Use of genomic and functional analysis to characterize patients with steroid-resistant nephrotic syndrome.

Background: Children with genetic causes of steroid-resistant nephrotic syndrome (SRNS) usually do well after renal transplantation, while some with idiopathic SRNS show recurrence due to a putative podocyte-toxic factor. Distinguishing different forms of SRNS based on clinical criteria has been dif...

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Publicado en:Pediatric Nephrology Vol. 33; no. 10; pp. 1741 - 1751
Autores principales: Kitzler, Thomas M., Kachurina, Nadezda, Bitzan, Martin M., Torban, Elena, Goodyer, Paul R.
Formato: pictorial research tables/charts Journal Article
Publicado: Springer Nature Oct2018
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Oct2018
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      pub: Springer Nature
      place: New York, New York
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        10.1007/s00467-018-3995-2
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        atl: Use of genomic and functional analysis to characterize patients with steroid-resistant nephrotic syndrome.
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          Kitzler, Thomas M.
          Kachurina, Nadezda
          Bitzan, Martin M.
          Torban, Elena
          Goodyer, Paul R.
        affil: Department of Medical Genetics, The Montreal Children’s Hospital, McGill University Health Center, Montreal, Quebec, Canada
      sug:
        subj:
          Nephrotic Syndrome Familial and Genetic
          Nephrotic Syndrome Diagnosis
          Steroids
          Drug Resistance
          Sequence Analysis Methods
          Biological Assay
          Human
          Epithelial Cells Analysis
          Mutation
          Recurrence Risk Factors
          Confidence Intervals
          Nephrotic Syndrome Blood
          Grafts
          Nephrotic Syndrome Surgery
          Postoperative Complications
          Kidney Transplantation
          Cell-Matrix Junctions
      ab: Background: Children with genetic causes of steroid-resistant nephrotic syndrome (SRNS) usually do well after renal transplantation, while some with idiopathic SRNS show recurrence due to a putative podocyte-toxic factor. Distinguishing different forms of SRNS based on clinical criteria has been difficult. The aim of our study was to test a novel approach that allows categorization of patients into clinically useful subgroups.Methods: Seventeen patients with clinically confirmed SRNS were analyzed by next-generation sequencing (NGS) of 37 known SRNS genes and a functional assay of cultured human podocytes, which indirectly tests for toxicity of patients’ sera by evidenced loss of podocyte focal adhesion complex (FAC) number.Results: We identified a pathogenic mutation in seven patients (41%). Sera from patients with monogenic SRNS caused mild loss of FAC number down to 73% compared to untreated controls, while sera from seven of the remaining ten patients with idiopathic SRNS caused significant FAC number loss to 43% (non-overlapping difference 30%, 95% CI 26-36%, P < 0.001). All patients with recurrent SRNS (n = 4) in the graft showed absence of podocyte gene mutations but significant FAC loss. Three patients had no mutation nor serum podocyte toxicity.Conclusions: Our approach allowed categorization of patients into three subgroups: (1) patients with monogenic SRNS; (2) patients with idiopathic SRNS and marked serum podocyte toxicity; and (3) patients without identifiable genetic cause nor evidence of serum podocyte toxicity. Post-transplant SRNS recurrence risk appears to be low in groups 1 and 3, but high in group 2.
      pubtype: Academic Journal
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        pictorial
        research
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      ougenre: Article
    language: English
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