Polycystic kidney disease in a Persian Cat

Signalment

A 4.4kg 7 year old male neutered Persian cat.

History

            Two years previously the cat had suffered three episodes of pollakuria and polydipsia in a twelve month period, all of which had resolved following antibiotic therapy within a few days. One of these episodes was accompanied by pyrexia and polydipsia. No diagnostic procedures were performed at this stage.

            The cat presented three weeks previously with inappetence, lethargy and polydipsia of 1 week’s duration. No vomiting had been noted by the owners, but mild diarrhoea was seen on examination at this point. The cat was found had enlarged, irregular kidneys. Haematology and biochemistry tests were performed which revealed a moderate to high azotaemia (urea 36.0mmol/l, reference range 5.71-12.85; creatinine 561umol/l, reference range 71-212). PCV was normal at 0.279 l/l (reference range 24.0-45.0) and phosphate was high at 4.73 mmol/l (reference range 1.00-2.42). The cat was treated with 125ug of vitamin B12 (Vitbee 250, Arnolds), 12.5mg nandrolone laurate (Laurabolin, Intervet) and prednisolone 1mg BID for 4 days, 1mg SID for 4 days and 1mg every other days for four days. Dietary therapy was also started (Whiskas low phosphorus/low protein). Some improvement was noted, with a reduction in polydipsia and an increase in appetite. However, three weeks after this, the cat presented again with anorexia, polyuria and polydipsia.

Physical Examination

T 38.6C                        P 180bpm        R 22/minute

The cat was bright, alert and active, but was quite underweight. Mucous membrane colour was normal, but gingivitis and stomatitis were present in the buccal cavity. Lymph nodes were normal on palpation and thoracic auscultation was unremarkable. Both kidneys were large and irregular. No other abnormalities were noted on abdominal palpation and the remainder of the physical examination was unremarkable.

Problem List

Enlarged, irregular kidneys

Anorexia and weight loss

PUPD

Gingivitis/stomatitis

Differential diagnosis

*=more likely based on history, clinical signs and disease incidence

(i) Enlarged irregular kidneys

            Renal lymphosarcoma*

            Other renal neoplasia*

            Polycystic kidney disease*

            Chronic nephritis*

            Granulomatous nephritis associated with feline infectious peritonitis

            Perinephric pseudocysts*

            Hydronephrosis*

(ii) PUPD

            Primary polydipsia

                        Pyschogenic

                        Neurologic

                        Fever, pain

            Polydipsia secondary to fluid loss (e.g. vomiting and diarrhoea)

            Polydipsia secondary to primary polyuria

                        Osmotic diuresis (e.g. diabetes mellitus)*

                        Chronic renal failure*

                        Hypercalcaemia*

                        Hyperadrenocorticism*

                        Hyperthyroidism*

                        Hepatic disease*

                        Hypoadrenocorticism

                        Renal medullary solute washout

                        Primary diabetes insipidus

(iii) Gingivitis/stomatitis

            Dental disease*

            Infectious disease +/- immunosuppression (e.g FeLV, FIV, FIP, calicivirus,                               herpesvirus, Candidiasis)*

            Immune mediated disease (e.g. Systemic lupus erythematosus, pemphigus,                                 toxic epidermal necrosis, lymphocytic-plasmacytic idiopathic)*

            Uraemia*

            Trauma

            Ingestion of caustic/corrosive toxins

Diagnostic plan

The palpably abnormal kidneys were suggestive of a renal cause of polyuria, polydipsia, anorexia and weight loss. Haematology and biochemistry were performed by an external laboratory to investigate the presence of azotaemia and rule out other causes of polyuria and polydipsia, and FeLV and FIV serology performed to rule out these diseases. Survey and contrast radiography and ultrasonography were used to further characterise the kidney disease.

Haematology and biochemistry (tables 1 and 2)

The cat was moderately anaemic with evidence of only a mild regenerative response. It was also severely azotaemic.

Serology

IFA for FeLV and FIV were negative.

Abdominal radiography (figs 1, 2, 3 and 4)

Plain abdominal radiography revealed a skeletally mature cat in relatively poor bodily condition. Both kidneys were grossly enlarged with a somewhat irregular contour. Positive contrast low volume bolus intravenous urography with iodine-based contrast media (Urografin 325, Schering) showed multiple radiolucent areas throughout both kidneys, with the contrast medium delineating a pattern of parenchymal loculation. The radiopacity of the contrast medium was lower than would be expected from a healthy kidney.

Ultrasonography (fig. 5)

Ultrasonographic examination with a B-mode 5MHz linear scanner revealed both kidneys were grossly enlarged. Both contained multiple, roughly spherical anechoic spaces distributed throughout the kidney.  Distant acoustic enhancement was observed. Ultrasound-guided fine needle aspirate of a cyst demonstrated that the cyst contained a yellow-brown fluid.

Diagnosis

Polycystic kidney disease

Treatment

Symptomatic treatment for anorexia and weight loss were continued. This consisted of 125 ug of vitamin B12 (Vitbee 250, Arnolds) and 12.5mg nandrolone laurate (Laurabolin, Intervet), as well as dietary treatment with low phosphorus and low protein diet (Whiskas low phos/low protein). Clavulanate/amoxycillin (Synulox, Pfizer) was given at 50mg BID.

Outcome

After diagnosis, the cat continued to deteriorate, becoming increasingly lethargic, eating very little and drinking excessively. The owners requested euthanasia and a post mortem examination was carried out.

Post mortem examination (fig. 6)

Gross post mortem examination revealed a cat in poor bodily condition. Stomatitis and mild oral ulceration was present. Both kidneys were grossly enlarged, the right having external dimesions of 6cm x 4cm and the left 4cm x 3.5cm. The surface of the kidneys were irregular and nodular. Transection of the kidneys revealed multiple cysts filled with a yellow-brown fluid. Little normal kidney tissue was visible. The ureters, bladder and urethra were normal and no abnormalities were noted in other abdominal organs. Histological examination (fig. 9.7) carried out by an external laboratory demonstrated that the cysts contained an eosinophilic colloid, and were lined by a single layer of flattened cells, which were probably epithelial. Remaining kidney tissue had many dilated tubules with interstitial fibrosis and occasional groups of macrophages or lymphoid cells within the tissue. The majority of the glomeruli looked reasonably normal.

Discussion

Polycystic kidney disease (PKD) is an inherited disease affecting Persian cats which has been reported sporadically in the veterinary literature over the last 30 years (Battershell and Garcia, 1969; Northington and Juliana, 1977; Crowell et al 1979).

            PKD is usually bilateral, but affected cats often do not show clinical signs of renal failure until adulthood and many reported cases were asymptomatic until older than 7 years (e.g. Miller et al 1999).

            The disease is characterised by multiple cysts throughout the kidney that increase in size with age. Cysts may arise from any nephron segment, but only a small percentage of nephrons are affected (Eaton et al 1997).

            Enlarged, irregular kidneys can occur in cats for a variety of reasons. Differentials include renal lymphosarcoma, other renal neoplasia, granulomatous nephritis associated with feline infectious peritonitis and perinephric pseudocysts. Bilateral hydronephrosis is more likely to produce a regular contour.

            Intravenous urography provided a good indication that the cat described here was suffering from PKD, as the radiographs showed the constrast meduim had delineated a pattern of parenchymal loculation. However, the contrast in the radiographs is not pronounced, probably due to the presence of uraemia. Since there is also the possibility that adverse reactions to intravenous contrast media may occur  (Douglas et al, 1987), urography is not ideal for diagnosing PKD.

            Ultrasonography is safe and non-invasive, and it has been reported that it can be used to diagnose feline PKD with a high level of confidence (Walter et al, 1988). The case described here had a multifocal distribution with anechoic cavitating lesions. On the basis of radiographic and ultrasonographic findings, polycystic kidney disease was diagnosed and this was later confirmed by histological examination of kidney tissue sampled at post mortem examination.

            The cat in this case study was showing clinical signs of chronic renal failure, and biochemical parameters showed a severe azotaemia. This had progressed since initial presentation 3 weeks earlier, and the cat had also become mildly anaemic, suggesting that the cat was suffering from severe renal failure. A low phosphorus and low protein diet was given to reduce clinical signs of uraemia and decrease the worsening of the disease from hyperphosphataemia. Vitamin B12 and anabolic steroids were given to improve appetite. Antibiotics were administered, since pyelonephritis and cystitis may occur secondary to PKD (Northington et al, 1977). The cat continued to deteriorate, however, and was euthanased on welfare grounds.

            Other treatment options not explored included erythropoietin for the anaemia, owner administered subcutaneous fluids and renal transplantation. Two other possible treatment options were ultrasound-guided percutaneous aspiration of cyst fluid, or surgical reduction of cyst volume (Bennet 1987). These were declined by the owner.

            Hypertension is commonly associated with chronic renal failure. A study was performed to see if enalapril was indicated in cats suffering from PKD (Miller et al, 1999). However, the study was flawed, in that nearly all the cases of PKD studied were in the early, asymptomatic stage of the disease and hence were normotensive. Further studies are needed in hypertensive cats suffering from PKD to see if ACE inhibitors have a therapeutic role in the disease. ACE inhibitors were therefore not used in the management of this case.

            Crowell et al (1979), reported a familial predisposition to PKD and subsequent studies (Biller et al, 1987, Biller et al, 1990), have demonstrated that the condition is inherited in an autosomal dominant pattern. PKD is an important genetic disease of Persian cats with a prevalence probably exceeding 45% in the UK. A screening programme has recently been instituted (Cannon et al, 2000) to assist breeds in eradicating the disorder. Because of the heritable nature of this disease, the cat’s breeder was informed of the findings.

References

BATTERSHELL, D., & GARCIA, J. P., (1969) Polycystic kidney in a cat. Journal of the American         

           Veterinary Medical Association 154, 665-666

                Biller et al, 1987,

BILLER, D. D., CHEW, D. J., DIBARTOLA, S. P., (1990) Polycystic kidney disease in a family of           

            Persian cats. Journal of the American Veterinary Medical Association 196, 1288-1290

CANNON, M., GRUFFYDD-JONES, T. & GUNN-MOORE, D., (2000) Screening for polycystic           

                                kidney disease in cats. Veterinary Record, 147, 639-640

NORTHINGTON, J. W., & JULIANA, M. M., (1977) Polycystic kidney disease in a cat. Journal of      

             Small Animal Practice 18, 663-666

CROWELL, W. A., HUBBELL, J. J., & RILEY, J. C., (1979) Polycystic renal disease in related cats.          

          Journal of the American Veterinary Medical Association 175, 286-288

MILLER, R. H., LEHMKUHL, L. B., SMEAK, D. D., DIBARTOLA, S. P. & RADIN, J. (1999)                        

                       Effect of enalapril on blood pressure, renal function and the renin-angiotensin-aldosterone       

                              system in cats with autosomal dominant polycystic kidney disease. American Journal of         

                                 Veterinary Research 60, 1516-1525

EATON, K. A, BILLER, S. D., DIBARTOLA, S. P., RADIN, M. J., & WELLMAN, M. L. (1997)                      

    Autosomal dominant polycystic kidney disease in Persian and Persian-cross cats. Veterinary                   

Pathology 34, 117-126

DOUGLAS, S. W., HERRTAGE, M. E., & WILLIAMSON, H. D., (Eds) (1987), Contrast radiography of the urinary system.

In: Principles of Veterinary Radiography, 4th Edn, pp256- 264 Bailliere                  Tindall, London

WALTER, P. A., JOHNSTOM, M. S., FEENEY, D. A. & O’ BRIEN, T. D., (1988) Applications of                

        ultrasonography in the diagnosis of parenchymal kidney disease in cats: 24 cases (1981-1986).           

       Journal of the American Veterinary Medical Association 192, 92-98

BENNET, W. M., ELZINGA, L., GOLPER, T. A. & BARRY, J. M. (1987) Reduction of cyst volume              

      for symptomatic management of autosomal dominant polycystic kidney disease. Journal of                 

      Urology 137, 620-2

Figs 1 and 2 Lateral and DV abdominal survey radiographs

Figs 3 and 4 Lateral abdominal radiographs post IVU after 2 minutes (fig 3) and after 1                          hour (fig4)

(a)

(b)

Fig 5 Renal ultrasonography

Fig 6 Polycystic kidneys at post mortem examination

Fig. 7 Histology of polycystic kidney x50 power

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