Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Athena Diagnostics | RCV000714152 | SCV000844835 | uncertain significance | not provided | 2018-04-03 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000714152 | SCV001815074 | uncertain significance | not provided | 2019-03-14 | criteria provided, single submitter | clinical testing | Not observed in large population cohorts (Lek et al., 2016); In silico analysis, which includes protein predictors and evolutionary conservation, supports a deleterious effect; Has not been previously published as pathogenic or benign to our knowledge |
Fulgent Genetics, |
RCV002499298 | SCV002812084 | uncertain significance | Familial juvenile hyperuricemic nephropathy type 1 | 2021-07-06 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004026832 | SCV004977862 | uncertain significance | Inborn genetic diseases | 2024-02-08 | criteria provided, single submitter | clinical testing | The c.116C>A (p.A39D) alteration is located in exon 3 (coding exon 2) of the UMOD gene. This alteration results from a C to A substitution at nucleotide position 116, causing the alanine (A) at amino acid position 39 to be replaced by an aspartic acid (D). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |