ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO455

Monogenic Causes Identified in 30.70% of Children with Steroid-Resistant Nephrotic Syndrome: A Single-Centre Study

Session Information

Category: Genetic Diseases of the Kidneys

  • 1202 Genetic Diseases of the Kidneys: Non-Cystic

Authors

  • Zhang, Luyan, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
  • Zheng, Bixia, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
  • Zhang, Aihua, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
Background

Steroid resistant nephrotic syndrome (SRNS) is the second most common cause of end-stage kidney disease in children, mostly associated with focal segmental glomerulosclerosis (FSGS). Advances in genomic science have enabled the identification of causative variants in 20 – 30% of SRNS patients.

Methods

We used whole exome sequencing (WES) to explore the genetic causes of SRNS in children. Totally 101 patients with SRNS, and 13 patients with subnephrotic proteinuria and FSGS were retrospectively enrolled in our hospital between 2018 and 2022. For the known monogenic causes analysis, we generated a known SRNS gene list of 71 genes through reviewing the OMIM database and literature.

Results

Causative variants were identified in 30.70% of our cohort, and the most frequently mutated genes in our cohort were WT1 (7/33), NPHS1 (3/33), ADCK4(3/33), TRPC6(3/33) and ANLN (3/33). Five patients carried variants in phenocopy genes, including MYH9, MAFB, TTC21B, AGRN, and FAT4. The variant detection rate was the highest in the two subtype groups with congenital nephrotic syndrome and syndromic SRNS. In total 68.75% of variants we identified were novel,and have not been previously reported in literature.

Conclusion

Comprehensive genetic analysis is key to realizing the clinical benefits of a genetic diagnosis. We suggest that all children with SRNS undergo genetic testing, especially those with early onset and extrarenal phenotypes.