| Literature DB >> 31472902 |
Ashish K Solanki1, Eugen Widmeier2, Ehtesham Arif1, Shailza Sharma1, Ankana Daga3, Pankaj Srivastava1, Sang-Ho Kwon4, Hannah Hugo3, Makiko Nakayama3, Nina Mann3, Amar J Majmundar3, Wei Tan3, Heon Yung Gee5, Caroline E Sadowski3, Choni Rinat6, Rachel Becker-Cohen6, Carsten Bergmann7, Seymour Rosen8, Michael Somers3, Shirlee Shril3, Tobias B Huber9, Shrikant Mane10, Friedhelm Hildebrandt11, Deepak Nihalani12.
Abstract
Steroid-resistant nephrotic syndrome is a frequent cause of chronic kidney disease almost inevitably progressing to end-stage renal disease. More than 58 monogenic causes of SRNS have been discovered and majority of known steroid-resistant nephrotic syndrome causing genes are predominantly expressed in glomerular podocytes, placing them at the center of disease pathogenesis. Herein, we describe two unrelated families with steroid-resistant nephrotic syndrome with homozygous mutations in the KIRREL1 gene. One mutation showed high frequency in the European population (minor allele frequency 0.0011) and this patient achieved complete remission following treatment, but later progressed to chronic kidney disease. We found that mutant KIRREL1 proteins failed to localize to the podocyte cell membrane, indicating defective trafficking and impaired podocytes function. Thus, the KIRREL1 gene product has an important role in modulating the integrity of the slit diaphragm and maintaining glomerular filtration function.Entities:
Keywords: KIRREL1; focal segmental glomerulosclerosis; minimal change disease; steroid-resistant nephrotic syndrome
Year: 2019 PMID: 31472902 PMCID: PMC6756928 DOI: 10.1016/j.kint.2019.06.016
Source DB: PubMed Journal: Kidney Int ISSN: 0085-2538 Impact factor: 10.612