Postinfectious Hemolytic Uremic Syndrome

Bitzan, Martin; Lapeyraque, Anne-Laure

doi:10.1007/978-3-662-52972-0_26

Cited by 7 publications

(10 citation statements)

References 677 publications

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“…Kidney biopsies, where obtained during acute and post-acute iHUS reveal varied features [ 25 , 33 , 37 , 38 , 92 , 93 ] that replicate key findings described in other forms of HUS [ 3 ], including endothelial cell swelling and luminal narrowing, focal mesangiolysis, intravascular deposition of fibrin, and diffuse granular staining for C3 [ 25 , 33 , 37 , 92 , 93 ], and in some cases, for IgG or IgM [ 25 , 37 , 92 ]. No electron-dense deposits, virus-like particles or tubuloreticular inclusions were described [ 93 ].…”

Section: Influenza Tma In Kidney Transplant Recipientsmentioning

confidence: 76%

“…pnHUS patients are commonly Coombs test-positive, a feature that has been related to Nan-mediated desialylation [ 3 , 84 , 85 ]. By comparison, the direct Coombs test was negative in 7 of the examined iHUS patients (Table 2 ).…”

Section: Neuraminidase and The Link Between Influenza And Smentioning

confidence: 99%

“…Patients with influenza-associated TMA benefit from best supportive care, similar to other forms of HUS [ 3 , 84 ]. The outcome of iHUS is generally favorable; in our analysis, 3 out of 22 patients died (14%; #3, 4, and 9; all before 2008).…”

Section: Therapeutic Management Outcome and Preventionmentioning

confidence: 99%

“…The current, interchangeable use of the epithet “atypical” that may or may not include HUS owing to pneumococcal infection and various metabolic and other conditions, including “secondary” forms of HUS [ 1 , 7 ] and HUS strictly caused by complement dysregulation (“primary complement-mediated HUS” or “HUS with dysregulation of the APC” [ 2 ]), leads to confusion about the etiology of and appropriate therapy for different forms of HUS. We argue in favor of etiologically defined designations that correspond to different pathomechanisms and lead to rational, mechanism-targeting therapies [ 2 , 3 , 94 ].…”

Section: Conclusion and Future Areas Of Researchmentioning

confidence: 99%

“…Infections by Shiga toxin-producing Escherichia coli (STEC or Stx HUS) are the most common cause of TMA (HUS) in children. Less frequently, HUS has been linked to infections by other bacteria, such as Shigella dysenteriae type 1, Clostridium perfringens or Streptococcus pneumoniae , and by HIV, coxsackie-, Epstein–Barr (EBV), varicella or influenza viruses [ 1 – 3 ].…”

Section: Introductionmentioning

confidence: 99%

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Influenza-associated thrombotic microangiopathies

Bitzan

Zieg

2017

Pediatr Nephrol

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Thrombotic microangiopathy (TMA) refers to phenotypically similar disorders, including hemolytic uremic syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP). This review explores the role of the influenza virus as trigger of HUS or TTP. We conducted a literature survey in PubMed and Google Scholar using HUS, TTP, TMA, and influenza as keywords, and extracted and analyzed reported epidemiological and clinical data. We identified 25 cases of influenza-associated TMA. Five additional cases were linked to influenza vaccination and analyzed separately. Influenza A was found in 83%, 10 out of 25 during the 2009 A(H1N1) pandemic. Two patients had bona fide TTP with ADAMTS13 activity <10%. Median age was 15 years (range 0.5–68 years), two thirds were male. Oligoanuria was documented in 81% and neurological involvement in 40% of patients. Serum C3 was reduced in 5 out of 14 patients (36%); Coombs test was negative in 7 out of 7 and elevated fibrin/fibrinogen degradation products were documented in 6 out of 8 patients. Pathogenic complement gene mutations were found in 7 out of 8 patients tested (C3, MCP, or MCP combined with CFB or clusterin). Twenty out of 24 patients recovered completely, but 3 died (12%). Ten of the surviving patients underwent plasma exchange (PLEX) therapy, 5 plasma infusions. Influenza-mediated HUS or TTP is rare. A sizable proportion of tested patients demonstrated mutations associated with alternative pathway of complement dysregulation that was uncovered by this infection. Further research is warranted targeting the roles of viral neuraminidase, enhanced virus-induced complement activation and/or ADAMTS13 antibodies, and rational treatment approaches.Electronic supplementary materialThe online version of this article (10.1007/s00467-017-3783-4) contains supplementary material, which is available to authorized users

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Section: Influenza Tma In Kidney Transplant Recipientsmentioning

confidence: 76%

Section: Neuraminidase and The Link Between Influenza And Smentioning

confidence: 99%

Section: Therapeutic Management Outcome and Preventionmentioning

confidence: 99%

Section: Conclusion and Future Areas Of Researchmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Influenza-associated thrombotic microangiopathies

Bitzan

Zieg

2017

Pediatr Nephrol

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Hemolytic Uremic Syndrome (HUS)

Gupta¹,

Gupta²

2022

Pathology of Glomerular Diseases

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Whole-genome characterization of hemolytic uremic syndrome-causing Shiga toxin-producing Escherichia coli in Sweden

et al. 2021

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Shiga toxin-producing Escherichia coli , a foodborne bacterial pathogen, has been linked to a broad spectrum of clinical outcomes ranging from asymptomatic carriage to fatal hemolytic uremic syndrome (HUS). Here, we collected clinical data and STEC strains from HUS patients from 1994 through 2018, whole-genome sequencing was performed to molecularly characterize HUS-associated STEC strains, statistical analysis was conducted to identify bacterial genetic factors associated with severe outcomes in HUS patients. O157:H7 was the most predominant serotype (57%) among 54 HUS-associated STEC strains, followed by O121:H19 (19%) and O26:H11 (7%). Notably, some non-predominant serotypes such as O59:H17 (2%) and O109:H21 (2%) also caused HUS. All O157:H7 strains with one exception belonged to clade 8. During follow-up at a median of 4 years, 41% of the patients had renal sequelae. Fifty-nine virulence genes were found to be statistically associated with severe renal sequelae, these genes encoded type II and type III secretion system effectors, chaperones, and other factors. Notably, virulence genes associated with severe clinical outcomes were significantly more prevalent in O157:H7 strains. In contrast, genes related to mild symptoms were evenly distributed across all serotypes. The whole-genome phylogeny indicated high genomic diversity among HUS-STEC strains. No distinct cluster was found between HUS and non-HUS STEC strains. The current study showed that O157:H7 remains the main cause of STEC-associated HUS, despite the rising importance of other non-O157 serotypes. Besides, O157:H7 is associated with severe renal sequelae in the follow-up, which could be a risk factor for long-term prognosis in HUS patients.

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Postinfectious Hemolytic Uremic Syndrome

Cited by 7 publications

References 677 publications

Influenza-associated thrombotic microangiopathies

Influenza-associated thrombotic microangiopathies

Hemolytic Uremic Syndrome (HUS)

Whole-genome characterization of hemolytic uremic syndrome-causing Shiga toxin-producing Escherichia coli in Sweden

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