Effects of coastal acidification on North Atlantic bivalves: interpreting laboratory responses in the context of in situ populations.

Experimental exposure of early life stage bivalves has documented negative effects of elevated pCO2 on survival and growth, but the population consequences of these effects are unknown. Following standard practices from population viability analysis and wildlife risk assessment, we substituted laboratory-derived stress-response relationships into baseline population models of Mercenaria mercenaria and Argopecten irradians. The models were constructed using inverse demographic analyses with time series of size-structured field data in NY, USA, whereas the stress-response relationships were developed using data from a series of previously published laboratory studies. We used stochastic projection methods and diffusion approximations of extinction probability to estimate cumulative risk of 50% population decline during ten-year population projections at 1, 1.5 and 2 times ambient pCO2 levels. Although the A. irradians population exhibited higher growth in the field data (12% per year) than the declining M. mercenaria population (-8% per year), cumulative risk was high for A. irradians in the first ten years due to high variance in the stochastic growth rate estimate (log λs = -0.02, σ2 = 0.24). This ten-year cumulative risk increased from 69% to 94% and >99% at 1.5 and 2 times ambient scenarios. For M. mercenaria (log λs = -0.09, σ2 = 0.01), ten-year risk was 81%, 96% and >99% at 1, 1.5 and 2 times ambient pCO2, respectively. These estimates of risk could be improved with detailed consideration of harvest effects, disease, restocking, compensatory responses, other ecological complexities, and the nature of interactions between these and other effects that are beyond the scope of available data. However, results clearly indicate that early life stage responses to plausible levels of pCO2 enrichment have the potential to cause significant increases in risk to these marine bivalve populations.

Canine tick-borne pathogens and associated risk factors in dogs presenting with and without clinical signs consistent with tick-borne diseases in northern Australia.

OBJECTIVES: To estimate the proportion of canine tick-borne disease (CTBD) pathogens in dogs from northern states of Australia presenting with and without clinical signs/laboratory abnormalities suggestive of CTBD and to evaluate associated risk factors. DESIGN: Client-owned dogs presented to a general practice clinic in the Northern Territory (NT; n = 138) and five referral hospitals in south-east Queensland (SEQ; n = 100) were grouped into CTBD-suspect and -control groups based on clinical and laboratory criteria. Blood and sera were screened for haemotropic Mycoplasma spp., Babesia spp., Anaplasma spp., Ehrlichia spp. and Hepatozoon spp. using microscopic examination, in-clinic ELISA testing and PCR assays. Dog-specific risk factors associated with the presence of CTBD pathogens were evaluated. RESULTS: Overall, 24.4% of the suspect group and 12.2% of the control group dogs were infected. The proportions of M. haemocanis, B. vogeli, A. platys, Candidatus Mycoplasma haematoparvum, and C. Mycoplasma haemobos were 7.1%, 5.0%, 3.8%, 1.7% and 0.4%, respectively. Dogs originating from the NT were 3.6-fold (95% confidence interval (CI) 1.51-8.62; P = 0.004) more likely to be infected with CTBD pathogens than those from SEQ. Male dogs were 2.3-fold (95% CI 1.17-4.80, P = 0.024) more likely to be PCR-positive to CTBD pathogens than female dogs. Dogs presenting with clinical signs consistent with CTBD and thrombocytopenia were more likely to be infected by CTBD pathogens (odds ratio 2.85; 95% CI 1.16, 7.02; P = 0.019). CONCLUSIONS: Haemotropic mycoplasmas were the most common tick-borne pathogen infecting client-owned dogs. Subclinical cases were common in dogs from the NT. Veterinary practitioners should be aware of the proportion of CTBD pathogens and the presenting features of clinical and subclinical disease in their area.

Associations between meal size, gastric emptying and post-prandial plasma glucose, insulin and lactate concentrations in meal-fed cats.

Plasma glucose and insulin concentrations are increased for 12-24 h in healthy cats following moderate- to high-carbohydrate meals. This study investigated associations between gastric emptying time and post-prandial plasma glucose, insulin and lactate concentrations in cats fed an extruded dry, high-carbohydrate, moderate-fat, low-protein diet (51, 28, 21% metabolizable energy, respectively) once daily by varying meal volume. Eleven healthy, non-obese, neutered adult cats were enrolled in a prospective study and fed to maintain body weight. Ultrasound examinations were performed for up to 26 h, and blood collections over 24 h after eating meals containing approximately 100% and 50% of the cats' daily caloric intake (209 and 105 kJ/kg BW, respectively). Gastric emptying time was increased after a meal of 209 kJ/kg BW compared with 105 kJ/kg BW (median gastric emptying times 24 and 14 h, respectively; p = 0.03). Time for glucose to return to fasting was longer after the 209 kJ/kg BW meal (median 20 h; 25th and 75th percentiles 15 and 23 h, respectively) than the 105 kJ/kg BW meal (13, 12 and 14 h; p < 0.01); however, peak glucose was not higher after the 209 kJ/kg BW meal compared with the 105 kJ/kg BW meal [(mean ± SD) 6.6 ± 0.6 and 7.8 ± 1.2 mmol/l, respectively, p = 0.07]. Times for insulin to return to fasting were not significantly longer after the 209 kJ/kg BW meal than the 105 kJ/kg BW meal (p = 0.29). d- and l-lactate concentrations were not associated with gastric emptying time or post-prandial blood glucose and insulin. Based on results obtained, prolonged gastric emptying contributes to prolonged post-prandial hyperglycemia in cats meal fed a high-carbohydrate, low-protein, dry diet and fasting times for cats' meal-fed diets of similar composition should be 14-26 h, depending on meal size.

Linking innovative measurement technologies (ConMon and Dataflow© systems) for high-resolution temporal and spatial dissolved oxygen criteria assessment.

One consequence of nutrient-induced eutrophication in shallow estuarine waters is the occurrence of hypoxia and anoxia that has serious impacts on biota, habitats, and biogeochemical cycles of important elements. Because of the important role of dissolved oxygen (DO) on these ecosystem features, a variety of DO criteria have been established as indicators of system condition. However, DO dynamics are complex and vary on time scales ranging from diel to decadal and spatial scales from meters to multiple kilometers. Because of these complexities, determining DO criteria attainment or failure remains difficult. We propose a method for linking two common measurement technologies for shallow water DO criteria assessment using a Chesapeake Bay tributary as a test case. Dataflow© is a spatially intensive (30-60-m collection intervals) system used to map surface water conditions at the whole estuary scale, and ConMon is a high-frequency (15-min collection intervals) fixed station approach. The former technology is effective with spatial descriptions but poor regarding temporal resolution, while the latter provides excellent temporal but very limited spatial resolution. Our methodology for combining the strengths of these measurement technologies involved a sequence of steps. First, a statistical model of surface water DO dynamics, based on temporally intense ConMon data, was developed. The results of this model were used to calculate daily DO minimum concentrations. Second, this model was then inserted into Dataflow©-generated spatial maps of DO conditions and used to adjust measured DO concentrations to daily minimum concentrations. This information was used to assess DO criteria compliance at the full tributary scale. Model results indicated that it is vital to consider the short-term time scale DO criteria across both space and time concurrently. Large fluctuations in DO occurred within a 24-h time period, and DO dynamics varied across the length and width of the tributary. The overall result provided a more detailed and realistic characterization of the shallow water DO minimum conditions that have the potential to be extended to other tributaries and regions. Broader applications of this model include instantaneous DO criteria assessment, utilizing this model in combination with aerial remote sensing, and developing DO amplitude as an indicator of impaired water bodies.

Consequences of a screening programme on the prevalence of congenital hereditary sensorineural deafness in the Australian Cattle Dog.

Genetic disease testing programmes are used in domestic animal breeds to guide selective breeding with the aim of reducing disease prevalence. We assessed the change in the prevalence of canine congenital hereditary sensorineural deafness (CHSD) in litters of Australian Cattle Dogs following the introduction of a brainstem auditory evoked response (BAER) testing programme. We studied 608 pups from 122 litters from 10 breeding kennels. Despite 10 years of testing (1998-2008), no substantial reduction in prevalence of CHSD was evident in these 10 breeding kennels. Even for the subset of litters in which both parents were BAER tested as normal hearing (305 pups from 58 litters), there was no evidence of substantial reduction in prevalence. Odds ratios for CHSD in pups for each extra year since testing in the kennel commenced were 1.01 (95% CI, 0.88-1.17) and 1.03 (95% CI, 0.82-1.30) respectively for these populations. Amongst 284 dogs from 54 litters with extended pedigrees and both parents BAER-tested normal hearing, observed prevalences of CHSD were highest in pups with no BAER-tested normal grandparents (17% or 5/29) and lowest in pups with all four grandparents tested normal (0% or 0/9). In pups for which one, two and three grandparents tested negative, prevalences of CHSD were 12% (9/74), 9% (9/101) and 8% (6/71) respectively. Hence, testing programmes based on phenotypic screening may not lead to a substantial reduction in recessive genetic disease prevalence over the medium term, even when only tested normal parents are used. Exclusive breeding of litters in which both parents and all four grandparents are BAER-tested normal is expected to reduce CHSD prevalence in pups to the greatest extent over the long term.

The inheritance of extra-hepatic portosystemic shunts and elevated bile acid concentrations in Maltese dogs.

OBJECTIVES: To determine the heritability of extra-hepatic portosystemic shunts and elevated post-prandial serum bile acid concentrations in Maltese dogs. MATERIALS AND METHODS: Maltese dogs were recruited and investigated by a variable combination of procedures including dynamic bile acid testing, rectal ammonia tolerance testing, ultrasonography, portal venography, surgical inspection or necropsy. In addition, nine test matings were carried out between affected and affected dogs, and affected and unaffected dogs. RESULTS: In 135 variably related Maltese, shunt status could be confirmed in 113, including 19 with an extra-hepatic portosystemic shunt (17 confirmed at surgery, 2 at necropsy). Rectal ammonia tolerance testing results and post-prandial serum bile acid concentrations were retrievable for 50 and 88 dogs, respectively. Pedigree information was available for these 135 and an additional 164 related dogs. Two consecutive test matings were carried out between two affected animals (whose shunts had been attenuated), with 2 of 8 (25%) of offspring having an extra-hepatic portosystemic shunt. Six test matings were carried out between an affected and an unaffected animal, with 2 of 22 (9%) offspring affected. Heritability of extra-hepatic portosystemic shunt was 0·61 calculated using variance components analysis [95% confidence interval (CI) 0·14 to 1·0, P=0·001]. The best fitting model from segregation analysis was a common, partially penetrant, recessive model (allele frequency 0·34, penetrance 0·99, CI 0·09 to 1·0). The heritability of elevated post-prandial serum bile acid (and thus likely portal vein hypoplasia) was 0·81 (CI 0·43 to 1·0, P=0·2) after logarithmic transformation of post-prandial serum bile acid concentrations. CLINICAL SIGNIFICANCE: There is strong support for extra-hepatic portosystemic shunts and elevated post-prandial serum bile acid concentrations both being inherited conditions in Maltese.

Investigation of diabetes mellitus in Burmese cats as an inherited trait: a preliminary study.

AIM: To investigate, in a pilot study, a possible genetic component to type 2 diabetes mellitus (T2D) in Burmese cats in New Zealand by analysing pedigree data. METHODS: Pedigrees were obtained for 305 Burmese cats living in New Zealand; diabetes was diagnosed in 19 of these due to presence of polyuria and polydipsia, persistent concentrations of glucose in plasma >16 mmol/L and glucosuria prior to insulin treatment. Pedigrees were also submitted for 16 cats with no clinical signs of T2D. The remaining 270 cats were unobserved relatives of these individuals. Inbreeding coefficients and heritability were calculated, and a single major locus model segregation analysis was conducted using pedigree analysis software. RESULTS: Nineteen cats were diagnosed with T2D. Males (n = 14) and females (n = 5) were both affected, suggesting that the gene or genes causing diabetes are autosomal rather than sex-linked. Examination of the pedigree revealed few signs of fully penetrant dominant gene action: diabetes was ostensibly rarely seen in sequential generations and nearly always skipped at least one and often more generations; apparently unaffected offspring of apparently unaffected parents sometimes produced affected progeny. The mean relatedness of the affected animals within the core pedigree (16 diabetic cats) was 0.049, and mean inbreeding 0.033. Based on 100,000 permutations of the trait values, the expected relatedness of a random sample of 16 animals taken from the phenotyped animals would be 0.013 (SD 0.007) (permutation p = 0.0009). The observed inbreeding was also significant (permutation p= 0.02). Heritability was estimated to be 9 (95% CI = 0-57)% assuming all animals with unknown status were unaffected. The best fitting genetic model was a major gene model with dominant expression with the risk allele frequency at 15% with 60% penetrance. CONCLUSIONS: In this pilot study the increased inbreeding in the cases, lack of likely sampling bias, the increased frequency of T2D in Burmese, and small number of breed founders are consistent with the involvement of a major locus in diabetes in Burmese cats with a significant risk allele prevalence. However, low case numbers meant this could not be unambiguously confirmed. A genome-wide association study may be useful for investigating the genetic cause of T2D.

Effect of dietary carbohydrate, fat, and protein on postprandial glycemia and energy intake in cats.

BACKGROUND: Reducing carbohydrate intake is recommended in diabetic cats and might also be useful in some healthy cats to decrease diabetes risk. OBJECTIVE: To compare postprandial glucose and insulin concentrations and energy intakes between cats fed diets high in protein, fat, or carbohydrate. ANIMALS: Twenty-four lean cats with normal glucose tolerance. METHODS: In a prospective randomized study, each of 3 matched groups (n = 8) received a different test diet for 5 weeks. Diets were high in either protein (46% of metabolizable energy [ME]), fat (47% ME), or carbohydrate (47% ME). Glucose and insulin were measured during glucose tolerance, ad libitum, and meal-feeding tests. RESULTS: During ad libitum feeding, cats fed the high-carbohydrate diet consumed 25% and 18% more carbohydrate than cats fed diets high in fat and protein, respectively, and energy intake was highest when the high-fat and high-protein diets were fed. Regardless of the feeding pattern, cats fed the high-carbohydrate diet had 10-31% higher peak and mean glucose compared with both other diets; peak glucose in some cats reached 10.4 mmol/L (188 mg/dL) in cats fed 47% ME carbohydrate and 9.0 mmol/L (162 mg/dL) in cats fed 23% ME. CONCLUSIONS AND CLINICAL IMPORTANCE: High-carbohydrate diets increase postprandial glycemia in healthy cats compared with diets high in fat or protein, although energy intake is lower. Avoidance of high- and moderate-carbohydrate diets can be advantageous in cats at risk of diabetes. Maintenance energy requirements should be fed to prevent weight gain when switching to lower carbohydrate diets.

Canine vector-borne disease pathogens in dogs from south-east Queensland and north-east Northern Territory.

OBJECTIVES: To determine the prevalence of canine vector-borne diseases (CVBD: Babesia spp., Anaplasma spp., Ehrlichia spp., haemotropic mycoplasmas and Hepatozoon) in Australian dogs; namely, dogs from pounds in south-east Queensland and an indigenous Aboriginal community in the north-east of the Northern Territory. DESIGN AND PROCEDURE: Blood samples were collected from 100 pound dogs and 130 Aboriginal community dogs and screened for the CVBD pathogens using polymerase chain reaction (PCR). All positive PCR products were sequenced for species confirmation. RESULTS: In total, 3 pound dogs and 64 Aboriginal community dogs were infected with at least one CVBD pathogen. Overall, B. vogeli was detected in 13 dogs, A. platys in 49, M. haemocanis in 23, Candidatus Mycoplasma haematoparvum in 3 and C. M. haemobos in 1 dog. Co-infections were detected in 22 Aboriginal community dogs. CONCLUSIONS: This study found B. vogeli, A. platys and haemotropic mycoplasma infections to be common in dogs in subtropical and tropical areas of Australia. This study also reports for the first time the prevalence and genetic characterisation of haemotropic mycoplasmas in dogs in Australia.

Cardiac valvular and vascular disease in Bull Terriers.

The hearts of 27 Bull Terriers and 6 control dogs were evaluated. Heart murmurs were auscultated in 14 (52%) Bull Terriers. At necropsy, 25 Bull Terriers (93%) had myxomatous degeneration of the mitral valve or abnormalities of the left ventricular outflow tract. Small vessel arteriosclerosis in the myocardium and fibrosis of cardiac conduction tissue were common histologic findings in Bull Terriers with clinical cardiac disease. These lesions were also detected in dogs without clinical evidence of cardiac disease and only mild murmurs or structural valvular disease.

Linkage confirms canine pkd1 orthologue as a candidate for bull terrier polycystic kidney disease.

Bull terrier polycystic kidney disease (BTPKD) is a Mendelian disorder with many features reminiscent of human autosomal dominant polycystic disease, the latter disease being due to mutations at PKD1 and PKD2 loci. We investigated the role of the canine pkd1 orthologue in BTPKD via linkage analysis of a large kindred in which the disorder is segregating. Twelve microsatellite markers around the canine pkd1 locus (CFA6) were amplified from the genomic DNA of 20 affected and 16 unaffected bull terriers. An additional 28 affected dogs were genotyped at five key microsatellites. A highly significant multi-point LOD score that peaked over the canine pkd1 locus was observed (LOD = 6.59, best two-point LOD score LOD = 6.02), implicating this as the BTPKD locus.

Auscultation and echocardiographic findings in Bull Terriers with and without polycystic kidney disease.

OBJECTIVE: To investigate a possible association between Bull Terrier polycystic kidney disease (BTPKD) and cardiac disease, to determine the prevalence of mitral valve disease (MVD) and left ventricular outflow tract obstruction (LVOTO) in the Australian Bull Terrier population, and to compare auscultation and echocardiography in detection of cardiac disease in Bull Terriers. DESIGN: Ninety-nine Bull Terriers, ranging in age from 8 weeks to 13 years and 11 months were auscultated and examined using renal ultrasonography; 86 were also examined using echocardiography. The prevalence and severity of heart defects in dogs with BTPKD was compared with that in dogs without BTPKD. RESULTS: Nineteen of these 99 dogs were diagnosed with BTPKD. Forty-two percent of Bull Terriers with BTPKD and 28% of those without BTPKD had murmurs characteristic of mitral regurgitation or LVOTO. How recently an animal was descended from an ancestor with BTPKD was associated with presence (P = 0.008) and loudness of a murmur (P = 0.009). Overall, echocardiography detected MVD in 39% of Bull Terriers, with increased prevalence in older animals (P = 0.003). Mitral stenosis was found in eight cases. Fifty-three percent of dogs in this study had evidence of LVOTO, with obstruction consisting of a complex of lesions including dynamic or fixed subvalvular LVOTO, significantly narrowed left ventricular outflow tract or valvular aortic stenosis. Dogs with BTPKD, or those descended from dogs with BTPKD, were more likely to have MVD (P = 0.006), and while LVOTO was not more common in these dogs, if they did have LVOTO, they were more likely to have severe obstruction than dogs with no ancestors with BTPKD (analysed in three ways P = 0.028 to 0.001). In this study, 46% of Bull Terriers without a murmur or arrhythmia had cardiac disease detected on echocardiographic examination. CONCLUSION: Cardiac disease, especially MVD and LVOTO, was common in Bull Terriers in this study, and those with BTPKD had an increased risk of cardiac abnormalities. Auscultation did not detect a significant number of Bull Terriers with cardiac disease.

Chronic renal failure in an English bull terrier with polycystic kidney disease.

An entire female English bull terrier, aged five years and one month, was diagnosed with polycystic kidney disease by renal ultrasonography. It had thickening and abnormal motion of the mitral valve on 2D and M mode echocardiography, and left ventricular outflow tract obstruction, characterised by turbulence in the left ventricular outflow tract and elevated aortic blood flow velocity, detected by colour flow and spectral Doppler echocardiography, respectively. Two years later, haematology, serum biochemistry and urinalysis data suggested the presence of compensated renal failure. The dog was euthanased at 10 years and eight months of age, with haematology, serum biochemistry and urinalysis data Indicating decompensated chronic renal failure. Postmortem examination confirmed polycystic kidney disease, chronic renal disease, mitral and aortic valvular myxomatous degeneration, and mixed mammary neoplasia. This case demonstrates that bull terriers with polycystic kidney disease may develop associated chronic renal failure.

No disease-associated mutations found in the coding sequence of the canine polycystic kidney disease gene 1 in Bull Terriers with polycystic kidney disease.

The aim of this study was to identify possible disease-associated mutations in the canine homologue of the polycystic kidney disease gene 1 (PKD1) in Bull Terriers with autosomal dominant polycystic kidney disease. Messenger RNA was obtained from the blood or renal tissue of five Bull Terriers with the disease and four close relatives without the disease. Reverse transcription, PCR and 3' rapid amplification of cDNA ends were used to amplify the coding and 3' untranslated regions of this transcript. Comparison of PKD1 sequence between the affected and unaffected Bull Terriers, revealed six polymorphisms, but no disease-associated mutations.

Echocardiographic parameters in 14 healthy English Bull Terriers.

OBJECTIVE: To determine the range of various cardiac parameters using echocardiography in apparently normal, healthy English Bull Terriers. DESIGN: Fourteen English Bull Terriers were selected for study. Cardiac auscultation of the parents of these dogs was normal. Echocardiographic examination of one parent of each animal showed: no mitral or aortic valve abnormalities; no myocardial lesions; no two dimensional evidence of fixed or dynamic left ventricular outflow tract obstruction; and no systolic aortic or left ventricular outflow tract turbulence on colour flow Doppler examination. The 14 selected dogs did not have arrhythmias or murmurs, and on echocardiographic examination had similar findings to their parents. Systolic blood pressure was measured in all dogs and they had no clinical evidence of Bull Terrier polycystic kidney disease or Bull Terrier hereditary nephritis. PROCEDURE: All dogs were auscultated and subjected to a sequential global echocardiographic assessment of the heart, including two dimensional long and short axis, and colour flow Doppler interrogation of the mitral and aortic valves. Dimensional measurements, including those from the left atrium, aortic annulus and left ventricle, were taken from a right parasternal window, and derived values such as fractional shortening, stroke volume and left atrial to aortic annulus ratio were calculated. Peak systolic aortic velocity was measured from the left parasternal window using two dimensional-guided pulsed wave Doppler with angle correction. Systolic blood pressure was measured using a Doppler monitor. The absence of Bull Terrier polycystic kidney disease was determined using renal ultrasonography, and of Bull Terrier hereditary nephritis using urinary protein to creatinine ratio. RESULTS: These 14 dogs had greater left ventricular wall thickness and smaller aortic root diameters than those reported as normal for other breeds of comparable body size. Left atrial dimensions were also larger, however this may have been due to the "maximising" method of measurement. These apparently normal English Bull Terriers also had higher aortic velocities than those reported for other breeds, possibly due to a smaller aortic root diameter or other anatomic substrate of the left ventricular outflow tract, lower systemic vascular resistance, or breed-specific "normal" left ventricular hypertrophy. While these dogs were selected to be as close to normal as possible, the breed may have a particular anatomy that produces abnormal left ventricular echocardiographic parameters. CONCLUSION: These echocardiographic parameters may be used to diagnose left ventricular outflow tract obstruction and left ventricular hypertrophy, and inaccurate diagnoses may result if breed-specific values are not used.

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers.

OBJECTIVE: To describe the renal lesions in Bull Terrier polycystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). DESIGN: Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. RESULTS: In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. CONCLUSION: This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously.

Polycystic kidney disease in bull terriers: an autosomal dominant inherited disorder.

The prevalence, mode of inheritance and urinalysis findings in Bull Terriers with polycystic kidney disease were assessed by screening 150 clinically normal dogs. The disorder was diagnosed in 39 dogs on the basis of renal ultrasound results and family history of the disease. In equivocal cases confirmation required gross and histopathological renal examination. Necropsy was performed on nine affected dogs and the kidneys from another five affected animals were also examined. Renal cysts were usually bilateral, occurred in cortex and medulla and varied from less than 1 mm to over 2.5 cm in diameter. Cysts were lined by epithelial cells of nephron origin. Abnormal urine sediment and proteinuria were common in affected dogs. The disease appears to be inherited in a highly penetrant autosomal dominant manner.