Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001938585 | SCV002189153 | pathogenic | not provided | 2024-09-02 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp71*) in the CFH gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CFH are known to be pathogenic (PMID: 11170896, 14978182, 16621965, 23870792, 25188723). This variant is present in population databases (no rsID available, gnomAD 0.0009%). This variant has not been reported in the literature in individuals affected with CFH-related conditions. ClinVar contains an entry for this variant (Variation ID: 1417726). For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002484526 | SCV002775742 | likely pathogenic | Basal laminar drusen; Factor H deficiency; Hemolytic uremic syndrome, atypical, susceptibility to, 1; Age related macular degeneration 4 | 2024-03-05 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004529049 | SCV004111995 | likely pathogenic | CFH-related disorder | 2023-03-28 | criteria provided, single submitter | clinical testing | The CFH c.213G>A variant is predicted to result in premature protein termination (p.Trp71*). This variant has been reported in an individual with atypical hemolytic uremic syndrome (Table 3, Sheerin et al. 2016 PubMed ID: 25899302). This variant is reported in 0.00089% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/1-196642262-G-A). Nonsense variants in CFH are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Genome- |
RCV003452163 | SCV004180679 | likely pathogenic | Factor H deficiency | 2023-04-11 | criteria provided, single submitter | clinical testing |