Polycystic Kidney Disease (PKD) in Cats: the PKD1 Test, Ultrasound Screening, and What Both Cost in India

Signs of Polycystic kidney disease in cats

The 10 signs to watch for are listed below. Any one of them is a reason to consult your nearby vet; none of them is a diagnosis.

• Drinking noticeably more water than the cat used to
• Passing more urine, so litter clumps get bigger or more frequent
• Losing weight slowly over months, often while still eating
• Eating less, or walking away from a full bowl
• Vomiting on and off over weeks rather than once
• Lethargy, hiding more, and a coat that looks unkempt
• Pale gums, which point to the anaemia of advancing kidney failure
• Kidneys that feel large or irregular when a vet palpates the belly
• Bad breath, sometimes with ulcers in the mouth
• No signs at all for the first several years, which is the usual picture

Breeds on this site that document this condition

Each breed page below carries the figure for this condition with its denominator and its source. The 10 breeds listed are the ones on this site that document it, not a ranking of risk.

What polycystic kidney disease in cats is, and why one copy of PKD1 is enough

Polycystic kidney disease in cats is an inherited condition in which fluid-filled cysts form in the kidneys from birth, grow slowly over years, and eventually crowd out working kidney tissue. It is caused in most affected cats by a single change in one gene, PKD1, and one copy of that change is enough to make a cat affected.

Cats with polycystic kidney disease have large, irregularly shaped kidneys containing multiple, variably sized epithelial-lined cysts in the cortex and the medulla, and renal failure frequently occurs by seven years of age. The testing laboratory names three features that mark the heritable form apart from a one-off cyst: early onset, bilateral presentation in both kidneys, and multiple cysts rather than one. Most affected cats develop multiple bilateral renal cysts. The cysts are present at birth, though minuscule, and may be diagnosed in kittens as young as six months of age; in a mature cat they typically range from less than one millimetre to more than a centimetre across. Some affected cats also carry hepatobiliary cysts, with biliary hyperplasia and fibrosis.

The disease is the feline version of a human one. Autosomal dominant polycystic kidney disease affects between 1 in 200 and 1 in 1,000 people, and PKD1 mutations cause about 85 percent of human cases Lyons LA, Biller DS, Erdman CA. Because the feline and human diseases behave alike, the domestic cat is described in the paper that found the feline variant as an ideal model for the human condition.

The variant, named exactly

Lyons and colleagues scanned the feline PKD1 gene in 2004 and identified a C to A transversion at c.10063 in exon 29, producing a stop at position 3284 and removing roughly 25 percent of the C-terminus of the polycystin-1 protein. They found it in the heterozygous state in all 48 affected cats examined, including 41 Persians, a Siamese and several other breeds known to outcross with Persians, found it segregating concordantly in every available PKD family, and found it in no unaffected cat.

The Online Mendelian Inheritance in Animals record for the disease is OMIA:000807-9685, it lists the key variant as first reported in 2004, and on 11 July 2025 it updated the coordinates to the current transcript, so the same change is now written NC_058383.1:g.39431089C>A, XM_023247051.2:c.9864C>A and XP_023102819.2:p.(C3288*). If a laboratory report in front of you names c.9864C>A rather than c.10063C>A, those are the same variant under two transcript versions, not two different tests.

Why one copy is enough, and what two copies do

There is no carrier state in this disease, which is the single fact most often got wrong about it. A cat with one normal and one variant copy will develop the disease, the severity cannot be predicted, and it will transmit the variant to 50 percent of its offspring. That is what autosomal dominant means here, and it is why a breeder cannot mate a positive cat carefully and get around it.

On the homozygous state the sources genuinely disagree, and both are worth having. Lyons and colleagues found no homozygous cat among the animals they examined, which supports the mutation being embryonic lethal in a double dose, and the 2021 review states flatly that to date no homozygous animals have been found for the PKD1 mutation, reinforcing the idea that it is lethal in utero. The testing laboratory is more cautious and says a positive cat could potentially be homozygous, that homozygotes are suspected not to be abundant, that the homozygous form could be lethal in utero or severely affected very early, and that further research is required to determine the effects of the homozygous condition. OMIA splits the difference and records the mode of inheritance as autosomal dominant plus recessive lethal.

The conventional variant is not the whole disease

A negative PKD1 result is very good news and it is not a guarantee that a cat will never grow a renal cyst. In the largest feline dataset published to date, covering 110,325 insured cats and 61,968 genetically tested cats across 14 breeds in Japan, 77.8 percent of the cats diagnosed with cystic kidneys carried the conventional PKD1 variant, which leaves about a fifth of them that did not, and exome and whole-genome sequencing of affected cats turned up eight potentially deleterious variants in other PKD-related genes.

Three other groups have found the same gap from different directions. A Tokyo study of 1,281 cats identified four variants unique to cats with cystic kidneys that were absent from wild-type normal cats, all of them in exon 15 rather than exon 29, and named two of them as candidates. An Ankara group sequencing a Siamese family with ancestral hereditary renal failure found novel variations in the fibrocystin gene PKHD1 that were not compatible with dominant inheritance of PKD. And several studies have reported that around 5 percent of cats with cysts on ultrasound or histopathology were wild-type homozygous, carrying no copy of the c.10063C>A change at all.

Signs, the age they appear, and the day to stop waiting

The signs of PKD in cats are the signs of kidney failure, and they arrive late. The average age at which clinical signs appear is seven years, with a range of roughly three to ten, so a cat can carry the variant and look completely well for most of its life.

The 2021 review sets the average age of appearance of clinical signs at seven years and notes they can appear anywhere between three and ten years of age, and describes the picture as apathy, anorexia, weight loss, a poor coat, polyuria and polydipsia, with gastrointestinal upset. Cornell puts the same thing in an owner's words and says clinical signs are most often recognised in cats that are around seven years of age, although the disorder may be diagnosed several years earlier or later.

The reason for the delay is mechanical. No failure of kidney function is seen until around 70 percent of the total kidney tissue is lost, which is roughly the whole of one kidney and half of the other. Everything before that point is silent, and the cysts are growing throughout it.

On examination the kidneys may feel unusually large and irregular in outline, and in an advanced case the sacs can become so large and numerous that the kidney's outline is visible when the cat lies on its back. Individual cysts are usually not palpable on their own, and they do not show on a plain radiograph.

One Japanese series of 377 cats sent in by referring veterinarians gives a useful marker for when the blood starts to move. Among cats carrying the PKD1 mutation, a high plasma creatinine of 1.6 mg/dl or above was commoner in cats aged three years and over, although a few cats aged nine and over still had a creatinine below that threshold. The same series found renal and hepatic cysts together in 12.6 percent of mutation-positive cats overall and in 31 percent of the Persians.

Straining, blood in the urine or repeated visits to the tray point at the lower urinary tract rather than the kidneys, and are covered on the FLUTD in cats page. A cat that has stopped eating and is drooling may be in dental pain instead, which the tooth resorption in cats page covers. The two are worth naming because both are commoner than PKD and both look like a sick cat.

• Take the cat's weight history. Slow weight loss over months is the earliest thing most owners can measure at home, and a kitchen scale beats an impression.
• Count litter clumps for a week. More urine and bigger clumps are the first change most owners notice, and a number is more useful to a vet than the word 'more'.
• Bring any previous blood report. A single creatinine means much less than two creatinines a year apart.
• Say the breed out loud. A veterinarian who knows the cat is a Persian or a Persian cross will scan the kidneys rather than treat a vague malaise.
• Ask for the parents' PKD status if the cat came from a breeder, because a positive parent changes the index of suspicion for everything that follows.

The PKD1 DNA test: what it detects, at what age, and what it cannot tell you

The PKD1 DNA test detects the c.10063C>A variant itself, at any age and at any stage of disease, from cells brushed off the inside of a cat's cheek. It is definitive about the genotype and silent about the severity.

A genetic test detects the PKD1 mutation at any age or stage of disease, while ultrasound is most sensitive only once the cat is over 10 months old, and the genetic test can be run after weaning. That gap is the whole argument for the DNA test in a buying decision, because a kitten leaves its breeder long before 10 months.

What the laboratory asks you to do

The sample is not blood. Cat DNA tests at the University of California, Davis are carried out using cells brushed from the cat's cheeks and gums with ordinary household cotton swabs, four swab heads in total, each rubbed or rotated between gum and cheek for 15 seconds and then waved in the air for 10 to 15 seconds to dry before being taped to a barcoded submission form printed from the owner's own account. Kits are no longer mailed.

Three instructions in that protocol are the ones people get wrong. The cat must have had nothing to eat or drink for at least an hour beforehand; a kitten must be isolated from its mother, littermates and shared toys for an hour, because the mother's genetic material rubs off in the kitten's mouth and contaminates the sample; and the swab must not pick up saliva or be rubbed on the tongue or teeth, because the point is cheek cells. Turnaround is at least 15 business days, and may be longer if the sample needs repeating.

What the result cannot tell you

The test reports a genotype, not a prognosis. The laboratory's own wording for an N/P result is that the cat has or will develop PKD and that the severity of symptoms cannot be predicted. Cornell puts the limitation more bluntly through Richard Goldstein, who says you can run a genetic test but that it will not tell you how seriously the cat is affected, and that the only way to get a definitive diagnosis is by using ultrasound.

That is a real disagreement between two credible sources and it is worth publishing rather than resolving. The welfare literature and the testing laboratories treat the DNA test as the instrument that identifies affected animals before breeding age; the clinical reference treats ultrasound as the instrument that tells you what is actually in this cat's kidneys today. Both are right about different questions, which is why the screening sections below use them for different jobs.

The microchip rule nobody mentions

For a pet owner satisfying their own curiosity, a swab taken at home and posted off is enough. For a result that will go on an official register the rules are stricter, and this catches breeders out. To be accepted onto a register of unaffected animals a cat has to be permanently identified with a microchip, and any sample for genetic testing has to be collected by a veterinary surgeon who has read that microchip; animals also have to be microchipped to have an official ultrasound evaluation. The laboratory that runs the United Kingdom scheme says the same thing in its own words, that for inclusion on the International Cat Care PKD negative register the sample must be taken by a veterinary surgeon and labelled with the cat's microchip number, on a vet-checked submission form.

The chemistry behind the test has more than one valid recipe, which matters when a certificate names a method you have not seen before. The Bristol laboratory runs a PCR-based pyrosequencing assay and reports excellent agreement with ultrasound screening. OMIA records real-time PCR and PCR-RFLP as available detection methods. An ARMS-PCR method published in 2010 reported 100 percent sensitivity and specificity with a smaller sample volume, a faster result and a lower cost. A certificate naming any of these is a real certificate.

Ultrasound against the DNA test, and the age at which each becomes reliable

Ultrasound and the DNA test answer different questions and become reliable at different ages. Ultrasound sees cysts and gets better as the cat gets older; the DNA test sees the variant and is the same at eight weeks as at eight years.

The published sensitivity of ultrasound rises steeply with age. It is quoted at 75 percent when performed at 16 weeks of age and 91 percent at 36 weeks, and specificity is quoted at 100 percent. A Tehran series found the same pattern from the other end, reporting that for each year of increase in age the detection probability of PKD on sonography increased about 2.62 times. The 2021 review, pooling the literature, gives ultrasound a sensibility of around 91 to 96.2 percent, a specificity of 91 to 100 percent and a repeatability of 100 percent, and says the diagnosis in Persian cats will preferably be carried out from 10 months of age because the cysts are hard to detect in young cats.

The one study that ran both tests on the same kittens

The head-to-head comparison is worth reading in detail because it is the only study on this page that scanned and genotyped the same animals at the same visit. Sixty-three Persians and seven Exotic Shorthairs, each with at least one parent already diagnosed with PKD, underwent both renal ultrasound with a 10 MHz linear transducer and a PCR/RFLP genetic test between 2.5 and 3.5 months of age, a mean of 12.1 weeks.

With ultrasound, 41.4 percent showed renal cysts, while 37.1 percent were PKD positive by genetic testing and DNA sequencing. Six cats with at least one renal cyst were negative by genetic testing, while only one cat negative at ultrasound was positive at the genetic test; when three of the polycystic, genetically negative cats were sequenced, they turned out to be heterozygous for the mutation after all. Agreement measured by Cohen's kappa was 0.85, and the sensitivity and specificity of ultrasound at three months came out at 96.2 percent and 91 percent.

Read that carefully before concluding that ultrasound beats the DNA test at three months. Sensitivity was higher and specificity lower than previously reported, the authors attribute the higher sensitivity to better machines and transducers, and they attribute the lower specificity to other causes of PKD, meaning cysts in cats that did not carry this variant. A different group looking at cats under three months of age concluded the opposite way round, that genotyping of the PKD1 variant is a more accurate diagnostic tool than ultrasonography at that age.

How many cysts count, by age

A scan is not a yes or a no, it is a count against a threshold, and the threshold moves with the cat's age. Working at a renal cyst resolution of 0.3 cm, one group proposed age-based diagnostic criteria that a sonographer can apply directly. The four bands are set out below.

• Up to 15 months of age. One renal cyst present is enough for a diagnosis.
• 16 to 32 months. Two cysts, unilateral or bilateral.
• 33 to 49 months. At least three cysts in one or both kidneys.
• 50 to 66 months. Four cysts, unilateral or bilateral.

Why the machine and the operator are part of the result

Ultrasound is operator-dependent in a way a DNA test is not, and the published surveys show it plainly because each one used different equipment and a different threshold. The Australian survey scanned 228 cats in Brisbane on a Medison 600 with a 7.5 MHz mechanical sector scanner and 92 in Sydney on an ATL UltraMark-9 with a 5 to 10 MHz linear array, and excluded cats under 10 months of age because of the increased likelihood of a false negative result. The United Kingdom survey used a 7.5 MHz sector scanner and examined six of its cats postmortem instead. The French survey classified a cat as positive when at least one anechoic cavity was found in at least one kidney. The Italian comparison used a 10 MHz linear transducer on three-month-old kittens.

The practical reading for an owner is that a scan is only as good as the probe frequency, the operator's patience with a wriggling cat, and the age at which it was done. Ask what the cat's age was on the day, ask what the sonographer counted, and ask for the report rather than a verbal summary. A DNA result, by contrast, is a letter pair on a certificate that means the same thing wherever it was read.

What the PKD1 test costs, which laboratories sell it, and what an Indian buyer pays

The single PKD1 test costs 47 US dollars at the University of California, Davis, with a turnaround of at least 15 business days. No Indian laboratory sells that single test, and the only route inside India is a 75-item feline panel at 17,999 rupees that happens to include it.

The price at the laboratory that published the variant is 47 US dollars for one test per animal, with a turnaround of at least 15 business days. The same laboratory sells it more cheaply in combination, at 71 US dollars for this test plus the Persian PRA (PRA-pd) test, 71 US dollars for this test plus the Scottish Fold test, and 71, 95 or 119 US dollars for this test plus one, two or all three of the Burmese Head Defect, Burmese Hypokalemia and GM2 Gangliosidosis in Burmese tests.

Do not carry a price across from another test at the same laboratory, because they are not the same. The single dog PRA-prcd test at the same institution is 58 US dollars, with 27 US dollars as an additional health test on the same animal and a 5 dollar discount on three or more dogs. The cat PKD1 test is 47, the dog PRA-prcd test is 58, and a page that quotes one figure for both is guessing.

The Indian route, and the premium it carries

There is one way to buy a PKD test inside India in rupees, and it is not the single test. EasyDNA India sells the CatCheck feline genetic disease panel at 17,999 rupees, printed on both its product page and its shop page as the glyph form ₹17,999, and described on its own page as screening more than 75 genetic diseases, coat colours and blood types. The complete list of items tested, published by the company as a two-page PDF, names Polycystic Kidney Disease in its Diseases block, alongside Progressive Retinal Atrophy (Persian Type), Hypertrophic Cardiomyopathy in the Maine Coon and Ragdoll forms, Autoimmune Lymphoproliferative Syndrome and about 50 other entries.

So the answer to the question an Indian Persian buyer is actually asking is yes, you can test for PKD in India, at 17,999 rupees, and the test that answers the same question from California is 47 US dollars. Run the exchange test on both before comparing them. At 84.38 rupees to the dollar, 47 US dollars is about 3,970 rupees, and at 74 it is about 3,480, so the imported single test lands at about a fifth of the Indian panel price, 19 to 22 percent of it depending on the rate you use. Dividing 17,999 by 84.38 gives 213 dollars and by 74 gives 243, neither of them a round figure, so the panel price reads as a genuine rupee price rather than a converted dollar list.

Two caveats on the panel, and both come from the seller's own page. EasyDNA states in its frequently asked questions that the CatCheck is a genetic screening of more than 75 genetic variants related to hereditary diseases and traits and that it is not a diagnostic test. And the panel price does not buy a cheaper answer to the one question a Persian buyer has; it buys 67 other answers the buyer did not ask for, at about four and a half times the price of the one they did Veterinary Genetics Laboratory. Count the seller's list rather than accepting the seller's count, because on this page the two do not agree. The product page claims 75 different characteristics and, in a separate line, more than 75 genetic diseases, while the CatCheck List of Items Tested that the same page links runs to 68 rows, 54 of them in the Diseases block, 7 Coat Colour rows and 7 Trait rows EasyDNA India, CatCheck List of Items….

How common it is, with a denominator, a population and a date on every figure

Published prevalence in Persian and Persian-related cats runs from about 36 to 49 percent, and the range is not noise. It is the difference between screening surveys done on healthy cats, referral queues enriched for suspicion, and modern genotyped populations after two decades of testing.

The welfare summary gives the headline band, that around 36 to 49 percent of all Persians have been reported to have the condition across surveys from the United Kingdom, continental Europe, the United States and Australia, and that it is believed to be the commonest genetic disease in cats. The paper that found the variant puts the worldwide Persian figure at approximately 38 percent, which is about 6 percent of all cats, making it the most prominent inherited feline disease. The testing laboratory's own estimate is over 37 percent of Persians.

The page ranking first on Google India for this query says the disease affects around one-third of Persian cats and names no study, no denominator, no country and no year to go with it. That number is not wrong, but it cannot be checked, compared or updated, and it is the reason the table below exists.

Three ways to misread that table

The first trap is the denominator. The 1.8 percent in the Tokyo row is the share of all cats of every breed walking into one university hospital, not the Persian rate, and quoting it as a Persian figure understates the risk by more than a factor of twenty. The Japanese review of the same phenomenon lists Persian at 46 percent, Scottish Fold at 54 percent and American Shorthair at 47 percent in the referral series, which is the opposite error waiting to be made.

The second trap is the queue. Every one of the 377 cats in the Japanese referral series was sent in by a veterinarian because it already had abnormal ultrasonography or was a relative of an affected cat. A 54 percent positive rate in that queue is a statement about who gets tested rather than about the breed. The cleanest comparison is inside the same country: the Tokyo hospital study took every cat that walked in, regardless of history, and its Table 2 puts the Scottish Fold at 6 of 87, 6.89 percent, against the referral queue's 54 percent, an eightfold gap produced by the sampling frame alone Sato R, Uchida N, Kawana Y, Tozuka M. An unselected Turkish sample put the breed at 1 of 22, 4.5 percent, which is the same order. The Tokyo odds were still significantly raised for the breed (odds ratio 5.129, 95 percent CI 1.968 to 13.36, p = 0.0033), so the predisposition is real and the headline percentage is not. The authors say themselves that the number of cats in each breed was small. Where a page prints a breed percentage with no sampling frame, assume it came from a queue.

The third trap is time. An ultrasound survey of Australian catteries in 2001 and a genotyped Japanese insurance population in 2026 are not measuring the same thing in the same world, because twenty-five years of DNA testing sit between them, and the second number is lower partly because the first number worked. Compare within a method and within a decade, or say plainly that you are not.

A fourth reading is worth making because two good studies disagree outright. The French ultrasound survey found the Exotic Shorthair at 39.1 percent against the Persian at 41.8 percent, with no significant difference between the two breeds. The Japanese genotyping series found the Exotic Shorthair at 16 of 71, or 23 percent, against the Persian at 36 of 79, or 46 percent, which is half the rate rather than the same rate. One survey scanned healthy French show cats for cysts and the other genotyped a Japanese referral queue for one variant, twenty years apart, so both can be right. Neither supports treating the Exotic Shorthair as lower risk than the Persian without testing.

The native-cat control, which matters most in India

One finding on that table deserves separating out, because it answers the question an Indian owner of an ordinary street-descended cat is really asking. In the Turkish study, none of the cats of the native breeds of Anatolia carried the mutation, neither the 35 Angoras nor the 56 Vans, and nor did the 9 Exotic Shorthairs or the 5 British Shorthairs in that sample. The French survey found no PKD at all outside the Persian and Exotic Shorthair groups, including in its 11 Chartreux, 4 British Shorthairs and 4 Norwegian Forest Cats.

That does not mean a non-pedigree cat cannot carry it. The Japanese referral series noted that mixed-breed cats also showed high rates of the mutation, and the testing laboratory lists Domestic Shorthair among the breeds appropriate for testing, on the reasoning that the heritable form may not have arisen in Persians at all but perhaps in random-bred cats. The honest position is that the variant travels with Persian ancestry, it has leaked into random-bred populations where Persians have been bred loosely, and no survey of Indian cats of any kind has ever been published.

Two breeds on this site have a single published case each rather than a prevalence, and they are worth naming so nobody reads their absence from the table as safety. A 12-year-old female Chartreux with polyuria, polydipsia and enlarged irregular kidneys had multiple renal cysts and a single liver cyst confirmed by PCR/RFLP, and the authors concluded that Chartreux cats should be included in PKD screening programmes. The Australian survey detected no disease in its Ragdolls, but only six were tested.

Screening, breeding rules, and the evidence that testing actually works

Testing works, and there are now two independent datasets that prove it in numbers rather than in principle. Where breeders adopted the DNA test, the share of cats carrying the variant fell; where they did not, it did not move.

The first piece of evidence is a single laboratory's submission record. Submissions to Langford Veterinary Services for AD-PKD genetic testing dropped from 29 percent positive in 2005 to 10 percent in 2009, and the drop is attributed to the screening programme set up by the Feline Advisory Bureau using both the genetic test and ultrasound examinations. The laboratory publishes its own version of the same curve, covering 2005 to 2018, and attributes the decline to AD-PKD screening and selective breeding.

The second is much larger and much more recent. Across 110,325 insured cats and 61,968 genetically tested cats covering 14 breeds in Japan, the carrier frequency of the PKD1 variant fell by 42.6 percent between 2019, when full-scale genetic testing of kittens began, and 2022. Genomic analysis in Scottish Folds and Persians found no substantial change in overall genetic structure or inbreeding levels across the same period, so the gain was not bought by narrowing the gene pool, although the effective population size of cats carrying the variant did decline.

The three breeds where nothing happened

The interesting half of that result is the half that did not move. Among the eight breeds with large enough samples for a separate analysis, significant reductions in the proportion of heterozygous cats appeared in Scottish Folds at 49.5 percent, Persians at 38.8 percent and Ragamuffins at 57.7 percent, while no statistically significant or suggestive reduction was observed in British Shorthairs, Minuets or Munchkins. The authors' conclusion is that testing and appropriate breeding need promoting particularly for the breeds in which no decrease has been observed.

That is the most directly useful sentence on this page for an Indian buyer, because the British Shorthair is one of the fastest-selling pedigree cats in Indian cities and it is one of the three breeds where the carrier frequency has not fallen. A buyer cannot assume the breed has been cleaned up. A buyer has to ask for the certificate.

What the registries and the welfare bodies actually require

Requirements vary by registry and by breed, and the gap between advice and rule is where most buyers get caught. The United Kingdom registry route runs through a negative register: a cat tested clear can be listed on the International Cat Care PKD negative register, and the sample has to be taken by a veterinary surgeon and labelled with the cat's microchip number on a vet-checked form Science for Animal Welfare (UFAW). OMIA's control statement is that testing is recommended for relatives of affected cats, and that cats carrying a causal variant should be removed from breeding programmes to prevent the production of affected cats and reduce the frequency of the variant in the gene pool.

The welfare position is the strongest statement any source on this page makes, and it is worth quoting as written. There is no justification to breed two AD-PKD positive cats together, and there is also no justification to breed any Persian cat, or a cat known to have a Persian ancestor, without testing for PKD first. International Cat Care's advice to a buyer is the practical form of the same rule, to always ask the breeder to show proof that they have tested negative for PKD, giving the queen's PKD certificate as the United Kingdom example.

Which breeds a laboratory says to test, and where two laboratories disagree

The testing laboratory's list of breeds appropriate for the PKD1 test is long and its logic is ancestry rather than observed disease. It names Persian, Persian crosses and Persian-derived breeds, spelling out British Longhair, British Shorthair, Burmilla, Domestic Shorthair, Exotic Longhair, Exotic Shorthair, Foldex, Highland Fold, Highland Straight, Himalayan, Maine Coon, Napoleon, Ragamuffin, Ragdoll, Scottish Fold, Scottish Straight and Selkirk Rex, plus Devon Rex and Siberian, on the stated reasoning that any breed that has used Persians in its foundation or propagation should have concerns for PKD1.

The Bristol laboratory groups the same breeds differently and the disagreement is worth knowing before you decide not to test. It puts Persian, Chinchilla, Exotic Shorthair, British Shorthair and Himalayan at moderate risk of PKD, and puts Asian, Birman, Burmilla, Bombay, Cornish Rex, Devon Rex, Ragdoll, Scottish Fold, Selkirk Rex, Siberian, Snowshoe and Tiffanie at low risk. The Scottish Fold sits in that low-risk group, and the Japanese referral series put the same breed at the highest PKD1 rate of any breed it tested. Two credible laboratories, two answers, and the cheap resolution is to run the test rather than pick a side.

The five questions below are the ones that change what happens to a cat, and they are worth asking in writing before money moves.

• What is the PKD1 result for both parents, N/N or N/P? A cat with one N/P parent has a 50 percent chance of inheriting the variant, and there is no carrier state to hide behind.
• Which laboratory ran it, and on what date? A result is a document from a named laboratory, not a sentence in an advertisement.
• Was the sample taken by a veterinarian against a microchip? That is what an official register requires, and it is the difference between a certificate and a printout.
• If there is no DNA result, has either parent had a renal ultrasound after 10 months of age? That is the age at which the scan becomes most sensitive.
• Will you put the result in writing on the receipt? A seller who will not is telling you what the result is.

What is different in India: no published series, no rule that covers cats, and one laboratory

Three things are different in India. No Indian study of feline polycystic kidney disease has ever been published, no Indian rule requires any genetic test on a cat, and the only in-country testing route is a 17,999 rupee panel while a government ultrasound costs 250 to 500 rupees.

Start with the market, because it explains the rest. India's cat population grew 13.6 percent a year from 2.4 million in 2020 to 4.5 million in 2025, an 11 percent share of a 33.4 million pet population, driven by urban households treating cats as low-maintenance pets. The Persian and the Persian cross are the pedigree cats that growth has mostly been made of, and they are the two groups the whole of this page is about.

The Indian evidence, searched and absent

There is no published Indian study of this disease, and that absence was tested rather than assumed. On 27 September 2026 the Europe PMC REST search for feline polycystic kidney disease with India restricted to the title and abstract returned a hit count of 0, and the same query with India restricted to the author affiliation field also returned 0. Three controls run in the same session in the same way all returned results, so the instrument was working: Labrador hip dysplasia returned 110 records, feline polycystic kidney disease without the India term returned 98, and canine parvovirus with India in the title and abstract returned 47.

So every prevalence figure, every survival figure and every sensitivity figure on this page comes from a British, Australian, French, Italian, Japanese, Turkish, Iranian or Mexican population. None of them was measured in an Indian cat. That is a reason to read them as the best available evidence rather than as a local statistic, and it is a gap an Indian veterinary school could close with one ultrasound survey of a few hundred Persians in one city.

The rule that covers cats, and the clause that does not

Indian law does require genetic testing of breeding animals, and it does not apply to cats. Clause 8(10) of the Prevention of Cruelty to Animals (Dog Breeding and Marketing) Rules, 2017 states that the dogs shall have been tested for genetic defects, including hip dysplasia, progressive retinal atrophy, night blindness, hypothyroidism, entropion, ectropion, overshot and undershot jaw, wry mouth, two or more missing teeth and cryptorchidism. Eleven defects are named and the word including makes the list illustrative, but the instrument is titled Dog Breeding and Marketing and it regulates dog breeders.

The instrument that does cover cats is the Prevention of Cruelty to Animals (Pet Shop) Rules, 2018, notified as G.S.R. 844(E) on 6 September 2018. Its rule 2(j) defines a pet animal to include dog, cat, rabbit, guinea pig, hamster, rodents of the rat or mice category and pet birds, and its schedule carries a dedicated block headed FOR CATS covering floor surface, elevated resting surfaces, matting, play toys, litter box area and separation from inimical species. Across all 30 pages and 338,356 extracted characters of that gazette, the words genetic and hereditary do not appear once.

Read together, those two documents say something precise, and the occurrence counts make it checkable rather than rhetorical. The word cat does not appear once across the 14 pages and 51,953 extracted characters of the 2017 dog rules, and the words genetic and hereditary do not appear once across the 30 pages and 338,356 extracted characters of the 2018 pet shop rules Ministry of Environment. An Indian dog breeder is required by rule to have tested for named genetic defects; an Indian cat breeder is required by rule to provide a litter tray and a resting shelf. Nothing in Indian law asks anybody to test a Persian for PKD1 before selling its kittens, which is exactly why the buyer asking the question is the only control in the system.

What the alternatives cost at an Indian government hospital

If the DNA test is out of reach, the ultrasound is not, and three government veterinary hospitals publish what they charge. Their rates are printed below exactly as their own pages give them.

Every rupee figure in that table has been through the exchange test. Divide 250 by 84.38 and by 74 and you get 2.96 and 3.38 dollars; 500 gives 5.93 and 6.76; 300 gives 3.56 and 4.05; 30 gives 0.36 and 0.41. None of them is a round dollar amount in disguise, so all four are genuine Indian rupee prices from Indian institutions rather than a converted foreign price list Bihar Animal Sciences University Tamil Nadu Veterinary and Animal Sciences….

The practical arithmetic for an Indian Persian buyer is therefore stark. A scan at a government teaching hospital costs between 250 and 500 rupees and tells you what is in this cat's kidneys today, but is most sensitive only after 10 months of age Bihar Animal Sciences University. A posted cheek swab to California costs 47 US dollars, roughly 3,970 rupees at 84.38, plus international postage that no laboratory on this page prices, and answers the question at any age. The Indian panel costs 17,999 rupees and answers it along with the other 67 rows on its own published list.

Geography makes that harder than the price makes it look. The three published rate cards on this page belong to government teaching hospitals at Izatnagar in Uttar Pradesh, Patna in Bihar and Chennai in Tamil Nadu Bihar Animal Sciences University Tamil Nadu Veterinary and Animal Sciences…, and an owner in Mumbai, Delhi, Bengaluru, Hyderabad, Pune, Kolkata or Ahmedabad is choosing instead between private clinics, none of which publishes a scan price the way those three do. The DNA route is geographically flat by comparison, because a cheek swab posted from any Indian city reaches the same laboratory on the same terms and the price on the laboratory's page is the price.

Heat, and why it changes the reading and not the disease

Indian summers and the humid weeks of the monsoon do not cause polycystic kidney disease, and they do change what its numbers look like. A dehydrated cat's creatinine rises whether or not its kidneys are diseased, so a single high reading taken in a Delhi or Nagpur May is weaker evidence than the same reading in January, and the correct response is to rehydrate and repeat rather than to stage the cat on one number. Keeping a PKD-positive cat drinking through the hot months is ordinary good sense and is covered in the heat safety for cats in India guide, and the staging arithmetic itself belongs on the chronic kidney disease in cats page rather than here.

One last India-specific warning. A Persian advertised cheaply in an Indian classified listing with no paperwork has almost certainly not been screened, because screening costs more than the margin on the kitten, and the seller who cannot produce a PKD certificate has not bought one. International Cat Care's instruction is to ask for proof rather than an assurance, and it names the queen's certificate as the document to ask for.

Living with a PKD-positive cat, and where this page hands over

A positive PKD1 result is not a short sentence. A Japanese life table of 300 PKD1-positive cats put life expectancy at birth at about 12.7 years, with 16.0 percent progressing to uraemia, and the survival curve turning down sharply between six and seven years of age.

The life table is the first published survival analysis of this disease and it is worth reading in full. A retrospective cohort followed 300 cats that had tested positive for the feline PKD1 c.10063C>A variant in Japan; life expectancy at birth came out at approximately 12.7 years, with cumulative survival of 95.1 percent at five years and 61.3 percent at ten. Of the 300, 48 cats, or 16.0 percent, progressed to uraemia, and 62, or 20.7 percent, died of renal failure and other causes.

Among those 62 cats the median age at death was 8 years and the first decile was 5 years, the largest single number of deaths fell at age seven, and the cumulative survival rate began to decline significantly between the ages of six and seven. The authors' own conclusion is a screening instruction rather than a reassurance, that the findings emphasise the importance of frequent examination at a young age given the marked fall in cumulative survival between six and seven.

What progression looks like when somebody measures it

An 18-month longitudinal study of 12 PKD-affected cats put numbers on the slope. Over the follow-up it documented a 14.00 percent increase in cyst volume and a 7.00 percent enlargement in kidney length, with significant rises in plasma creatinine, phosphorus and blood urea nitrogen, and progressive anaemia associated with the advancing chronic kidney disease stages. Its authors emphasise that the disease progressed despite diligent care by owners and veterinarians, and recommend routine sonographic evaluation alongside haematology and biochemistry. Twelve cats is a small denominator and the study says so itself, calling for expanded cohorts.

Treatment, in general terms, and what it is not

There is no cure for feline polycystic kidney disease, and current treatment is palliative rather than curative. Cornell describes the only feasible approach as the same one used for kidney failure in general, a combination of diet control, fluid therapy and medications prescribed by a veterinarian, with the goal of keeping the kidneys as happy as possible for as long as possible. Draining the cysts with a needle under ultrasound guidance is conceivable but not viable, because there are usually too many of them and they refill.

Which drugs, at what point, and in what amounts is a decision for the veterinarian who has examined your cat and has its blood results in front of them, and this page prints no dose for that reason. What an owner controls is the monitoring interval, the water, the weight record and the willingness to go in when something changes.

The staging and the management of the kidney failure that follows do not belong on this page and they are not repeated here. Once a cat is azotaemic it is being managed as a cat with chronic kidney disease, staged from 1 to 4 on fasting creatinine and SDMA, and everything that follows from that stage, including the renal diet trials and their survival numbers and the Indian prices for a kidney panel, sits on the chronic kidney disease in cats page. Use this page to decide whether to test and that page to decide what to do next.

Three things owners of positive cats get wrong

The commonest mistake is starting a prescription renal diet on a well cat because it tested positive. A renal therapeutic diet is a treatment for diagnosed chronic kidney disease at a defined stage, not a preventive measure for a cat carrying the variant whose bloods are normal, and putting a healthy young cat on one is a decision for a veterinarian rather than a shelf.

The second is stopping monitoring after a positive result, on the reasoning that nothing can be done. The life table says the opposite, that survival falls away sharply from age six, which is an argument for examining frequently at a young age rather than waiting. A twice-yearly weight, a urine specific gravity and a blood panel in a senior cat are the ordinary schedule, and the senior cat care in India guide sets out what that costs here.

The third is breeding from the cat anyway. A positive cat transmits the variant to 50 percent of its offspring and each of those kittens will develop the disease, which is why the welfare position is that cats with a causal variant should be removed from breeding programmes. Neutering a positive pet cat ends the problem in that line permanently, and the Persian and Exotic Shorthair pages carry the Indian cost of doing it.