Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001056876 | SCV001221341 | pathogenic | not provided | 2023-11-05 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Lys497*) in the SLC12A3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC12A3 are known to be pathogenic (PMID: 20848653, 22009145, 25841442). This variant is present in population databases (rs746818109, gnomAD 0.004%). This premature translational stop signal has been observed in individuals with Gitelman syndrome (PMID: 11168953). ClinVar contains an entry for this variant (Variation ID: 852297). For these reasons, this variant has been classified as Pathogenic. |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV001276375 | SCV005395697 | pathogenic | Familial hypokalemia-hypomagnesemia | 2024-09-05 | criteria provided, single submitter | clinical testing | Variant summary: SLC12A3 c.1489A>T (p.Lys497X) results in a premature termination codon, predicted to cause a truncation of the encoded protein or absence of the protein due to nonsense mediated decay, which are commonly known mechanisms for disease. The variant allele was found at a frequency of 1.7e-05 in 230414 control chromosomes (gnomAD). c.1489A>T has been reported in the literature in at least an individual affected with Gitelman Syndrome (Palazzo_2022). The following publication has been ascertained in the context of this evaluation (PMID: 35628451). ClinVar contains an entry for this variant (Variation ID: 852297). Based on the evidence outlined above, the variant was classified as pathogenic. |
Natera, |
RCV001276375 | SCV001462610 | pathogenic | Familial hypokalemia-hypomagnesemia | 2020-09-16 | no assertion criteria provided | clinical testing |