Dataset Information

Severe SARS-COV-2 infection in pediatric patient with atypical Hemolytic Uremic Syndrome: A case report.

ABSTRACT:

Introduction and important

There is a high incidence of acute kidney injury with COVID-19 infections. We report a child with atypical Hemolytic Uremic Syndrome (aHUS) admitted to Intensive care Unit (ICU) due to severe SARS-COV-2 infection. Children are recognised as at lower risk of severe COVID-19 compared with adults, but the impact of atypical Hemolytic Uremic Syndrome is yet to be determined.

Case presentation

An eleven years old male presented to Mohammed Alamin Hamid Pediatric Hospital with generalize body swelling, skin rash and red urine. Examination reveal hepatomegaly and hemic murmur. Investigations reveal anemia, normal platelets, and impaired renal function. Peripheral blood picture shows shistocytes, crenated RBCs, occasional poikilocytes and mild neutrophilia.During hospital stay the patient developed severe shortness of breath and fever, diagnosed as COVID-19 and required ICU admission 2 days later due to severe respiratory compromised.

Clinical discussion

An atypical Hemolytic Uremic Syndrome with normal platelets is extremely rare condition. SARS-COV-2 infection in patients atypical Hemolytic Uremic Syndrome has not been reported in literature.

Conclusion

Our study shown that severe SARS-COV-2 infection can be developed in pediatric patients patients with co-existing atypical Hemolytic Uremic Syndrome.

SUBMITTER: Hamza SB

PROVIDER: S-EPMC8867980 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Publications

Severe SARS-COV-2 infection in pediatric patient with atypical Hemolytic Uremic Syndrome: A case report.

Hamza Salih Boushra SB

Annals of medicine and surgery (2012) 20220224

<h4>Introduction and important</h4>There is a high incidence of acute kidney injury with COVID-19 infections. We report a child with atypical Hemolytic Uremic Syndrome (aHUS) admitted to Intensive care Unit (ICU) due to severe SARS-COV-2 infection. Children are recognised as at lower risk of severe COVID-19 compared with adults, but the impact of atypical Hemolytic Uremic Syndrome is yet to be determined.<h4>Case presentation</h4>An eleven years old male presented to Mohammed Alamin Hamid Pediat ...[more]

PMID: 35228868

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Project description:BackgroundThe hemolytic-uremic syndrome consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. The common form of the syndrome is triggered by infection with Shiga toxin-producing bacteria and has a favorable outcome. The less common form of the syndrome, called atypical hemolytic-uremic syndrome, accounts for about 10% of cases, and patients with this form of the syndrome have a poor prognosis. Approximately half of the patients with atypical hemolytic-uremic syndrome have mutations in genes that regulate the complement system. Genetic factors in the remaining cases are unknown. We studied the role of thrombomodulin, an endothelial glycoprotein with anticoagulant, antiinflammatory, and cytoprotective properties, in atypical hemolytic-uremic syndrome.MethodsWe sequenced the entire thrombomodulin gene (THBD) in 152 patients with atypical hemolytic-uremic syndrome and in 380 controls. Using purified proteins and cell-expression systems, we investigated whether thrombomodulin regulates the complement system, and we characterized the mechanisms. We evaluated the effects of thrombomodulin missense mutations associated with atypical hemolytic-uremic syndrome on complement activation by expressing thrombomodulin variants in cultured cells.ResultsOf 152 patients with atypical hemolytic-uremic syndrome, 7 unrelated patients had six different heterozygous missense THBD mutations. In vitro, thrombomodulin binds to C3b and factor H (CFH) and negatively regulates complement by accelerating factor I-mediated inactivation of C3b in the presence of cofactors, CFH or C4b binding protein. By promoting activation of the plasma procarboxypeptidase B, thrombomodulin also accelerates the inactivation of anaphylatoxins C3a and C5a. Cultured cells expressing thrombomodulin variants associated with atypical hemolytic-uremic syndrome had diminished capacity to inactivate C3b and to activate procarboxypeptidase B and were thus less protected from activated complement.ConclusionsMutations that impair the function of thrombomodulin occur in about 5% of patients with atypical hemolytic-uremic syndrome.

Dataset Information

Severe SARS-COV-2 infection in pediatric patient with atypical Hemolytic Uremic Syndrome: A case report.

Introduction and important

Case presentation

Clinical discussion

Conclusion

Publications

Severe SARS-COV-2 infection in pediatric patient with atypical Hemolytic Uremic Syndrome: A case report.

Similar Datasets

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