Hemolytic uremic syndrome

Hemolytic uremic syndrome is characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney failure ^[1]. It is presented in the sources as a heterogeneous syndrome rather than a single entity, with most cases caused by Shiga-toxin-producing bacteria, especially Escherichia coli, and a smaller atypical subgroup driven by complement dysregulation ^[1][3]. The available material also identifies pregnancy-related and severe hypertension-associated forms within the broader complement-associated spectrum ^[3].

The core clinical pattern is the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney failure ^[1]. The syndrome is described within the thrombotic microangiopathy spectrum, which is associated with occlusive microvascular or macrovascular thrombosis and may produce end-organ ischemia ^[2]. Atypical hemolytic uremic syndrome is reported to have a relapsing course, and more than half of patients may progress to end-stage kidney failure ^[1]. The sources also note that hemolytic uremic syndrome is associated with significant morbidity and mortality, although detailed symptom timing and complication frequencies are not provided in the snippets ^[2].

The sources identify Shiga toxin-associated hemolytic uremic syndrome as the main cause of acute renal failure in children ^[1]. Most cases are attributed to Shiga-toxin-producing bacteria, especially Escherichia coli, placing the syndrome in a foodborne exposure context ^[1]. Atypical hemolytic uremic syndrome is reported to represent about 5% of cases ^[1]. The available snippets do not provide population incidence, seasonality, or geographic distribution, so source-backed detail on those topics is not yet available ^[1][3][2].

For the common Shiga toxin-associated form, transmission occurs through exposure to ground beef and unpasteurized milk ^[1]. The sources do not provide further detail on person-to-person spread, environmental persistence, or outbreak dynamics, so additional transmission pathways should not be inferred from this material ^[1]. Complement-mediated and atypical forms are described as pathobiologically distinct, but not as directly transmissible ^[3].

The sources explicitly identify children as an important affected group because Shiga toxin-associated hemolytic uremic syndrome is described as the main cause of acute renal failure in children ^[1]. Atypical and complement-mediated forms are linked in the literature to genetic or acquired complement dysregulation, and the review also notes pregnancy-related and severe hypertension-associated hemolytic uremic syndrome ^[3]. No further source-backed high-risk demographic or exposure-group detail is provided in the snippets ^[1][3].

The source material supports food exposure control as the principal preventive approach for the Shiga toxin-associated form, given transmission through ground beef and unpasteurized milk ^[1]. For complement-inhibition therapy in atypical hemolytic uremic syndrome, the literature warns of increased meningococcal infection risk and states that suitable prophylaxis must be addressed ^[3]. Beyond these points, the snippets do not provide a detailed prevention schedule or broader public-health control package, so source-backed detail is not yet available ^[1][3].

In surveillance terms, hemolytic uremic syndrome should be interpreted as a syndrome with multiple etiologic pathways rather than a single uniform disease entity ^[1][3]. The available sources support separating Shiga toxin-associated cases from complement-mediated, pregnancy-related, and severe hypertension-associated forms because prognosis and management context differ ^[1][3]. The syndrome is associated with substantial morbidity, and in children it is an important cause of acute renal failure ^[1][2].

1. 1 Boyer O et al. Hemolytic-Uremic Syndrome in Children. Pediatr Clin North Am. 2022 Dec. PMID: 36880929. doi: 10.1016/j.pcl.2022.07.006. PubMed: https://pubmed.ncbi.nlm.nih.gov/36880929/
2. 2 Abou-Ismail MY et al. Thrombotic microangiopathies: An illustrated review. Res Pract Thromb Haemost. 2022 Mar. PMID: 35615754. doi: 10.1002/rth2.12708. PubMed: https://pubmed.ncbi.nlm.nih.gov/35615754/
3. 3 Leon J et al. Complement-driven hemolytic uremic syndrome. Am J Hematol. 2023 May. PMID: 36683290. doi: 10.1002/ajh.26854. PubMed: https://pubmed.ncbi.nlm.nih.gov/36683290/
4. 4 Hemolytic-Uremic Syndrome. Pediatric Emergency Medicine. 2008. doi: 10.1016/b978-141600087-7.50134-3. DOI: https://doi.org/10.1016/b978-141600087-7.50134-3
5. 5 Hemolytic uremic syndrome. Rheumatology and Immunology Therapy. None. doi: 10.1007/3-540-29662-x_1196. DOI: https://doi.org/10.1007/3-540-29662-x_1196
6. 6 Hemolytic Uremic Syndrome. Transfusion Medicine and Hemostasis. 2009. doi: 10.1016/b978-0-12-374432-6.00092-0. DOI: https://doi.org/10.1016/b978-0-12-374432-6.00092-0

ICD-10

ICD-11

Total cases

601

Peak month

2019-12

Coverage

1 reporting countries · 2019-02-02 → 2026-06-20