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The D +/D − dichotomy fails to differentiate postinfectious forms, such as S. The historical terms diarrhea-positive (D +) and diarrhea-negative (D −) HUS, introduced to distinguish STEC-induced HUS from “atypical” forms, should be abandoned since at least one third of patients with complement-mediated “atypical” HUS present with diarrhea or even colitis. (c) HUS caused by endotheliotoxic therapeutics (examples: cancer drugs, endotheliotropic antibodies, such as anti-VEGF)ĪWhile influenza virus expresses neuraminidase (NA), its causal role in HUS has yet to be provenīThe mechanism underlying HIV HUS is not clear the majority of patients appear to present HUS-like features ĬForms involving unregulated alternative pathway of complement activation are differentiated from others for therapeutic purposes combinations of various factor mutations and/or autoantibodies existĮA recent publication implicates cases with DGKE mutation that demonstrate complement consumption įCombination with genetic complement regulator mutations have been described (b) “Secondary forms” (examples: HUS associated with bone marrow transplantation, f anti-phospholipid syndrome, malignant hypertension etc. (a) Spontaneous forms without known co-morbidities (b) Autoimmune TTP (due to anti-ADAMS13 antibody) (a) Hereditary TTP (Upshaw Shulman Syndrome, autosomal recessive mutation of ADAMS13) Thrombotic thrombocytopenic purpura (TTP) (a) Autoantibodies against complement regulatory proteins (example: anti-CFH antibody)Ĥ. (b) Genetic abnormalities without known complement dysregulation, usually autosomal recessive (examples: defective cobalamin metabolism due to mutations in MMACHC mutation of DGKE ) e (ii) Membrane-bound regulator deficiencies (examples: MCP) (i) Soluble regulator deficiencies (examples: CFH, CFI etc.) (a) HUS associated with mutations of regulatory proteins and components of the complement and coagulation pathways c (i) Shiga toxin-producing / enterohemorrhagic Escherichia coli (STEC/EHEC) (a) Shiga toxin-producing bacteria (STPB) Infection-induced HUS (caused by endothelial injury due to specific infectious agents) However, HUS can arise following infection by a “specific” agent in a patient with a complement defect the “atypical” nature of such HUS is usually uncovered by its atypical presentation (relapsing course, recurrence after transplantation or family history).ġ. This contrasts with HUS causally linked to the deficiency of proteins that regulate the alternative pathway of complement, either due to genetic mutations or the presence of autoantibodies (mainly to complement factor H), or to other genetic and metabolic causes (Box 26.1). In children, more than 80 % of cases of HUS are due to STEC infection. Stx and NA are thought to injure vascular endothelial and perhaps circulating red blood cells and platelets leading to thrombotic microangiopathy with intravascular hemolysis (TMA). Major triggers of postinfectious HUS are Shiga toxin (Stx) producing bacteria (STPB, mainly Escherichia coli and Shigella dysenteriae type 1) and neuraminidase (NA) producing organisms (mainly Streptococcus pneumoniae). pneumoniae, influenza A and HIV and discusses potential interactions between these pathogens and the complement system.įor the purpose of this section, we define postinfectious hemolytic uremic syndrome as HUS caused by specific infectious organisms in patients with no identifiable HUS-associated genetic mutation or autoantibody. The remainder of this chapter highlights rarer forms of (post-infectious) HUS due to S. The outcome of STEC-HUS is generally favorable, but chronic kidney disease, permanent extrarenal, mainly cerebral complication and death (in less than 5 %) occur and long-term follow-up is recommended. Treatment of STEC-HUS is supportive more investigations are needed to evaluate the efficacy of putative preventive and therapeutic measures, such as non-phage-inducing antibiotics, volume expansion and anti-complement agents. Clinicians should always strive for an etiological diagnosis through the microbiological or molecular identification of Stx-producing bacteria and Stx or, if negative, serological assays. STEC disease is characterized by hematological (microangiopathic hemolytic anemia), renal (acute kidney injury) and extrarenal organ involvement.

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This chapter reviews the epidemiology and pathogenesis of STEC-HUS, including bacterial-derived factors and host responses. The majority of episodes is due to infections by Shiga toxin (Stx) producing Escherichia coli (STEC).

Post-infectious hemolytic uremic syndrome (HUS) is caused by specific pathogens in patients with no identifiable HUS-associated genetic mutation or autoantibody.