Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Revvity Omics, |
RCV003137004 | SCV003822896 | pathogenic | Polycystic kidney disease, adult type | 2023-02-17 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV003368059 | SCV004082629 | pathogenic | Inborn genetic diseases | 2023-08-14 | criteria provided, single submitter | clinical testing | The c.9584G>A (p.W3195*) alteration, located in exon 28 (coding exon 28) of the PKD1 gene, consists of a G to A substitution at nucleotide position 9584. This changes the amino acid from a tryptophan (W) to a stop codon at amino acid position 3195. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This alteration has been detected in the heterozygous state in two individuals with clinical features of PKD1-related polycystic kidney disease (Kim, 2021; Obeidova, 2014). A different nucleotide substitution resulting in the same nonsense variant, c.9585G > A (p.W3195*), has also been reported in patients with PKD1-related polycystic kidney disease (Kim, 2019; Neumann, 2013). Based on the available evidence, this alteration is classified as pathogenic. |