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The current study aimed to investigate the clinical and pathological features, complement activation status, and the genetic variations in a <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>hinese cohort of patients with renal biopsy\u2010proven postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method of study<\/jats:title><jats:p>Five patients with postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content> were recruited. Renal biopsy specimens were examined and scored. Plasma levels of complements were detected, and coding sequences of complement regulators were screened. Anti\u2010<jats:styled-content style=\"fixed-case\">CFH<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content> autoantibodies were further detected.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Patients with postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content> patients presented with severe clinical manifestations and renal involvement. The renal biopsies of the five patients showed typical features of thrombotic microangiopathies. The levels of the following complement components, <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>4d, <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>b, <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3a, <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a, and <jats:styled-content style=\"fixed-case\">SC<\/jats:styled-content>5b\u20109, were significantly elevated in patients with postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content> compared with normal non\u2010pregnant controls. The plasma levels of <jats:styled-content style=\"fixed-case\">CFH<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CFI<\/jats:styled-content> significantly decreased in patients with postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content> compared with normal pregnant women. Three <jats:styled-content style=\"fixed-case\">CFH<\/jats:styled-content> single nucleotide polymorphisms (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s) were identified in the five patients. Two patients presented with <jats:styled-content style=\"fixed-case\">CFH<\/jats:styled-content> autoantibodies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content> is a clinical syndrome with severe renal damage. Genetic deficiencies and autoantibodies of <jats:styled-content style=\"fixed-case\">CFH<\/jats:styled-content> may lead to alternative pathway overactivation and participated in the pathogenesis of postpartum a<jats:styled-content style=\"fixed-case\">HUS<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aji.12404","type":"journal-article","created":{"date-parts":[[2015,5,25]],"date-time":"2015-05-25T14:19:19Z","timestamp":1432563559000},"page":"345-356","source":"Crossref","is-referenced-by-count":19,"title":["Overactivation of Complement Alternative Pathway in Postpartum Atypical Hemolytic Uremic Syndrome Patients with Renal Involvement"],"prefix":"10.1111","volume":"74","author":[{"given":"Di","family":"Song","sequence":"first","affiliation":[{"name":"Renal Division Department of Medicine Peking University First Hospital Beijing China"},{"name":"Peking University Institute of Nephrology Beijing China"},{"name":"Key laboratory of Renal Disease Ministry of Health of 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