Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000049930 | SCV000800329 | pathogenic | Finnish congenital nephrotic syndrome | 2018-05-31 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001034959 | SCV001198262 | likely pathogenic | not provided | 2019-02-18 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 5 of the NPHS1 gene. It is expected to disrupt RNA splicing and likely results in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). This variant has been observed in several individuals affected with congential nephrotic syndrome (PMID: 18614772, 25720465). ClinVar contains an entry for this variant (Variation ID: 56517). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site, but this prediction has not been confirmed by published transcriptional studies. Donor and acceptor splice site variants typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in NPHS1 are known to be pathogenic (PMID: 11317351, 11854170, 12039988). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Juha Muilu Group; Institute for Molecular Medicine Finland |
RCV000049930 | SCV000082339 | probable-pathogenic | Finnish congenital nephrotic syndrome | no assertion criteria provided | not provided | Converted during submission to Likely pathogenic. |