HCM, or hypertrophic cardiomyopathy

It is the most frequent heart disease in cats, all breeds included and non-pedigree cats too. The muscle of the left ventricle thickens, the heart fills less well, and the disease most often stays silent until the accident: acute heart failure, pulmonary oedema, or arterial thrombosis. It is this mute character that makes it fearsome — a cat can seem perfectly healthy the day before.

PKD, or polycystic kidney disease

Polycystic kidney disease is a hereditary condition in which cysts form in the kidneys and slowly grow, until they compromise renal function. It is linked to a mutation of the PKD1 gene, with autosomal dominant transmission: a single mutated copy is enough for the cat to be affected, and a carrier passes the mutation to half its offspring on average.

Historically associated with the Persian and the breeds descending from it, it concerns the Ragdoll through its ancestry — the breed’s founding cats, in 1960s California, included Persian-type individuals. That is why it belongs to the standard screening with us, even though it is less frequent there than HCM.

Two tools, complementary here again: the genetic test, which gives a definitive status from kittenhood, and the kidney ultrasound, which visualises the cysts but only becomes reliable from a certain age. An N/N status on PKD1 is solid — the mutation is well characterised and there is not, here, the same uncertainty as with HCM.

Blood groups: the screening nobody talks about

This one almost never appears in listings, and yet it is the only one whose omission can kill an entire litter within the first forty-eight hours. If you had to remember one thing from this page, it would be this paragraph.

Where we stand, precisely

A breeder who writes “tested parents” without explaining what they mean is asking to be trusted on their word. We prefer to give you the material to verify, and to write the real state of things rather than a reassuring formula. Here is the situation to date.

• Our breeding cats’ parents are tested N/N for HCM and PKD. On Bijou’s and Brontë’s profiles, we chose to keep this information in a deliberately simple, readable form.
• Brontë was tested in September 2026. Full genetic panel: 49 diseases screened, none found — neither affected nor a carrier. The detail is further down this page, and the results are publicly viewable ↗. An N/N status in both parents made the R820W mutation very improbable in her, but improbable is not ruled out: it is the cat itself you test, and that is now done.
• Bijou was tested in September 2026, on the same panel and in the same laboratory. Same outcome: 49 diseases screened, none found — neither affected nor a carrier. The detail is further down this page, and the results are publicly viewable ↗. Both our breeding cats are therefore screened on their own DNA, not on their parents’.
• The blood group: settled on both sides. This is where the A/A versus A/b nuance matters most: knowing that a cat “is group A” is not enough, you need to know whether it is a carrier. Both typings are done, on the CMAH gene: Brontë is A/A, Bijou is A/A. Neither carries the b allele. The isoerythrolysis scenario described above is therefore closed to this pair — and their kittens can be neither group B nor carriers.
• The echocardiogram will complete the genetics, and will be renewed throughout the breeding career — a genetic test is never redone, a scan is.

Our first litters are expected in 2027. Until then, nothing is urgent: these examinations will be done before, not after. This page will be updated as we go, and the results carried onto the individual profiles.

Brontë’s results, in detail

Brontë was tested in September 2026 on the Wisdom Panel feline DNA panel — the Finnish laboratory Genoscoper, the very one that runs MyCatDNA in Europe. 49 genetic diseases, 29 traits, blood group and genetic diversity. No anomaly detected: she is neither affected by nor a carrier of any of the 49 diseases screened.

The panel covers the two mutations that matter in the Ragdoll — Ragdoll HCM (MYBPC3 R820W) and PKD — as well as Maine Coon HCM, pyruvate kinase deficiency, mucopolysaccharidosis types I, VI and VII, cystinuria, haemophilia B and MDR1 drug sensitivity.

Blood group A, genotype A/A. That is what her dam’s typing gave us reason to hope for, and it is confirmed: she does not carry the b allele. The isoerythrolysis scenario described above is closed to her, and to her future kittens, whatever the sire’s group.

Genetic diversity: 35 % heterozygosity, average for the breed — the usual Ragdoll range runs from 32 to 37 %. The figure does not read alone: it matters mainly against a partner’s, since it is the distance between two lines that makes a litter diverse, not one cat’s value.

On colour, the test confirms what the pedigree suggested: two copies of the Siamese colourpoint, two copies of white, two copies of long hair, and a single copy of non-agouti — hence her tabby pattern. Above all it establishes her two recessive alleles, both predictable from parentage: carries chocolate from her sire, a chocolate tabby point mitted, and carries dilution from her dam, a blue tabby bicolour — a blue dam is d/d and necessarily passes on the dilute allele. The pedigree predicted them, the test establishes them: that is what separates a deduction from a verified fact. These are the two alleles to weigh against the sire’s in our future pairings.

The full report, test by test, is freely viewable ↗ — we publish not a chosen summary but the page as the laboratory renders it. An echocardiogram will complete this follow-up before any breeding: a genetic test alone does not rule out HCM.

Bijou’s results, in detail

Bijou was tested in September 2026, on the same panel as Brontë and in the same laboratory: Wisdom Panel — that is, the Finnish Genoscoper, the very lab that runs MyCatDNA in Europe. 49 genetic diseases, 29 traits, blood type and genetic diversity. Nothing found: he is neither affected by nor a carrier of any of the 49 diseases screened.

The panel covers the two mutations that matter in the Ragdoll — Ragdoll HCM (MYBPC3 R820W) and PKD — as well as Maine Coon HCM, pyruvate kinase deficiency, mucopolysaccharidosis types I, VI and VII, cystinuria, haemophilia B and MDR1 drug sensitivity.

Blood type A, genotype A/A. This is the result that changes the most, because it reads as a pair: Brontë is A/A, Bijou is A/A. Neither carries the b allele, so none of their kittens can be group B — nor even a carrier. Neonatal isoerythrolysis, described above, is entirely out of reach for this pair. That is not a breed inference or a probability: it is the typing of both individuals.

Genetic diversity: 34 % heterozygosity, average for the breed — the usual Ragdoll range runs from 32 to 37 %. Brontë is at 35 %. Two average figures, and that is normal: the value reads poorly on its own. What will make a litter diverse is the distance between the two lines, not each parent’s individual score — hence the inbreeding coefficient we calculate on the shared ancestry before every mating.

On colour, the test confirms what his coat announces: two copies of the Siamese colourpoint, two copies of white, two copies of non-agouti — hence the absence of tabby markings, unlike Brontë who has only one — and a long coat. The important point lies elsewhere, in what he does not have: no colour recessive at all. No chocolate, no dilution, no cinnamon.

Set against Brontë’s two recessives, that translates simply. She carries chocolate and carries dilution; he carries neither. Their kittens can therefore be neither chocolate nor blue — a recessive needs two copies to show, and Bijou supplies none — but roughly half of them will be carriers, invisibly. Put plainly: to breed blue bicolour here, we will need a partner other than Bijou. We would rather write it than let you find out. And since he is homozygous non-agouti where she is only half, we expect roughly one tabby point kitten in two.

The full report, test by test, is freely viewable ↗ — as with Brontë’s, we publish no hand-picked summary, but the page exactly as the laboratory renders it. An echocardiogram will complete this follow-up before any breeding: a genetic test alone does not rule out HCM.