POLYCYSTIC KIDNEY DISEASE IN WHITE DOMESTIC PIGS

Robert Paslawski¹, Adrian Janiszewski², Agnieszka Noszczyk-Nowak², Dorian Nowacki¹, Urszula Paslawska^2
1 Department and Clinic of Internal and Occupational Diseases and Hypertension Wroclaw Medical University
² Department of Internal Diseases with Clinic for Horses, Dogs and Cats Faculty of Veterinary Medicine Wroclaw University of Environmental and Life Sciences

ABSTRACT

Polycystic kidney disease (PKD) is a rare form of swine congenital renal malformation in contrast to other species, especially cats and humans. The most affected animals developed renal failure which can lead to death at the neonatal age. PKD was detected in 5 white domestic pigs (Polish Landrasse). All affected pigs are descendants of the same males, but they came from two litters, in one litter 2 of 10 pigs were affected by the disease, in the second litter 3 of 10 pigs. The pigs did not have symptoms of renal failure (to 50 kg of body weight), and the disease was detected incidentally during a routine autopsy examination. Despite PKD is a rare disorder in the swine, it should be monitored in the pig population to avoid its expansion because of its genetic origin.

 

Key words: cysts, kidney disease, swine, urinary tract, pig.

INTRODUCTION

Polycystic kidney disease (PKD) is a rare form of swine congenital renal malformation in contrast to other species, especially cats [1] and humans [16,17]. The anomaly is characterized by the presence of numerous, mostly small cysts located in the renal parenchyma. The most affected animals developed renal failure which can lead to death at the neonatal age [15]. Sometimes cysts may be present in the liver and rarely in the pancreas or spleen [9]. PKD seems to be connected with increased risk of subarachnoid hemorrhage and cranial aneurysms [3].

Congenital polycystic kidney disease has not been documented previously in pigs in Poland.

MATERIAL AND METHODS

PKD was detected in 5 white domestic pigs (Polish Landrasse). The pigs did not have symptoms of renal failure, and the disease was detected incidentally during a routine autopsy examination. The autopsy was performed immediately after the pigs were euthanized with an overdose of pentobarbital. All the animals received human care in compliance with the Guide for the Care and Use of Laboratory Animals as published by the National Institutes of Health in 1985. All experiments were performed in compliance with the Bioethical Committee of the Wroclaw University of Environmental and Life Sciences guidelines for the experimentation on animals.

RESULTS AND DISCUSSION

PKD was recognized in 5 white domestic pigs at a body weight of 30-50 kg, out of 30 that participated in the experiment of heart infarct and were examined at autopsy - which is 17%. All tested pigs are descendants of the same parents, but they came from three litters, in one litter 2 of 10 pigs were affected by the disease, in the second litter 3 of 10 pigs, and the last litter was free of congenital disorders. In both kidneys of the diseased animals, a number of fluid cysts of various sizes, in most cases small, were found (Fig. 1). Morphological and biochemical examinations of blood didn’t detect any alterations: White blood cells 20.96 G/L, Red blood cells 6.41 T/L, Hemoglobin 6.1 mmol/L, Hematocrite 0.283 L/L, urea 3.58, creatinine 111.7 µmol/L, Total protein 50.78 g/L, Albumin 28.89 g/L.

Fig. 1. Necropsy of PKD in the swine. Visible cysts drained from fluid during incision of the kidney and a smaller cyst filled with fluid content

So far PKD in pigs has not become a clinical or economical problem, and therefore it aroused no particular interest to researchers. Wells and Herbert described the results of investigation conducted at the slaughterhouse, where they investigated the presence of renal cysts in fattening pigs from a single manufacturer. They showed a prevalence of 47.5 percent in that particular pig population. Affected pigs were the progeny of a landrace boar [16]. A breeding experiment done with suspected boar revealed congenital origin of disorders with prevalence of 62 per cent, what documented autosomal dominant inheritance. They suggested that a number of cysts may be determined by polygenic inheritance. Study of the pathology of the cysts performed in one-day-old, 25-32-day-old and 370-day-old progeny indicated a complex pathogenesis including probable recruitment to the cyst population throughout the studied period. In our cases the prevalence of the disease was lower, but breeders lack the interests for further investigation. Recent studies confirm that PKD is inherited in a very similar manner to human form of diseases and this monogenic autosomal dominant defect is caused by two mutations PKD1 and PKD2. It has been found that the porcine PKD1 cDNA has 14,209bp length and encodes a 4305-residue polypeptide. The genomic sequence of PKD1 is ≈50kb with 46 exons. An alternative splice acceptor site was identified in intron 9 [5]. The pig PKD2 cDNA consist of 3370 bases. Wang and colleagues provided evidence that affected region, responsible for the severity of PKD is localized between 3 to 9 exons [14].

PKD is a rare disorder in the swine and has not yet been described in Poland and other countries of Central and Eastern Europe. We do not know whether the absence of such reports is related to the real lack of affected animals, or PKD was not previously recognized because they do not cause obvious symptoms, or significant economic loss. We do not know if that is the actual spread of the defect and whether its presence is maintained at a constant level, or has some dynamics. In humans and in cats PKD is of great of importance, while leads often to chronic renal failure. Moreover the last research documented an association between PKD and renal cell carcinoma in humans [2,6,7]. Despite knowledge of the location of abnormal mutations, it seems that attempts to monitor the disease with the (most reliable method) genetic testing - would be economically unjustified. Moreover the genetic defect as a primary cause of PKD does not predicts the precise anatomical manifestation in a particular animals. This clinical variability fluctuates not only between different families, but also between affected members of the same family. Therefore the intrafamiliar variability suggests an additional role for other genetic or environmental factors eg. breeds, protein or salt enriched diets, ageing. Few research suggest that male hormones may be important factors in renal cystic disease, based on the faster or earlier growth of kidney cysts in male individuals [4,10]. Salt in diet and other risk factor resulting in high blood pressure are charged with responsibility for more rapid progression renal failure in patients with PKD especially in male humans [12]. In contrast the low-protein intake or the addition of flaxseed may be beneficial [8,11].

It seems that more rational to the general monitoring of PKD prevalence should be drawing attention of veterinarians on the morphology of kidneys during a routine abdominal ultrasound (eg. pregnancy control) or during post-mortem examination in the abattoir.

It should be remembered that cystic diseases of the kidney encompass a wide spectrum of causes that should be considered in differential diagnosis: localized cystic disease, unilateral autosomal dominant polycystic kidney disease, multilocular cystic nephroma, or cystic neoplasm [13]. 

CONCLUSION

According to the best of our knowledge, this is a first case of described PKD in pigs in Poland. PKD has had so far no impact on the economy of the pig production. Monitoring of expansion of this genetically originated disease could be done using abdominal ultrasound or after slaughtering of animals.

ACKNOWLEDGEMENTS

The Ph.D. scholarship in this task is co-financed by the European Union as part of the European Social Fund. 

REFERENCES

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Accepted for print: 17.05.2013

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Robert Paslawski
Department and Clinic of Internal and Occupational Diseases and Hypertension
Wroclaw Medical University
Borowska 213, 50-556 Wrocław, Poland
Phone: +48 602 752 908
email: robertpaslawski@wp.pl

Adrian Janiszewski
Department of Internal Diseases with Clinic for Horses, Dogs and Cats
Faculty of Veterinary Medicine
Wroclaw University of Environmental and Life Sciences
47 Grunwaldzki sq.
50-366 Wroclaw, Poland
Phone: +48 71 320 10 11
email: ajanisz@gmail.com

Agnieszka Noszczyk-Nowak
Department of Internal Diseases with Clinic for Horses, Dogs and Cats
Faculty of Veterinary Medicine
Wroclaw University of Environmental and Life Sciences
47 Grunwaldzki sq.
50-366 Wroclaw, Poland
Phone: (+4871) 320 10 09
email: agnieszka.noszczy-nowak@up.wroc.pl

Dorian Nowacki
Department and Clinic of Internal and Occupational Diseases and Hypertension
Wroclaw Medical University
Borowska 213
50-556 Wrocław, Poland
Phone: +48 505 852 881
email: dorian.nowacki@wp.pl

Urszula Paslawska
Department of Internal Diseases with Clinic for Horses, Dogs and Cats
Faculty of Veterinary Medicine
Wroclaw University of Environmental and Life Sciences
47 Grunwaldzki sq.
50-366 Wroclaw, Poland
Phone: +48 71 320 53 67
email: urszula.paslawska@up.wroc.pl

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Responses to this article, comments are invited and should be submitted within three months of the publication of the article. If accepted for publication, they will be published in the chapter headed 'Discussions' and hyperlinked to the article.

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