Autosomal dominant medullary cystic kidney disease with or without hyperuricemia: genes and variants

Autosomal dominant medullary cystic kidney disease with or without hyperuricemia is linked to 2 analyzed proteins (UMOD and MUC1). 3 DNA variants are known to cause it; 4 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Autosomal dominant medullary cystic kidney disease with or without hyperuricemia

Known disease-causing variants in Autosomal dominant medullary cystic kidney disease with or without hyperuricemia

VariantPositionProtein partClinical label
UMOD C106Y106EGF-like 2Disease-causing (★★)
UMOD A461E461ZPDisease-causing (★★)
UMOD C137W137EGF-like 3Disease-causing

Same protein, different disease

Diseases related to Autosomal dominant medullary cystic kidney disease with or without hyperuricemia

Frequently asked questions

Which genes are linked to Autosomal dominant medullary cystic kidney disease with or without hyperuricemia?

In CATVariant, Autosomal dominant medullary cystic kidney disease with or without hyperuricemia is linked to 2 analyzed proteins: UMOD (Uromodulin) and MUC1 (Mucin-1).

How many genetic variants are linked to Autosomal dominant medullary cystic kidney disease with or without hyperuricemia?

8 variants: 3 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 4 are of uncertain significance or have conflicting reports.

Which uncertain variants in Autosomal dominant medullary cystic kidney disease with or without hyperuricemia look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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