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Use GeneFoundry to build an ACMG/AMP evidence worksheet for HNF1B NM_000458.4:c.529C>T (p.Arg177Ter), ClinVar VCV000012635, in autosomal dominant renal cysts and diabetes syndrome. Resolve the GRCh38 allele, retrieve its ClinVar record and gnomAD frequency, inspect AutoPVS1 and VEP, and confirm ClinGen validity and dosage context. Separate source classifications from candidate criteria, identify missing evidence and avoid double counting. Do not produce an autonomous final classification.

The result

ClinVar reports Pathogenic with two review stars for the resolved GRCh38 allele. AutoPVS1 suggests VeryStrong loss-of-function evidence, but this remains a candidate for expert review. The gnomAD lookup returned not_found, so no population-frequency criterion is assigned.

Retrieved evidence for one allele · GRCh38 17-37739455-G-A
Source / observationCaptured result
ClinVar identityVCV000012635 · NM_000458.4:c.529C>T · p.Arg177Ter
ClinVar aggregate classificationPathogenic · 2/4 stars · criteria provided, multiple submitters, no conflicts · 7 submitters
ClinVar datesLast evaluated 7 March 2025; weekly release 31 August 2026
ClinGen gene-disease contextHNF1B–renal cysts and diabetes syndrome (MONDO:0007669) · autosomal dominant · Definitive
ClinGen mechanism contextHaploinsufficiency score 3: sufficient evidence for dosage pathogenicity
AutoPVS1NM_000458.4 · exon 2/9 · predicted NMD · NF1 path · VeryStrong (source: inferred)
VEPstop_gained; ENST00000617811.5:c.529C>T / ENSP00000480291.1:p.Arg177Ter among returned transcripts
gnomAD 4.1.1 / r4Resolver: zero matches. Frequency call: not_found. No AF, AC, AN or coverage returned.
ACMG/AMP worksheet · interpretation, not an assigned classification
Criterion / evidenceStatus in this worksheetWhat still needs review
PVS1Candidate; AutoPVS1 suggests VeryStrong, not independently assignedConfirm relevant transcript/exon expression, predicted NMD and HNF1B loss-of-function mechanism for this disease. Apply current SVI and any applicable gene-specific specification.
PM2UnassignedNo frequency or callable allele number was returned. Verify site coverage and ancestry-relevant rarity against an appropriate disease threshold; general SVI guidance reduces PM2 to Supporting.
PP3 / PM4Not added for the same predicted truncationVEP stop_gained, CADD and the NMD prediction do not supply independent support to stack on PVS1 for the same effect.
PP5 / source assertionNot usedClinVar’s aggregate classification is reported separately. Inspect the underlying evidence; a reputable-source label is not an independent pathogenic criterion.
PS2 / PM6 / PP1 / PP4UnassignedNo parental testing, confirmed de novo event, segregation or sufficiently specific patient phenotype was provided.
PS3 / PS4UnassignedNo validated functional assay or independently reviewed case-enrichment evidence was retrieved.
Overall classificationNot assignedComplete and critically review the missing evidence before applying an ACMG/AMP combination framework.

This is an actual execution with a documented failed lookup, not a successful frequency measurement. VEP also returned an empty frequencies array; that does not repair the missing gnomAD denominator.

The worksheet focuses on renal cysts and diabetes syndrome. ClinVar also returned a composite condition label; its aggregate must not be silently generalized to every listed condition.

The separate ClinGen validity and dosage records provide disease and mechanism context. They do not prove the variant’s effect independently of AutoPVS1.

AutoPVS1 is an automated, HTML-derived assessment and its final strength was marked inferred. Predicted NMD is not an experimentally demonstrated RNA result.

Original source records
How GeneFoundry got this
  1. Resolve the exact ClinVar allele

    Read VCV000012635 and preserve its transcript, GRCh38 allele, submitted classification and condition context.

    clinvar_get_variant

    {
      "identifier": "VCV000012635",
      "id_type": "vcv",
      "response_mode": "full"
    }
  2. Confirm the disease relationship

    Check HNF1B specifically for autosomal dominant renal cysts and diabetes syndrome.

    clingen_get_gene_validity

    {
      "gene_symbol": "HNF1B",
      "response_mode": "standard"
    }
  3. Check the assembly-matched population identifier

    Search the ClinVar-resolved GRCh38 allele in gnomAD r4.

    gnomad_resolve_variant_id

    {
      "query": "17-37739455-G-A",
      "dataset": "gnomad_r4",
      "enrich": true,
      "limit": 5
    }
  4. Record the unavailable frequency

    Request frequency for that exact allele and retain the not_found response.

    gnomad_get_variant_frequencies

    {
      "variant_id": "17-37739455-G-A",
      "dataset": "gnomad_r4",
      "response_mode": "compact"
    }
  5. Inspect the automated loss-of-function suggestion

    Run AutoPVS1 for the same hg38 allele and inspect its transcript-specific decision path.

    autopvs1_get_variant_pvs1_data

    {
      "variant_id": "17-37739455-G-A",
      "genome_build": "hg38",
      "response_mode": "standard",
      "meta_mode": "compact"
    }
  6. Cross-check consequence without counting it twice

    Annotate the same GRCh38 allele with VEP and preserve versioned transcript consequences.

    vep_annotate_variant

    {
      "variant": "17-37739455-G-A",
      "assembly": "GRCh38",
      "response_mode": "standard",
      "transcripts": "auto"
    }
  7. Review the loss-of-function mechanism

    Read ClinGen dosage sensitivity before interpreting the PVS1 suggestion.

    clingen_get_gene_dosage

    {
      "gene_symbol": "HNF1B",
      "response_mode": "full"
    }

This educational worksheet is not a complete ACMG/AMP assessment, clinical classification or patient report. No genotype, phenotype, segregation, de novo or case-level evidence was supplied.

The exact gnomAD lookup failed with not_found. No allele frequency, coverage or allele number was returned; absence and PM2 cannot be inferred from that failure.

The automated PVS1 strength is a source suggestion marked inferred. Assignment requires review of gene-disease mechanism, biologically relevant transcript and nonsense-mediated decay.