Late Onset of Congenital TTP: Case Presentation and Review of the Literature.

Background: Congential thrombotic thrombocytopenic purpura (cTTP) is a ultrarare genetic disorder caused by reduced or absent ADAMTS13 enzyme activity. In contrast to the acquired form of TTP, which results from inhibitory autoantibodies against ADAMTS13, cTTP arises due to mutations in the ADAMTS13...

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Publicado en:Clinical Medicine Insights: Case Reports Vol. 19; pp. 1 - 9
Autores principales: Chatzisfetkos, Athanasios, Bergmann, Carsten, Janssen, Ulf
Formato: algorithm case study tables/charts Journal Article
Publicado: Sage Publications Inc. 2/18/2026
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 2/18/2026
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      pub: Sage Publications Inc.
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        atl: Late Onset of Congenital TTP: Case Presentation and Review of the Literature.
      aug:
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          Chatzisfetkos, Athanasios
          Bergmann, Carsten
          Janssen, Ulf
        affil: Department of Nephrology and Diabetology, Kliniken Maria Hilf, Mönchengladbach, Germany
      sug:
        subj:
          Purpura, Thrombotic Thrombocytopenic Familial and Genetic
          Anemia, Hemolytic
          Purpura, Thrombotic Thrombocytopenic Symptoms
          Purpura, Thrombotic Thrombocytopenic Physiopathology
          Kidney Failure, Acute
          Adult
          Purpura, Thrombotic Thrombocytopenic Diagnosis
          Female
          Genetic Screening
          Treatment Delay
          Diagnosis, Differential
          Thrombosis
          Blood Coagulation Disorders, Inherited
          Adult: 19-44 years
          Female
      ab: Background: Congential thrombotic thrombocytopenic purpura (cTTP) is a ultrarare genetic disorder caused by reduced or absent ADAMTS13 enzyme activity. In contrast to the acquired form of TTP, which results from inhibitory autoantibodies against ADAMTS13, cTTP arises due to mutations in the ADAMTS13 gene and lacks such inhibitors. cTTP commonly manifests during infancy through recurrent episodes of hemolytic anemia and signs of microvascular damage. Episodes are often precipitated by infections or physical stressors. Case presentation: A 23-year-old female patient presented to the emergency department with microangiopathic hemolytic anemia (MAHA), a reduced platelet count and acute kidney injury stage 3 (AKI 3). Three days before she had suffered a knee injury, which was treated with fentanyl. The peripheral-blood smear showed many schistocytes. A thrombotic microangiopathy was suspected and therapeutic plasma exchange (TPE) was initiated. ADAMTS13 activity on admission was 4% without a detectable inhibitory antibody and an inherited ADAMTS13 deficiency was suspected. Genetic testing revealed 2 presumably compound heterozygous variants in the ADAMTS13 gene, confirming the diagnosis of cTTP. After 3 TPE platelet count raised significantly with improvement of renal function. Thereafter the patient received prophylactic plasma infusions every 2 to 3 weeks. At 1-year follow-up she had a normal renal function and no recurrence of hemolytic anemia. Conclusion: The present case of cTTP is notable for its late onset at first presentation, with unusual severe renal impairment. Rapid diagnosis and timely initiation of treatment are critical. Differential diagnoses such as malignant hypertension, sepsis, and autoimmune diseases like systemic lupus erythematosus must be excluded.
      pubtype: Academic Journal
      doctype:
        algorithm
        case study
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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