Feline PKD-Autosomal dominant polycystic kidney genetic non sex, non color linked cat disease can be diagnosed as early as seven weeks old with abdominal ultrasound. The cysts will appear as black and round. Persians and Persian crossbred cats are most often affected by this disease which can result in renal failure. Not all cats will show signs of the disease which are classic signs of renal failure:Weight loss, poor appetite, increased thirst and urination, lack of energy, and vomiting
The iohexol clearance test is a sensitive blood test that may detect kidney problems before the symptoms emerge usually after 2/3s of damage. Dietary citrate treatment and flaxseed may help..research on cats is needed(please check out the research abstracts below)
Breeders are growing more knowledgeable and responsible.
A website devoted totally to this disease is has been created by Marie Thiers
J Vet Intern Med. 2003 Jan-Feb;17(1):21-7. :
Increased mean arterial pressure and aldosterone-to-renin ratio in Persian cats with polycystic kidney disease.
Pedersen KM, Pedersen HD, Haggstrom J, Koch J, Ersboll AK.
Department of Clinical Studies, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark.
Polycystic kidney disease (PKD) in Persian cats has been increasingly reported and compared to human autosomal dominant polycystic kidney disease (ADPKD) in the last decade. In cats, however, few studies have dealt with the occurrence and hormonal determinants of hypertension, one of the most common extrarenal manifestations of ADPKD in humans. The purpose of this study was to compare Persian cats >4 years old with PKD to unaffected control cats with regard to blood pressure (BP), plasma renin activity (PRA), serum aldosterone concentration, plasma atrial natriuretic peptide (ANP) concentration, and aldosterone-to-renin ratio (ARR). Three gender- and age-matched groups were studied, each consisting of 7 cats: (1) a control group without cysts, (2) a group with mild PKD, and (3) a group with severe PKD (multiple cysts and renal enlargement). Mild renal insufficiency was found in only 1 of 14 cats with PKD. Cats with PKD had a higher mean arterial pressure (P = .04) and more often had a high ARR (P = .047) than did control cats. Tendencies toward higher diastolic and systolic arterial pressures (DAPs and SAPs, respectively) and lower PRAs were observed in cats with PKD compared to controls (.05 < P < or = .1). No significant differences were found between the groups in serum aldosterone and plasma ANP concentrations. None of the cats had echocardiographic evidence of cardiac hypertrophy. In conclusion, cats with PKD had a minor increase in mean arterial pressure compared to control cats, and half of the cats had a high ARR.
Vet Radiol Ultrasound. 2002 Jul-Aug;43(4):368-73. :
Renal ultrasonographic and computed tomographic appearance, volume, and function of cats with autosomal dominant polycystic kidney disease.
Reichle JK, DiBartola SP, Leveille R.
Department of Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine, Columbus 43210-1089, USA.
The purpose of this study was to describe the ultrasonographic (US) and computed tomographic (CT) appearance of autosomal dominant polycystic kidney disease (ADPKD) in cats; to compare renal volume in cats with ADPKD (n = 5; mean age 59 +/- 10 months)) and normal cats (n = 5; mean age 66 +/- 10 months) using 2 imaging modalities, US and CT; and to calculate cyst volume using CT. Glomerular filtration rate (GFR) was determined by 2 methods: 99mTc-diethylene-triaminepentaacetic acid (99mTc-DPTA) scintigraphic uptake and 99-Tc-DTPA plasma clearance. Sonographically, ADPKD affected kidneys were characterized by multiple anechoic to hypoechoic, round to irregularly shaped structures with variation in size. Affected kidneys had indistinct corticomedullary junctions and foci of mineralization. Intravenous (IV) contrast medium administration allowed more definitive identification of cysts with CT, and identification of distortion of renal pelves by cysts. A significant difference (Welch ANOVA, P = 0.05) was detected between the US-estimated renal volumes of normal and affected cats. No statistically significant differences were detected in CT volume (between the normal and affected cats, or between US and CT volume measurements) or the 2 GFR methods. In this group of clinically normal, middle-aged ADPKD cats, renal function was within normal limits and not significantly different than normal.
Nephron Physiol. 2003 Jan;93(1):P14-20. :
Dietary citrate treatment of polycystic kidney disease in rats.
Tanner GA, Tanner JA.
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Ind 46202, USA.
Progression of autosomal-dominant polycystic kidney disease (ADPKD) in the heterozygous male Han:SPRD rat is dramatically slowed by ingestion of potassium or sodium citrate. This study examined the efficacy of delayed therapy with sodium citrate, the effect of sodium citrate therapy on kidney cortex levels of transforming growth factor-beta (TGF-beta), and the response to calcium citrate ingestion. Rats were provided with citrate salts in their food, and renal clearance, blood pressure, blood chemistry, and survival determinations were made. Sodium citrate therapy was most effective when started at age 1 month, and delay of therapy until age 3 months produced no benefit. Kidney cortex TGF-beta levels were elevated in 3- and 8-month-old rats with ADPKD, but not in 6-week-old rats. Sodium citrate treatment, started at age 1 month, lowered TGF-beta levels to normal in 3-month-old rats, but this is probably not the primary mechanism of citrate's beneficial effect. Calcium citrate had only a modest effect in preserving glomerular filtration rate. Effective treatment of ADPKD in this rat model requires early administration of a readily absorbed alkalinizing citrate salt. Existing data on ADPKD patients on vegetarian diets or with kidney stones should be studied in light of these findings. Copyright 2003 S. Karger AG, Basel
Srp Arh Celok Lek. 2002 Jul-Aug;130(7-8):251-7. :
[Effect of a modified low protein and low fat diet on histologic changes and metabolism in kidneys in an experimental model of polycystic kidney disease]
[Article in Serbo-Croatian (Cyrillic)]
Bankovic-Calic N, Ogbori MR, Nicman E.
Monitoba Institute of Child Health, Canada.
BACKGROUND: Dietary protein restriction slows progression in numerous animal models of renal diseases. Flax seed has also demonstrated useful anti-inflammatory properties in a number of animal models and human diseases. We undertook several studies to determine if feeding with low protein casein, soy diet and flax seed diet would ameliorate renal injury in Han:SPRD-cy rat model of polycystic kidney disease. METHODS: Male offspring of Han:SPRD-cy heterozygotes received protein modified diet: ad libidum LP 8% casein in test or 20% casein in control group for 8 weeks; 20% heat treated soy protein or 20% casein in control group two separate studies for 8 weeks ad libidum and pair feeding in 6 weeks; and 10% flax seed diet or control rat chow for 8 weeks from weaning. Tissue was harvested for histological assessment and metabolic changes in lipids, citric acid metabolites and osmolytes. Morphometrically after histochemical and immunohistochemical staining cystic changes, renal tubular proliferation and apoptosis, number of interstitial cells/macrophages infiltration and interstitial fibrosis were measured. Gas chromatography was used for lipid analysis in renal and liver tissue. 1-HNMR spectroscopy was used for urine and tissue organic anion and osmolytes content analysis. RESULTS IN PROTEIN MODIFIED DIET: Casein low protein as well as soy protein fed animals demonstrated reduced PKD pathology: significant reduction in cystic changes, interstitial inflammation and fibrosis and also reduction in tubular cells proliferation and apoptosis. Pair feeding protocol in second soy diet study confirmed that significant effect on renal histology was not because of protein deprivation and growth retardation. 1-H NMR spectroscopy revealed that progression of chronic renal failure in Han:SPRD-cy rat PKD is associated with renal depletion of citric acid cycle metabolite and betaine. Amelioration of PKD by soy protein diet is associated with renal retention of citric acid cycle anions, despite increased excretion and preservation of betaine in renal tissue. Soy feeding increased both hepatic and renal content of linoleic acid and increased renal alpha linolenic acid content, while decreased arachidonic hepatic content. RESULTS IN FLAX SEED SUPPLEMENTATION IN DIET: Flax seed fed animals had moderate decrease in cystic size and less interstitial inflammation and fibrosis while there were no differences in epithelial cell apoptosis and proliferation. Lipid analysis revealed significant renal enrichment of 18 and 20 carbon omega 3 polyunsaturated fatty acids. In flax fed animals there was an increased urinary citrate excretion without significant changes in urinary ammonia excretion, so increased citrate excretion was not due to alkaline effect of the diet. Kidney tissue 1H NMR spectroscopy revealed that disease amelioration was associated with tissue retention of succinate and betaine. CONCLUSION: Effect on histology: Low casein and soy feeding ameliorates Han: SPRD-cy rat polycystic kidney disease reducing both tubular remodeling and interstitial inflammation and fibrosis, while flax seed diet effect appears to be through moderation of associated interstitial nephritis. Metabolic effect: Soy diet alters the renal content of polyunsaturated fatty acids and enriched renal betaine content with retention of citric acid cycle metabolites despite increased excretion. Flax seed diet alters renal content of polyunsaturated fatty acids and promotes the formation of less inflammatory classes of renal prostanoides. Flax seed diet also enriched renal content of betaine and succinate. Amelioration of Hans:SPRD-cy rat polycystic kidney disease by diet is associated with alteration in the handling of citric acid cycle metabolites and betaine, and also in content of polyunsaturated fatty acids in kidneys and liver. Metabolic pathways in dietary modified renal pathology have to be established.
J Am Soc Nephrol. 1998 Jul;9(7):1242-8. :
Potassium citrate/citric acid intake improves renal function in rats with polycystic kidney disease.
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202, USA.
Polycystic kidney disease (PKD) has been shown to be exacerbated by acidosis or a low potassium intake, and there is evidence that administration of alkali might have a beneficial effect. This study determined whether ingestion of potassium citrate and citric acid would ameliorate PKD. Healthy normal and heterozygous littermate Han:SPRD rats with autosomal dominant PKD were provided with either tap water or 55 mM K3citrate/67 mM citric acid solution (KCitr) to drink starting at the age of 1 mo. Renal clearance measurements and histologic assessments were performed when the rats were 3 mo old. KCitr intake did not affect body weight or urine flow, but completely prevented the decline in GFR found in untreated rats with PKD. In rats that drank tap water, left kidney GFR averaged (in microliter/min per 100 g body wt) 503 +/- 78 (n = 9) in normal animals and 242 +/- 56 (n = 6) in rats with PKD. In rats that drank KCitr, GFR averaged 562 +/- 123 (n = 7) in normal animals and 534 +/- 103 (n = 7) in rats with PKD. Kidneys of rats with PKD were approximately double normal size. KCitr treatment did not affect kidney size, but led to fewer interstitial abnormalities and smaller cysts in cystic kidneys. KCitr ingestion led to a significantly lower (P < 0.001) plasma [K+] in rats with PKD (3.3 +/- 0.2 versus 4.1 +/- 0.2 mEq/L in rats on tap water). Chronic KCitr intake in the young heterozygous Han:SPRD rat with PKD yields a modest improvement of kidney histology and a dramatic improvement in GFR. The mechanism of action of KCitr and the long-term effects of this treatment on renal structure and function in PKD deserve further study.
Vet Rec. 2001 Oct 6;149(14):409-11. :
Prevalence of polycystic kidney disease in Persian cats in the United Kingdom.
Cannon MJ, MacKay AD, Barr FJ, Rudorf H, Bradley KJ, Gruffydd-Jones TJ.
The Feline Centre, Department of Clinical Veterinary Science, School of Veterinary Science, University of Bristol, Langford.
The prevalence of polycystic kidney disease was assessed in 132 Persian cats, 46 of them referred for the investigation and treatment of medical or surgical conditions, and 86 apparently healthy cats referred specifically to be screened for the disease. Cats referred for the investigation of renomegaly or renal failure were excluded, and cats under 10 months old were only included if they had been examined postmortem. One hundred and twenty-six of the cats were examined ultrasonographically with a 7.5 MHz sector scanner, and the other six cats were examined postmortem. Forty-nine of the 86 cats referred specifically for screening (57.0 per cent) and 16 of the 46 cats referred for other clinical reasons (34.8 per cent) were affected by the disease, giving an overall prevalence of 49.2 per cent.
Aust Vet J. 2001 Mar;79(3):181-4. :
Feline polycystic kidney disease in Persian and other cats: a prospective study using ultrasonography.
Beck C, Lavelle RB.
University of Melbourne Veterinary Clinic and Hospital, 250 Princess Highway Werribee, Victoria 3030.
OBJECTIVE: To determine the prevalence of feline polycstic kidney disease in Persian cats presented to the University of Melbourne Veterinary Clinic and Hospital between February and August 1999. DESIGN: A prospective clinical study using client owned animals was performed. PROCEDURE: Two hundred and fifty Persian cats, ranging in age from 13 weeks to 10 years, were presented to the University of Melbourne Veterinary Clinic and Hospital for ultrasound examination of both kidneys. The cats were placed in dorsal and lateral recumbency and alcohol and ultrasonic coupling gel were applied to the skin. The kidneys were examined ultrasonographically in longitudinal, sagittal and transverse planes. Results were recorded for each cat at the time of examination as either negative or positive for PKD. In addition 14 Exotics (short-haired Persians), 4 Ragdolls and 3 British Short-Hair cats were examined. RESULTS: Forty five percent of Persian cats examined were found to be positive for feline polycystic kidney disease on the basis of presence of anechoic cysts within the renal parenchyma. These cats ranged in age from 13 weeks to 10 years. Fifty per cent of the Exotic cats were positive for polycystic kidney disease whereas all Ragdolls and British Short Hairs were negative for the disease. Only one positive cat was reported to be showing clinical signs of renal disease. CONCLUSION: The prevalence of feline polycstic disease in Persian cats presented to the University of Melbourne between February and August 1999 was 45%. Exotic cats were found to have the slightly higher incidence of 50%.
Aust Vet J. 2001 Apr;79(4):257-9. :
Prevalence of autosomal dominant polycystic kidney disease in Persian cats and related-breeds in Sydney and Brisbane.
Barrs VR, Gunew M, Foster SF, Beatty JA, Malik R.
Department of Veterinary Clinical Sciences, University of Sydney, New South Wales 2006.
OBJECTIVE: A form of autosomal dominant polycystic kidney disease has been identified in Persian cats and related breeds. Two features make elimination of this disease from future generations an achievable goal: the autosomal dominant mode of inheritance and the availability of a noninvasive technique, renal ultrasonography, to identify affected cats. The aims of this study were; to determine the prevalence of the disease in Persian cats and related breeds in Sydney and Brisbane, to determine any effect of domicile and breed on disease prevalence, to alert veterinary practitioners to the prevalence of autosomal dominant polycystic kidney disease and to propose methods of eliminating the disease from future generations of cattery-bred cats. DESIGN: To be included in this scheme, cats had to be of Persian or related breed and be older than 10 months-of-age. Younger cats were excluded because of the increased likelihood of a false negative result. Renal ultrasonography was performed using either a Medison 600 with a 7.5 MHz mechanical sector scanner (n = 228, Brisbane) or using an ATL UltraMark-9 with a 5 to 10 MHz linear array transducer (n = 92, Sydney). The effects of domicile (Sydney versus Brisbane) and breed on the prevalence of autosomal dominant polycystic kidney disease were tested using two-tailed Fisher's Exact tests. RESULTS: A total of 320 cats were tested comprising 230 Persians, 48 Himalayans, 17 Exotics, 14 Burmillas, 6 Ragdolls and 5 Chinchillas. The prevalence of autosomal dominant polycystic kidney disease in Sydney (45%) and Brisbane (42%) was comparable and no sex predilection was identified. The disease was not detected in Ragdolls, although only a small number was tested. Two of 14 Burmilla cats were positive (14%), demonstrating that long hair coat and brachycephalic features do not segregate with the polycystic kidney disease trait. CONCLUSION: These results show that the prevalence of autosomal dominant polycystic kidney disease amongst purebred, long-haired cats in Australia is currently very high. Ultrasound detection schemes are easy to establish and breeder participation can be encouraged through subsidisation.
Am J Vet Res. 1999 Dec;60(12):1516-25. :
Effect of enalapril on blood pressure, renal function, and the renin-angiotensin-aldosterone system in cats with autosomal dominant polycystic kidney disease.
Miller RH, Lehmkuhl LB, Smeak DD, DiBartola SP, Radin J.
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus 43210, USA.
OBJECTIVE: To evaluate blood pressure, renal function, and the renin-angiotensin-aldosterone system (RAAS) in cats with autosomal dominant polycystic kidney disease (ADPKD) and to assess the effect of enalapril on these variables. ANIMALS: 6 cats with ADPKD and 6 age-matched healthy cats. PROCEDURE: To measure blood pressure and heart rate, a radiotelemetry catheter was placed in the left femoral artery of each cat. Baseline data collection included 24-hour blood pressure, heart rate, and motor activity. Blood was then collected for analysis of RAAS status and renal function. Enalapril (0.5 mg/kg of body weight, p.o., q 24 h) was administered for 1 week, and data collection was repeated. RESULTS: Differences in baseline blood pressure, heart rate, motor activity, RAAS status, and renal function were not detected between cats with ADPKD and control cats. Hypertension was not documented in cats with ADPKD. Blood pressure was significantly reduced for 15 to 17 hours after treatment with enalapril in both groups. Administration of enalapril also resulted in significant increases in plasma renin activity and significant decreases in angiotensin converting enzyme activity and atrial natriuretic peptide concentration but only minimal changes in glomerular filtration rate and effective renal plasma flow in both groups of cats. CONCLUSIONS AND CLINICAL RELEVANCE: Although hypertension is common in humans with ADPKD, cats with ADPKD were normotensive. Treatment with enalapril (0.5 mg/kg, p.o., q 24 h) significantly reduced blood pressure in normotensive healthy cats and cats with ADPKD, and resulted in predictable changes in RAAS enzyme activities and hormone concentrations. Enalapril had minimal effects on renal function.
Vet Q. 1998 Oct;20(4):136-9. :
Polycystic kidney and liver disease in cats.
Bosje JT, van den Ingh TS, van der Linde-Sipman JS.
Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht, The Netherlands.
This paper reviews 27 cases of polycystic disease of the kidneys and/or liver in cats. The multiple cysts in the kidneys were rounded in all but one case, as described in adult polycystic kidney disease in humans. In 68% of the cats presented with polycystic kidneys, there were also cystic changes of the liver (uni- or multilocular cysts and/or congenital hepatic fibrosis (CHF)). In 1 cat polycystic changes of kidneys and liver were accompanied by cysts in the pancreas. In 5 cases there was severe pancreas fibrosis. Twenty-one of the 27 cats were Persian or Persian-crossbred.
J Hered. 1996 Jan-Feb;87(1):1-5. :
Inheritance of polycystic kidney disease in Persian cats.
Biller DS, DiBartola SP, Eaton KA, Pflueger S, Wellman ML, Radin MJ.
Department of Veterinary Clinical Sciences, Ohio State University, Columbus 43210, USA.
Polycystic kidney disease in Persian cats culminates in chronic renal failure after a variable clinical course. An affected 6-year-old Persian cat was used to establish a colony of cats with polycystic kidney disease. In affected cats, cysts could be detected by ultrasonography as early as 7 weeks of age. Absence of cysts on ultrasound examination at 6 months of age was correlated with absence of polycystic kidney disease at necropsy. Both males and females were affected and, of progeny from affected x unaffected crosses, 42% were affected and 58% were unaffected. In affected x affected crosses, 73% of progeny were affected and 27% were unaffected. These results are compatible with autosomal dominant inheritance of this trait. Polycystic kidney disease in Persian cats resembles autosomal dominant polycystic kidney disease (ADPKD) in human beings, and represents a valuable animal model of the human disease.