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Canine Mendelian disease record

Cystinuria Type I-B (SLC7A9 p.A217T)

Cystinuria Type I-B (SLC7A9 p.A217T). Autosomal recessive (incomplete penetrance). Observed in 64 of 266 breeds tested in the Sniff Atlas, with measured carrier frequencies drawn from 242,662 dogs (Donner 2023). Per-dog phenotype outcome depends on penetrance, modifiers, and environment; the carrier frequencies below describe variant prevalence, not disease incidence.

OMIA identifier
OMIA:001880-9615
Autosomal recessive (incomplete penetrance)
Linked gene
SLC7A9
Human counterpart
In humans, this gene is SLC7A9. OMIM 604144
Source dataset
Sniff Atlas v1.0.1 / DOI
The human connection

A model of human cystinuria

Dogs with this condition carry a change in SLC7A9. In people, changes in the same gene cause cystinuria. That makes affected dogs a naturally-occurring model of the human disease, and it is part of why studying dogs moves medicine forward for everyone. It does not mean your dog has the human disease. It means the two share an underlying biology.

In people, the disease is described as: Cystinuria is a renal tubular amino acid transport disorder characterized by recurrent formation of kidneys cystine stones.

In humans it is also called: CSNU, cystinuria (disease), cystinuria, type non-I, cystinuria-lysinuria, cystinuria-lysinuria syndrome.

Mapped from OMIA via the human disease's OMIM entry to the Mondo Disease Ontology (Monarch Initiative, CC-BY 4.0). Sniff renders this as a model-of link; the canine disease remains the subject of this page.

About this disease

From OMIA's curated record

Documented in OMIA (Online Mendelian Inheritance in Animals). This describes the disease as recorded in the published literature, not a prediction for any individual dog. As of 2026-06-03.

Summary

The name of this entry has been created in line with the new expanded classification system for canine cystinuria suggested by Brons et al. (2013): "type I cystinuria when the disease shows autosomal recessive inheritance, type II when it shows autosomal dominant inheritance, and type III for sex-limited inheritance. . . . Involvement of the SLC3A1 gene is indicated by adding A, and similarly B indicates mutations in SLC7A9".

Clinical features

As summarised by Brons et al. (2013), cystinuria type II - B is characterised by: occurs in males and females; not androgen-dependent; COLA [μmol/g creatinine (normal ≤500)] ≥ 700 in heterozygotes.

Molecular genetics

Using the direct candidate gene strategy, based on clinical signs, Brons et al. (2013) identified "a single base missense mutation (c.964G>A) [in SLC7A9] changing the small hydrophobic glycine residue to the larger, charged basic amino acid arginine (p.Gly322Arg) in transmembrane domain 9 of the light subunit bo,+AT" as causal in Miniature Pinschers.
A SLC7A9 variant (c.649A>G; p.(A217T) has been identified by Harnevik et al. (2006) in English bulldogs, but there appears to be no support for the variant to be causal (Harnevik et al., 2006; Ruggerone et al., 2016; Fitzwilliams et al. 2023). It appears that all affected English bulldogs in these three studies were also homozygous for two likely causal SLC3A1 variants (p.(I192V) and p.(S698G) (see OMIA:000256-9615 : Cystinuria, type I - A in Canis lupus familiaris). The affected dogs were reported to be also either heterozygous or homozygous for the SLC7A9 variant (Harnevik et al., 2006; Ruggerone et al., 2016, Fitzwilliams et al. 2023), which according to Fitzwilliams et al. (2023) is a common allele in the breed (allele frequency for c.649A is 0.52 in English bulldogs from Denmark). The data presented by Fitzwilliams et al. (2023) showed that 10 out of 14 non cystinuric male dogs were heterozygous or homozygous for the A allele. Fitzwilliams et al. (2023) strongly recommend not to use "the variant in SLC7A9 as a test to predict the risk of developing cystinuria in male English bulldogs.”

Inheritance

Brons et al. (2013) provided evidence consistent with autosomal dominant inheritance.

Human analog

OMIA links this condition to its human counterpart in OMIM (Mendelian Inheritance in Man), the place to read across to the deeper human literature for the same biology.

Source: OMIA (Nicholas, Tammen & the Sydney Informatics Hub), entry OMIA:001880-9615, doi:10.25910/2AMR-PV70 (CC-BY 4.0).

The evidence

Published references

The peer-reviewed papers behind this disease, curated by OMIA. Starred entries are OMIA-designated landmark papers. Showing 6 of 7.

  1. Cystinuria in dogs and cats: What do we know after almost 200 years? · Animals (Basel) · 2021 · PMID 34438894
  2. Urolithiasis. · Vet Clin North Am Small Anim Pract · 2015 · PMID 26002797

References curated by OMIA (Nicholas, Tammen & the Sydney Informatics Hub), doi:10.25910/2AMR-PV70 (CC-BY 4.0). Full list at the OMIA entry.

Predict a litter

Set each parent's status for Cystinuria Type I-B (SLC7A9 p.A217T) and see the odds for their puppies. Single recessive variant, exact Mendelian math.

Parent A
Parent B
NNClear
NmCarrier
NmCarrier
mmAffected
Clear25%
Carrier50%
Affected25%

These are the genetic odds for one known variant, not a promise: a real litter varies around them, and penetrance or other genes can change whether the condition ever appears. Use it to avoid pairing two carriers and to keep a line healthy, not to engineer a dog. Inheritance mode per OMIA.

Your breed

See what Cystinuria Type I-B (SLC7A9 p.A217T) looks like in your dog's breed.

Carrier frequency by breed

Top 25 well-sampled breeds (n ≥ 50)

Maximum per breed across variants in the Donner 2023 cohort, with . The list below is split into well-sampled breeds (n ≥ 50 tested) and small-sample breeds (n < 50, where the Wilson CI typically spans more than 20 percentage points and frequencies should not be compared directly to the well-sampled entries). Frequencies are population-level, not per-litter or per-line.

0%38%75%
Bulldog Standard55.5% · n 4,816
Swedish Vallhund25.6% · n 88
Golden Retriever23.7% · n 12,881
Bull Terrier Standard22.7% · n 468
Bulldog American15.0% · n 540
Boerboel11.2% · n 165
Parson Russell Terrier8.6% · n 181
Catahoula Leopard Dog6.8% · n 154
Dalmatian6.4% · n 820
Maltese5.3% · n 2,413
Great Dane4.2% · n 3,266
n = 28,685 dogs · Donner et al. 2023 carrier-screening cohort · Sniff Atlas
Each bar is one well-sampled breed; the whisker is its Wilson 95% CI, and fainter bars have wider intervals. Frequencies are population-level, not per-litter. Carrier status for Cystinuria Type I-B (SLC7A9 p.A217T) is measured; phenotype outcome depends on penetrance and modifiers.
▸ Full table with Wilson 95% confidence intervals
Breed Carrier frequency n tested
Bulldog Standard 55.5% 4,816
Swedish Vallhund 25.6% 88
Golden Retriever 23.7% 12,881
Bull Terrier Standard 22.7% 468
Bulldog American 15.0% 540
English Cocker Spaniel 12.2% 580
Boerboel 11.2% 165
Parson Russell Terrier 8.6% 181
Catahoula Leopard Dog 6.8% 154
Soft Coated Wheaten Terrier 6.8% 607
Dalmatian 6.4% 820
Maltese 5.3% 2,413
English Springer Spaniel 4.4% 751
Great Dane 4.2% 3,266
Bernese Mountain Dog 4.0% 955
Mastiff 3.3% 767
American Staffordshire Terrier 2.9% 42,793
Cairn Terrier 1.9% 183
Blue Tick Coonhound 1.4% 104
Border Terrier 1.4% 71
Saint Bernard 0.97% 721
Chinese Shar Pei 0.88% 400
Schnauzer Giant 0.87% 230
Russell Terrier 0.84% 239
Danish Swedish Farmdog 0.82% 61

Top 25 of 55 well-sampled breeds with at least one observed carrier shown.

▸ Also observed in 9 small-sample breeds (n < 50)

Frequencies in this section are statistical estimates with wide Wilson 95% confidence intervals (typically >20 percentage points). Treat these as "carriers observed but the true population frequency is not yet measurable" rather than as comparable to the well-sampled entries above.

Breed Estimate n tested
Bedlington Terrier 40.9% 11
Kuvasz 28.6% 7
Polish Tatra Sheepdog 25.0% 8
Briard 10.7% 14
German Pinscher 10.0% 30
Xoloitzcuintli 6.3% 8
Black Russian Terrier 4.3% 23
Lacy Dog 1.6% 32
Mudi 1.2% 42

202 additional breeds in the Donner 2023 cohort were tested but showed no carriers.

Scope of this record

Scope

This record carries the breed-level carrier frequencies from the Donner 2023 cohort. Penetrance data (the fraction of at-risk dogs that develop the phenotype) is not yet quantified for this disease in the Sniff Atlas v1.0.1. The OMIA entry is the authoritative reference for the clinical phenotype, inheritance pattern, and gene assignment.

Predicted disease relevance at the per-dog level is UNPROVEN. The carrier frequency is measured; phenotype outcome depends on penetrance, environment, and modifier loci. Consult a veterinarian for clinical interpretation.

How to cite this record

Citations

If you use this record in published work, cite the Sniff Atlas (the published dataset that carries the breed-level carrier frequencies) and the upstream sources:

  • Sniff Atlas v1.0.1 for the per-breed carrier frequencies:

    Gehring, M. (2026). Sniff Atlas v1.0.1. Zenodo. https://doi.org/10.5281/zenodo.20566358. CC-BY 4.0.

  • OMIA for the disease definition, inheritance, and gene assignment:

    Nicholas, F. W., & Tammen, I. (2024). OMIA. Sydney Informatics Hub, The University of Sydney. https://doi.org/10.25910/2AMR-PV70. Entry: OMIA:001880-9615.

  • Donner et al. 2023 for the breed × variant carrier-frequency cohort:

    Donner, J., Freyer, J., Davison, S., Anderson, H., Blades, M., Honkanen, L., et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics, 19(2), e1010651. https://doi.org/10.1371/journal.pgen.1010651.

Full citation formats (BibTeX, RIS, CITATION.cff) at sniff.world/cite.

Related

Related

Last updated
Sources: Sniff Atlas v1.0.1 · OMIA OMIA:001880-9615 · Donner et al. 2023