

Views: 8

Downloads: 13

Author Affiliation:

¹Senior Consultant, Department of Internal Medicine, Hamad General Hospital, Doha, Qatar,

² Senior Consultant, Department of Pediatrics, Pediatric Hospital, Tripoli, Libya,

³Medical Student, Department of  Hematolotugy, Faculty of Medicine, Tripoli University, Tripoli, Libya,

⁴Consultant Physician, Department of Medicine, Alwakra Hospital, Alwakra, Qatar,

⁵Assistant Professor, Department of Human Physiology, Biotechnology Research Center, Tripoli, Libya,

⁶ Senior Consultant, Department of Medicine, Hamad General Hospital, Doha, Qat

Abstract

Hemolytic uremic syndrome (HUS) is a microangiopathic thrombotic disease, which is classified into atypical, typical, and secondary types. Thrombocytopenia, acute kidney failure, and hemolysis are the main features of HUS regardless of its type. Infection with Shiga toxin-producing Escherichia coli causes typical HUS, and gene mutations trigger atypical HUS, while secondary HUS is associated with bone marrow transplantation, autoimmunity, cancer, and other diseases. New insights into the pathogenesis of HUS have emerged over the past decades, suggesting an important role of the complement system in disease pathogenesis, which has been reinforced by the efficacy of plasma exchange and monoclonal antibodies in its treatment. In this review, we performed an updated review of HUS with a focus on understanding its pathogenesis.