Phenotypic Spectrum of Children with Nephronophthisis and Related Ciliopathies

Clin J Am Soc Nephrol. 2017 Dec 7;12(12):1974-1983. doi: 10.2215/CJN.01280217. Epub 2017 Nov 16.

Abstract

Background and objectives: Genetic heterogeneity and phenotypic variability are major challenges in familial nephronophthisis and related ciliopathies. To date, mutations in 20 different genes (NPHP1 to -20) have been identified causing either isolated kidney disease or complex multiorgan disorders. In this study, we provide a comprehensive and detailed characterization of 152 children with a special focus on extrarenal organ involvement and the long-term development of ESRD.

Design, setting, participants, & measurements: We established an online-based registry (www.nephreg.de) to assess the clinical course of patients with nephronophthisis and related ciliopathies on a yearly base. Cross-sectional and longitudinal data were collected. Mean observation time was 7.5±6.1 years.

Results: In total, 51% of the children presented with isolated nephronophthisis, whereas the other 49% exhibited related ciliopathies. Monogenetic defects were identified in 97 of 152 patients, 89 affecting NPHP genes. Eight patients carried mutations in other genes related to cystic kidney diseases. A homozygous NPHP1 deletion was, by far, the most frequent genetic defect (n=60). We observed a high prevalence of extrarenal manifestations (23% [14 of 60] for the NPHP1 group and 66% [61 of 92] for children without NPHP1). A homozygous NPHP1 deletion not only led to juvenile nephronophthisis but also was able to present as a predominantly neurologic phenotype. However, irrespective of the initial clinical presentation, the kidney function of all patients carrying NPHP1 mutations declined rapidly between the ages of 8 and 16 years, with ESRD at a mean age of 11.4±2.4 years. In contrast within the non-NPHP1 group, there was no uniform pattern regarding the development of ESRD comprising patients with early onset and others preserving normal kidney function until adulthood.

Conclusions: Mutations in NPHP genes cause a wide range of ciliopathies with multiorgan involvement and different clinical outcomes.

Keywords: Adolescent; Bardet-Biedl syndrome; COACH syndrome; Ciliopathies; Congenital oculomotor apraxia; Cross-Sectional Studies; Genetic Heterogeneity; Homozygote; Joubert-like syndromes; Kidney Diseases, Cystic; Kidney Failure, Chronic; Mainzer-Saldino syndrome; Mutation; NEPHREG registry; Nephronophthisis (NPH); Nephronophthisis related ciliopathy; Nephronophthisis, familial juvenile; Prevalence; Registries; Senior-Løken syndrome.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Adolescent
  • Anemia / genetics
  • Antigens, Neoplasm / genetics
  • Calmodulin-Binding Proteins / genetics
  • Carrier Proteins / genetics
  • Cell Cycle Proteins
  • Child
  • Ciliopathies / complications
  • Ciliopathies / genetics*
  • Cross-Sectional Studies
  • Cytoskeletal Proteins
  • Female
  • Glomerular Filtration Rate / genetics
  • Homozygote
  • Humans
  • Kidney / diagnostic imaging
  • Kidney Diseases, Cystic / complications
  • Kidney Diseases, Cystic / congenital*
  • Kidney Diseases, Cystic / diagnostic imaging
  • Kidney Diseases, Cystic / genetics
  • Kidney Failure, Chronic / genetics*
  • Kidney Failure, Chronic / physiopathology
  • Kinesins / genetics
  • Longitudinal Studies
  • Male
  • Membrane Proteins / genetics*
  • Neoplasm Proteins / genetics
  • Nervous System Diseases / genetics
  • Phenotype*
  • Polyuria / genetics
  • Proteins / genetics
  • Ultrasonography
  • Young Adult

Substances

  • Adaptor Proteins, Signal Transducing
  • Antigens, Neoplasm
  • Calmodulin-Binding Proteins
  • Carrier Proteins
  • Cell Cycle Proteins
  • Cep290 protein, human
  • Cytoskeletal Proteins
  • IFT140 protein, human
  • IQCB1 protein, human
  • Membrane Proteins
  • NPHP1 protein, human
  • NPHP4 protein, human
  • Neoplasm Proteins
  • Proteins
  • TMEM67 protein, human
  • nephrocystin-3, human
  • Kinesins

Supplementary concepts

  • Nephronophthisis, familial juvenile