Literature DB >> 29058154

Clinical and genetic heterogeneity in familial steroid-sensitive nephrotic syndrome.

Guillaume Dorval1,2, Olivier Gribouval3,4, Vanesa Martinez-Barquero3,4, Eduardo Machuca3, Marie-Josèphe Tête3,4, Véronique Baudouin5, Stéphane Benoit6, Imen Chabchoub7, Gérard Champion8, Dominique Chauveau9, Hassib Chehade10, Chokri Chouchane11, Sylvie Cloarec6, Pierre Cochat12, Karin Dahan13, Jacques Dantal14, Yahsou Delmas15, Georges Deschênes5, Phillippe Dolhem16, Dominique Durand9, Zelal Ekinci17, Khalil El Karoui18, Michel Fischbach19, Jean-Pierre Grunfeld18, Vincent Guigonis20, Mongia Hachicha7, Julien Hogan21, Maryvonne Hourmant14, Aurélie Hummel18, Nassim Kamar9, Thierry Krummel22, Didier Lacombe23, Brigitte Llanas24, Laurent Mesnard25,26,27, Nabil Mohsin28, Patrick Niaudet29,30, Hubert Nivet6, Paloma Parvex31, Christine Pietrement32,33, Loic de Pontual34, Claire Pouteil Noble35, David Ribes9, Pierre Ronco25,26,27, Eric Rondeau25, Marion Sallee36, Michel Tsimaratos37, Tim Ulinski21, Rémi Salomon3,4,29,30, Corinne Antignac3,4,30,38, Olivia Boyer3,4,29,30.   

Abstract

BACKGROUND: Familial steroid-sensitive nephrotic syndrome (SSNS) is a rare condition. The disease pathophysiology remains elusive. However, bi-allelic mutations in the EMP2 gene were identified, and specific variations in HLA-DQA1 were linked to a high risk of developing the disease.
METHODS: Clinical data were analyzed in 59 SSNS families. EMP2 gene was sequenced in families with a potential autosomal recessive (AR) inheritance. Exome sequencing was performed in a subset of 13 families with potential AR inheritance. Two variations in HLA-DQA1 were genotyped in the whole cohort.
RESULTS: Transmission was compatible with an AR (n = 33) or autosomal dominant (AD, n = 26) inheritance, assuming that familial SSNS is a monogenic trait. Clinical features did not differ between AR and AD groups. All patients, including primary (n = 7) and secondary steroid resistant nephrotic syndrone (SRNS), (n = 13) were sensitive to additional immunosuppressive therapy. Both HLA-DQA1 variations were found to be highly linked to the disease (OR = 4.34 and OR = 4.89; p < 0.001). Exome sequencing did not reveal any pathogenic mutation, neither did EMP2 sequencing.
CONCLUSIONS: Taken together, these results highlight the clinical and genetic heterogeneity in familial SSNS. Clinical findings sustain an immune origin in all patients, whatever the initial steroid-sensitivity. The absence of a variant shared by two families and the HLA-DQA1 variation enrichments suggest a complex mode of inheritance.

Entities:  

Keywords:  EMP2; Familial nephrotic syndrome; Genetics; HLA-DQA1; Immunity; Podocyte; Steroid resistance; Steroid sensitivity

Mesh:

Substances:

Year:  2017        PMID: 29058154     DOI: 10.1007/s00467-017-3819-9

Source DB:  PubMed          Journal:  Pediatr Nephrol        ISSN: 0931-041X            Impact factor:   3.714


  48 in total

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