Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center for Genomic Medicine, |
RCV001533185 | SCV001746631 | pathogenic | Polycystic kidney disease 2 | 2021-01-04 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV001533185 | SCV001752715 | likely pathogenic | Polycystic kidney disease 2 | 2021-06-30 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001548698 | SCV001768656 | pathogenic | not provided | 2022-12-02 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Not observed in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 34426522, 36177613, 22863349, 34008892, 22508176) |
Laboratory of Medical Genetics, |
RCV001533185 | SCV001976970 | pathogenic | Polycystic kidney disease 2 | 2021-10-01 | criteria provided, single submitter | clinical testing | PVS1, PM2, PP3, PP5 |
Prevention |
RCV003908885 | SCV004726855 | pathogenic | PKD2-related disorder | 2023-10-25 | no assertion criteria provided | clinical testing | The PKD2 c.1837C>T variant is predicted to result in premature protein termination (p.Gln613*). This variant has been reported to be pathogenic for autosomal dominant polycystic kidney disease (ADPKD) (see for example at Robinson et al. 2012. PubMed ID: 22863349). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Nonsense variants in PKD2 are expected to be pathogenic. This variant is interpreted as pathogenic. |