Genetic welfare problems of companion animals

 

Polycystic Kidney Disease

 

Breed: Persian and Persian-related cats

 

Condition:  Polycystic Kidney Disease

Related terms: autosomal dominant polycystic kidney disease (AD-PKD)

Outline: Polycystic kidney disease affects about one in three Persian cats. A genetic fault in kidney cell development leads to mutliple cysts forming in the kidneys. These grow and eventually cause kidney failure. Often this is not until after breeding age has been reached but it can be much sooner. The disease is progressive and there is no cure, but treatment can alleviate it in the early stages. Kidney failure causes malaise and inappetance and, in later stages, muscle weakness, vomiting and seizures, and so is likely to cause unpleasant feelings of moderate to severe intensity. Affected animals can be detected and should not be used for breeding. The prevalence of this disease is declining because of testing and it should be possible to eliminate it. 



 

Summary of Information

(for more information click on the links below)

 

 

1.           Brief description

Polycystic kidney disease (PKD) is characterised by the presence of multiple fluid-filled sacs or cysts in the kidneys. They can be present at birth but initially are microscopic and enlarge throughout life. The rate of growth varies but, at some stage, chronic renal failure (CRF) occurs as the enlarging cysts damage normal kidney tissue. Typical signs of PKD are those also associated with chronic renal failure reduced appetite, weight loss, increased thirst and urine volume, muscle weakness, vomiting, seizures (fits) and death.

 

2.           Intensity of welfare impact             

Renal failure causes malaise and inappetance and, in later stages, muscle weakness, vomiting and seizures. These are likely to cause unpleasant feelings of a moderate to severe intensity.  Treatment can help to control the disease but treatment can itself have adverse welfare consequences. For example, special diets may be of low palatability, frequent administration of tablets may be aversive, as may frequent travel to and from veterinary practices and veterinary interventions.

 

3.           Duration of welfare impact

 

Most cats affected with PKD will have a normal life until signs of CRF occur. Once signs associated with CRF appear they will persist until death. This may be weeks or years. During this period the welfare impact will vary from mild to severe depending on the stage of disease and the effectiveness of any treatments.

 

4.           Number of animals affected

 

 

PKD has been very common in Persian cats. Around 36-49% of all Persians have been reported to have the condition (Cannon et al 2001, Barrs et al 2001, Beck & Lavelle 2001, Barthez et al 2003, Cooper 2000, Bonazzi et al 2007.  Domanjko-Petri et al 2008, Bonazzi et al 2009). However, the number with the condition may be decreasing due to the effectiveness of ongoing control schemes. It is believed to be the commonest genetic disease in cats.

 

Breeds related to Persians: Himalayans, Exotic shorthairs, Ragdolls, and Chinchillas, have also been shown to be affected by the condition (Barrs et al 2001).

 

5.           Diagnosis

The diagnosis of renal failure (CRF) rests upon clinical examination and the results of laboratory tests. The presence of the cysts in the kidneys can be detected by ultrasound examination which can indicate the presence, number and size of the cysts within each kidney. This method of detection is most sensitive when the cat is over 10 months of age. A genetic test is available which detects the presence or absence of the PKD1 genetic mutation that underlies the disease.

 

6.           Genetics

 

The form of PKD detailed here is an autosomal dominant condition with variable penetrance (Biller et al 1990, Biller et al 1996). The affected gene is PKD1 (Lyons et al 1994).

 

7.           How do you know if an animal is a carrier or likely to become affected?

In contrast to conditions caused by recessive genes, all cats with the gene will be affected and will go on to develop signs of the disease in due course. However, although strictly there is therefore no carrier state, the disease tends not to manifest until relatively late in life and often not until after breeding age. It is therefore necessary to use special tests to detect affected animals before breeding age. Both ultrasound examination after 10 months of age or use of the genetic test after weaning are reliable in identifying affected and unaffected animals and combining both has its advantages.

 

8.          Methods and prospects for elimination of the problem

 

All cats that carry the abnormal gene are affected with AD-PKD and this makes it relatively easy to eliminate the disease from a breeding group. If all cats in the high-risk breeds were to have their kidneys scanned or be gene tested before they were used for breeding, and if affected cats were not then used for breeding, PKD could be eradicated in a single generation. This would, however, significantly decrease the number of cats within the Persian breed which could be bred from, and hence restrict their gene pool. Such a restriction could increase the risk of other diseases with genetic influences

 

 


 

For further details about this condition, please click on the following:

 

 

 

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1.           Clinical and pathological effects

 

Polycystic kidney disease (PKD) is characterised by the presence of multiple fluid-filled sacs or cysts in the kidneys (Biller et al 1990). They can be present at birth but initially are microscopic and subsequently enlarge during the lifetime of the cat. The rate of growth varies, both from one individual cat to another, but also over time so individual cysts can expand quickly at times and then remain static for an unpredictable period (Biller 1994).

The cysts form because of a genetic defect in cell maturation. The defective gene in Persian (and related cats) is called PDK1. This is responsible for the autosomal dominant polycystic kidney disease (AD-PKD) that is the focus of the information given here (Biller et al 1996). Considerable detail is known about the feline PDK1 defect. A substitution of cytosine for adenine in the PDK1 gene leads to a defective version of the protein polycystin-1 being produced and because of this kidney cells fail to grow and develop normally (Torres & Harris 2006, Al-Bhalal & Akthar 2008).

 

This is not the only possible cause of a cyst in a cat’s kidney. Other genetic forms of PKD are seen in humans where they make up around 15% of cases (Torres & Harris 2006). AD-PKD1 is the only form recognised in cats but there are suspicions that other forms occur; albeit much less commonly (Kappe et al 2005, Helps et al 2007, Bonazzi et al 2009, Lee et al 2010). Kidney cysts can also occasionally form in cats secondary to other causes of chronic kidney disease; these are most likely in older cats (Norsworthy 2003).

 

A small number of cats with AD-PKD have cysts in the liver and pancreas as well as the kidneys (Domanjko-Petri et al 2008) and some cats have other pathological liver damage associated with the AD-PKD condition but the clinical significance of this is uncertain (Eaton et al 1997).

 

Exactly how the kidney cysts cause kidney failure is poorly understood. Their physical presence is partly, but not solely, the cause. Typical changes in kidney tissue seen in other forms of CRF – inflammation and ineffectual attempts at repair (tubulointerstitial nephritis and fibrosis, tubular epithelial atropy and regeneration) are also seen around the cysts (Eaton et al 1997). The kidneys have considerable reserve capacity and no failure of kidney function is seen until around 70% of the total kidney tissue is lost (ie approximately equivalent to theloss of the whole of one kidney and half of the other).


The age of onset of signs of kidney disease varies considerably (Biller 1994) and depends upon how quickly the cysts enlarge and affect the surrounding kidney tissue, and whether any concurrent, unrelated kidney disease is present. 


PKD
impacts on the welfare of the cat through disruption of the functions of the kidney and produces signs that are commonly seen in other forms of chronic renal failure (Biller 1994). The kidneys perform excretory and certain regulatory functions. They are the source of the hormone erythropoietin (EPO) which stimulates red blood cell production in the bone marrow. Loss of functional kidney tissue causes low EPO levels which results in anaemia (low numbers of circulating red blood cells). As the excretory functions are compromised by the cysts, substances that should be excreted from the body remain, others that should be retained by the kidneys are lost in excessive quantities. Some metabolic waste products, such as phosphate, build up in the body. Some are toxins which make the animal nauseous and reluctant to eat. The increase in levels of phosphate can lead to hormonal changes that result in calcium loss from bones weakening them. Amongst the substances lost excessively is water, which results in dehydration unless the animals can drink enough to compensate. Potassium is another and it’s loss can cause muscle weakness.

A regulatory mechanism that the body uses to try to maintain renal function in the face of failing kidneys is to increase blood pressure. Over time, this often leads to damage to sensitive parts of the body such as the eyes, heart and brain and it also further damages the remaining kidney tissue.

Initial signs of chronic renal failure are often non-specific: an insidious (gradual) onset of reduced appetite, weight loss and reduced activity may progress to the owner noticing an obvious increase in the volume of urine produced and the amount of water drunk each day. The time taken for the cat to progress from these earlier signs to more advanced signs varies greatly. It may be a few weeks or a few years, but progression will occur, largely because of growth of the cysts but also because CRF itself induces progressive damage to the tissue of the remaining kidney, for example: raised blood pressure causes further damage (Ross et al 2006).

In more advanced disease there is further weight loss and loss of muscle mass causing weakness and difficultly in performing normal activities such as jumping and running. Large amounts of watery urine is constantly produced. The cat may feel too ill to want to move around and may have little appetite. Anaemia resulting from low EPO levels may also contribute to this. Food and water intake therefore may be inadequate for the cat’s needs, leading to additional weight loss and dehydration, which in turn makes the cat’s condition worse.


Build up of toxic waste products can cause ulcers to form in the mouth which can lead to further reduction in food intake. Likewise, ulcers may form in the stomach and these contribute to the nausea and may lead to vomiting of food and fluid. Once vomiting starts, calorie intake falls further and it becomes even more difficult for the body to maintain its metabolic functions as electrolytes (salts) are lost. The acidity of the body changes and this further disturbs metabolism. Bleeding from ulcers also causes loss of blood cells and electrolytes. Significant amounts of protein can be lost from the damaged kidneys into the urine (Ross et al 2006).

The dilute urine running through the lower urinary tract is susceptible to infection from bacteria that find it difficult to survive in normal urine. Urinary tract infections cause painful cystitis and can spread up into the kidneys causing further damage there (pyelonephritis) (Norsworthy 2003). This may also be facilitated as a result of the immune system becoming compromised. Affected cats become susceptible to other infections also; most commonly disease of the eyes and nose from a “cat flu” virus previously kept dormant in the body by a functional immune system.

Terminally, a build up of toxins (coming from normal metabolic process but which can not be excreted) and loss of control of electrolyte levels and basic metabolic functions leads to seizures, coma, heart failure and death.


As a separate process to illness from CRF, some animals may become acutely ill when a cyst becomes infected (Norsworthy 2003).



Most Persian cats with AD-
PKD become ill when they are older rather than at a young age. This is one reason why the condition has become so common in the breed. Most affected cats will show no obvious signs (disregarding any cysts that are found by ultrasound examinations) until after they have reached breeding age. In fact most cats probably have become grandparents by the time they become ill. In the study by Domanjko-Petri et al (2008) the average age of PKD cats with clinical signs of renal failure was 12.2 years.

 

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2.               Intensity of welfare impact

Once around ¾ of kidney tissue has been lost signs of CRF start to be occur. The severity of these signs then increases until terminal CRF and death occur. The development of the disease brings with it a progression of the welfare issues as affected cats become weaker and more unwell. Feeling ill, nauseous and weak are likely early signs of more mild to moderate welfare concerns. In later disease vomiting, mouth and stomach ulcers, and secondary infections and complications that may occur, can cause severe discomfort, irritation and pain. Treatment can help but treatments may have side effects that are detrimental to welfare: for example, low palatability of special diets, frequent administration of tablets and frequent travel to and from veterinary practices and multiple veterinary interventions.

The PKD itself, separate from the CRF it eventually causes, is recognised to cause persistent pain that is difficult to characterise and localise in affected humans. Indeed, in a retrospective survey by Bajwa et al (2004) persistent pain in the lower back, abdomen, head, chest or legs was a common reason for clinical investigations to be started that ended with a diagnosis of PKD. It is reasonable to assume that affected cats suffer in an analogous way.

In areas of the world where veterinary facilities are available, the terminal stages of kidney failure should be avoidable if recognised and prevented by euthanasia.

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3.           Duration of welfare impact

 

Most affected cats will have a normal life until signs of CRF occur. The age this happens is very variable. It is usually over seven years (Eaton et al 1997) but does happen sometimes to kittens (Norsworthy 2003). Once signs start they will continue until death. This may be weeks to years in duration. During this period the welfare impact will vary from mild to severe depending on the stage of disease and the effectiveness of any treatments.

 

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4.           Number of animals affected

 

PKD has been very common in Persian cats. A number of surveys, from the UK, continental Europe, the USA and Australia have established that around 36-49% of all Persians have the condition (Cannon et al 2001, Barrs et al 2001, Beck & Lavelle 2001, Barthez et al 2003, Cooper 2000, Bonazzi et al 2007.  Domanjko-Petri et al 2008, Bonazzi et al 2009). It is believed to be the commonest genetic disease in cats.

 

The prevalence of the AD-PKD gene is known to be decreasing in UK Persians, probably as a result of the successful implementation of a pre-breeding screening programme for the disease. But it is still common (see below).

 

Breeds related to Persians: Himalayans, exotic shorthairs, ragdolls, and chinchillas, have also been shown to be affected by the disease (Barrs et al 2001).



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5.           Diagnosis

 

The presence of multiple cysts in the kidneys is diagnostic of PKD. In advanced disease irregular masses may be felt by a veterinary surgeon palpating the kidneys on general examination but other conditions e.g. tumours could feel the same. Usually, when obvious cysts can be felt, the affected cat will have clinical signs of chronic kidney failure (see above). Ultrasound examination gives characteristic findings both in the kidneys and in the liver (when affected) (Cannon et al 2001, Barrs et al 2001, Beck & Lavelle 2001, Barthez et al 2003, Bonazzi et al 2007, Domanjko-Petri et al 2008, Bonazzi et al 2009). The effectiveness of ultrasonography depends on the skill of the ultrasonographer, the quality of the ultrasound equipment and the size of the cysts. Ultrasound transducers with a frequency of 10-14 MHz are recommended to produce optimum ultrasound image quality (Bonazzi et al 2009). The size of the cysts tends to reflect the age of the cat so the younger the age of the kitten the harder it is  to detect cysts (Biller et al 1996). Bonazzi et al (2009) found that, with their skill levels, the use of modern ultrasound equipment compared very closely to results of genetic testing in a group of Persian cats examined at three months old. Repeatability of ultrasound findings has been demonstrated (Wills et al 2009).

 

In the study by Bonazzi et al (2009) cysts were not detected in one cat that was found to be positive using the genetic test., and several cats in which  cysts were seen by ultrasound were negative on the genetic test. Further investigations regarding the latter suggested that some of these may have had clinically insignificant, small cysts that may not progress but others did have the AD-PKD mutation that had not been detected on the initial genetic screen (but which was detected on detailed genetic sequencing). Two cats were found to have two copies of the AD-PKD gene (ie to be homozygous for the gene – see below); a condition that previously was thought to always be fatal prior to birth. At least one cat was thought to have PKD with a yet undetected genetic mutation – as has been described in humans (see above).

 

Despite these few false negative results, genetic tests to detect the AD-PKD are highly predictive of the results of ultrasound examination (Helps et al 2007). Tests are available from the following organisations:

 

University of Bristol – Langford Veterinary Services http://www.langfordvets.co.uk/lab_pcr_pkd.htm

Animal Health Trust, Genetic Services http://www.aht.org.uk/genetics_polycystic.html

University of California, David, Veterinary Genetics Laboratory http://www.vgl.ucdavis.edu/services/pckd1.php

The presence of chronic renal failure is a separate issue from the presence or absence of the PKD1 mutant gene and the presence of cysts. Chronic renal failure is a clinical diagnosis relying on the history of disease being present for at least two weeks and abnormalities on laboratory tests including elevated levels of urea, creatinine (azotaemia) and phosphate in the blood and dilute urine, all indicating that the kidneys are failing to function normally. A non-regenerative anaemia may also be detected (Ross et al 2006). PKD is not the only cause of CRF.

 

The diagnosis of CRF due to PKD rests upon clinical examination and the results of haematology, biochemistry and urine analysis (blood and urine tests) to determine the clinical situation ie the current degree to which kidney function has been lost; ultrasound examination to detect the presence number and size of cysts and genetic testing to detect the presence or absence of the genetic mutation in that individual.

 

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6.           Genetics

The form of PKD discussed here is an autosomal dominant condition with variable penetrance (Biller et al 1990, Biller et al 1996). Thus the presence or absence of just one gene determines if a cat will be affected or not, but the effect that it has on the individual varies in the age at which the cat is affected and the speed of progression. As it is a dominant trait carriers do not exist; only one copy of the gene (coming either from the father or mother) is needed to cause cysts to develop. These animals are said to be heterozygous (they have one dominant abnormal gene and one recessive normal gene). Affected animals always develop the cysts. If they live long enough they will develop kidney disease and failure. When the gene is passed on by both parents the resultant individual is said to be homozygous (having two dominant abnormal genes) and in the case of Persian cats with AD-PKD, were believed always to die before birth (Lyons 1994, Domanjko-Petri et al 2008). However, recently, Bonazzi et al (2009) have described two homozygous kittens alive at three months old.

The affected gene of autosomal dominant polycystic kidney disease has been identified and labelled PKD1 after the analogous human gene (Lyons et al 1994). It is this science that has enabled a genetic test to be developed to identify affected individuals at any age or stage of disease.


In humans other forms of
PKD are known to exist, for example there is an autosomal recessive polycystic kidney disease (Biller et al 1996, Barrs et al 2001, Beck & Lavelle 2001, Young et al 2005). Around 85% of human PKD cases are associated with the AD-PKD condition analogous to the cat disease discussed here. It is likely that there are other forms of polycystic disease in cats. Whether these are more common in Persians than other breeds has not been discovered but cats with cysts found on ultrasound scanning or at post-mortem examination but which are negative on the genetic test for mutant PKD1 gene do occur (Bonazzi et al 2009, Helps et al 2007, Kappe et al 2005). There can be no doubt, however that the autosomal dominant form discussed here is the most important condition, by far.

 

Other factors, besides the presence of this gene, also play a part in the expression of the AD-PKD gene. Whether these other factors are genetic or environmental is not known  (Lee et al 2010).

 

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7.           How do you know if an animal is a carrier or likely to become affected?

Ultrasound examination after 10 months of age and  genetic testing performed after weaning are both very reliable methods and combining both has advantages. The laboratories providing these tests should be contacted for details of the processes required. Generally, the genetic test can be performed either using a blood sample collected by a veterinary surgeon or using a mouth swab which can be collected by the cat’s owner. However, to be accepted on to a register of unaffected animals an individual 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 this microchip. Animals also have to have a microchip to have an official ultrasound evaluation. If both parents are free from the disease then offspring will not be affected.

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8.          Methods and prospects for elimination of the problem

All cats that carry the abnormal gene are affected with AD-PKD, and affected cats can be identified before they reach breeding age using a combination of ultrasound examination and genetic testing. This makes it relatively easy to eliminate the disease from a breeding group; if all cats in the high-risk breeds were to have their kidneys scanned or be gene tested before they were used for breeding, and if affected cats were not then used for breeding, then PKD could be eradicated from those breeds in a single generation.

A scheme to eliminate PKD was started by the UK’s Feline Advisory Bureau (FAB) in 2001. Details can be found at : http://www.fabcats.org/breeders/infosheets/pkd/pkd_gene_test.html

There is however, concern that removal of all these cats from the breeding pool might cause excessive restriction in the choice of cats to breed from, and hence a reduction in the Persian’s gene pool (Bell 2004) with the risk that other genetic defects may inadvertently increase in frequency. The UK’s Feline Advisory Bureau suggested that some cats positive for AD-PKD may be allowed to breed with AD-PKD negative cats to help preserve genetic diversity

(http://www.fabcats.org/breeders/infosheets/pkd/pkd_gene_test.html accessed 13th October 2010). However, as acknowledged, a large number of kittens that will go on to suffer from PKD and chronic renal failure will be born from these matings and a better way of preserving and increasing genetic diversity seems to be to allow out-breeding of Persian cats with cats free from genetic defects that are not Persians.

There is no justification to breed two AD-PKD positive cats together. There is also no justification to breed any Persian cat, or a cat known to have a Persian ancestor, without testing for PKD first. Persian cats that have been tested negative can be placed on to a register kept by the FAB (http://www.fabcats.org/breeders/infosheets/pkd/pkd_negative_register.html). As well as being tested either by an FAB-approved veterinary ultrasonographer or by the genetic test, these cats must be permanently identified using a microchip.

Submissions to Langford Veterinary services for AD-PKD genetic testing have shown a drop in numbers of positives. In 2005 29% were positive and in 2009 it was 10%. It has been suggested that this shows that the screening process set up by FAB (and using both the genetic test and ultrasound examinations) is succeeding http://www.langfordvets.co.uk/lab_pcr_pkd.htm (accessed 13th October 2010).

 
 

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9.          Acknowledgements

UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.

 

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10.          References

Al-Bhalal L and Akthar M (2008) Molecular basis of autosomal recessive polycystic kidney disease (ARPKD). Advances in Anatomical Pathology 15: 54-58

Bajwa ZH, Gupta S, Warfield CA and Steinman TI (2001) Pain management in polycystic kidney disease. Kidney International 60: 1631–1644

 

Barrs SV, Gunew M, Foster S, Beatty J and Malik R (2001) Prevalence of autosomal dominant polycystic kidney disease in Persian cats and related-breeds in Sydney and Brisbane. Australian Veterinary Journal 79 : 257–259

 

Barthez PY, Rivier P and Begon D (2003) Prevalence of polycystic kidney disease in Persian and Persian related cats in France. Journal of Feline Medicine and Surgery 5: 345-347

Beck C and Lavelle RB (2001) Feline polycystic kidney disease in Persian and other cats: a prospective study using ultrasonography. Australian Veterinary Journal 3: 181-186

Bell JS (2004) Common Genetic Disorders: Diagnosis and Counselling. Western Veterinary Conference 2004

 

Biller DS (1994) Polycystic Kidney Disease, In: Consultations in Feline Internal Medicine Volume 2. Editor J.R. August. Elsevier, St Louis. pp.325

Biller DS, Chew DJ and DiBartola SP (1990) Polycystic kidney disease in a family of Persian cats. Journal of the American Veterinary Medical Association196: 1288-90

 

Biller DS, DiBartola SP, Eaton KA, Pflueger S, Wellman ML and Radin MJ (1996) Inheritance of polycystic kidney disease in Persian cats. Journal of Heredity 87: 1-5

Bonazzi M, Volta A, Gnudi G, Bottarelli E, Gazzola M and Bertoni G (2007) Prevalence of the polycystic kidney disease and renal and urinary bladder ultrasonographic abnormalities in Persian and Exotic Shorthair cats in Italy. Journal of Feline Medicien and Surgery 9: 387-391

Bonazzi M, Volta A, Gnudi G, Cozzi MC, Strillacci MG, Polli M, Longeri M, Manfredi S and Bertoni G (2009) Comparison between ultrasound and genetic testing for the early diagnosis of polycystic kidney disease in Persian and Exotic Shorthair cats. Journal of Feline Medicine and Surgery (2009) 11: 430-434

Cannon MJ, MacKay AD, Barr FJ, Rudorf H, Bradley KJ, Gruffydd-Jones TJ (2001). Prevalence of polycystic kidney disease in Persian cats in the UK. Veterinary Record 149: 409-11

Cooper B. (2000) Autosomal dominant polycystic kidney disease in Persian cats. Feline Practice 28: 20-21

Domanjko-Petri A., Cernec D and Cotman M (2008) Polycystic kidney disease: a review and occurrence in Slovenia with comparison between ultrasound and genetic testing. Journal of Feline Medicine and Surgery 10: 115-119

Eaton KA, Biller DS, DiBartola SP, Radin MJ and Wellman ML (1997) Autosomal Dominant Polycystic Kidney Disease in Persian and Persian-cross Cats. Veterinary Pathology 34: 117-126

 

Helps CR, Tasker S, Barr F, Wills S and Gruffydd-Jones TJ (2007) Detection of the single nucleotide polymorphism causing feline autosomal-dominant polycystic kidney diseasein Persians from the UK using a novel real-time PCR assay. Molecular and Cellular Probes 21: 31-4

Helps C, Tasker S and Harley R (2007) Correlation of the feline PKD1 genetic mutation with cases of PKD diagnosed by pathological examination. Experimental and Molecular Pathology 83: 264-8

Kappe EC, Hecht W, Gerwing M, Michele U and Reinacher M (2005) Polycystic kidney disease in the German population of Persian cats. A comparative study of ultrasonographical examination and genetic testing. Tierarztl Prax Ausg K Kleintiere Heimtiere 33: 413-8

Lee Y-J, Chen H-Y, Wong M-L, Hsu W-L, Ou C-M and Wong M-L (2010) Diagnosis of feline polycystic kidney disease by a combination of ultrasonographic examination and PKD1 gene analysis. Veterinary Record 167: 614-7

Lyons LA, Biller DS, Erdman CA, Lipinski MJ, Young AE, Roe BA, Qin B and Grahn RA (2004) Feline Polycystic Kidney Disease Mutation Identified in PKD1. Journal of the American Society of Nephrology 15: 2548-2555

Norsworthy GD (2003) Polycystic Kidney Disease. In: The Feline Patient: Essentials of Diagnosis and Treatment 2nd edition. Editors: G.D. Norsworthy, M.A. Crystal, S. Fooshee Grace & L.P. Tilley. Lippincott Williams & Wilkins, Baltimore pp 415

Ross SJ, Polzin DJ and Osborne CA (2006) Clinical progression of early chronic renal failure and implications for management. In: Consultations in Feline Internal Medicine Volume 5. Editor J.R. August. Elsevier, St Louis. pp 389

Torres VE and Harris PC (2006) Mechanisms of Disease: autosomal dominant and recessive polycystic kidney diseases Nature Clinical Practice Nephrology 2: 40-55

Wills SJ, Barrett EL, Barr FJ, Bradley KJ, Helps CR, Cannon MJ and Gruffydd-Jones TJ (2009) Evaluation of the repeatability of ultrasound scanning for detection of feline polycystic kidney disease. Journal of Feline Medicine and Surgery 11: 993-996

Young AE, Biller DS, Herrgesell EJ, Roberts HR and Lyons LA (2005) Feline polycystic kidney disease is linked to the PKD1 region. Mammalian Genome 16: 59-65

 

http://www.fabcats.org/breeders/infosheets/pkd/pkd_gene_test.html accessed 13th October 2010

Veterinary Genetics Laboratory (VPL, California, UK. www.vgl.ucdavis.edu.

Langford Veterinary Diagnostics, University of Bristol, UK. www.bris.ac.uk/lvd/lvd.htm.

Genetic Services, Animal Health Trust, Newmarket, UK. www.aht.org.uk.

 

 

© UFAW 2011

 

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