Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Prevention |
RCV003417691 | SCV004112947 | pathogenic | CLCN5-related disorder | 2022-12-07 | criteria provided, single submitter | clinical testing | The CLCN5 c.100C>T variant is predicted to result in premature protein termination (p.Arg34*). This variant has been reported to have occurred de novo or be inherited from a mother with nephrolithiasis in two hemizygous patients with Dent disease (Hoopes et al. 1998. PubMed ID: 9734595; Wen et al. 2018. PubMed ID: 30581818). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Nonsense variants in CLCN5 are expected to be pathogenic. This variant is interpreted as pathogenic. |
Neuberg Centre For Genomic Medicine, |
RCV004546452 | SCV005042922 | likely pathogenic | Familial X-linked hypophosphatemic vitamin D refractory rickets | criteria provided, single submitter | clinical testing | The stop gained c.310C>Tp.Arg104Ter variant in CLCN5 gene has reported in hemizygous state in an individual affected with CLCN5 related disorders Wen M, et. al., 2018. The c.310C>T variant is novel not in any individuals in gnomAD Exomes and 1000Genomes. This variant has been reported to the ClinVar database. The nucleotide change c.310C>T in CLCN5 is predicted asconserved by GERP++ and PhyloP across 100 vertebrates. Loss of function variants have been previously reported to be diseasecausing. For these reasons, this variant has been classified as Likely Pathogenic. | |
Gene |
RCV000192273 | SCV000243781 | not provided | Dent disease type 1 | no assertion provided | literature only |