To report the incidence of metastatic calcification in cats with renal failure presenting for renal transplantation, and to determine if metastatic calcification detected prior to renal transplantation is associated with complication rates and patient survival.Retrospective case series.Seventy-four cats.In imaging studies, 178 feline renal transplant recipients from 1998 to 2020 were evaluated for metastatic calcification. Demographic, clinicopathological data, intraoperative complications, postoperative complications, need for hemodialysis, and survival times were recorded. Exclusion criteria were cats lacking imaging reports and cats with gastric, renal, or tracheal/bronchial calcification alone. Univariable and multivariable analyses were performed to determine variables that were independently associated with survival. Kaplan-Meier analysis was used to generate survival plots and estimate median survival times with a 95% confidence interval (CI).Seventy four of 178 cats met the inclusion criteria. Fifteen of 74 (20.3%) cats had metastatic calcification prior to renal transplantation. Twelve of 74 (16.2%) cats developed calcification following transplantation, and 47 of 74 (63.5%) cats had no calcification during the study period. Median follow-up time was 472 days, with a range of 0-1825 days. Cats with pretransplant calcification had shorter median survival times (147 days) than cats without calcification (646 days) (p = .0013). Metastatic calcification pretransplant was associated with an increased risk of death by 240% (95% CI, 1.22-4.71).Metastatic calcification in renal transplant cats is a negative prognostic indicator and is associated with decreased survival times.These findings may help guide therapeutic recommendations and owner expectations in cats undergoing renal transplantation.
Abstract Background Differentiation of the subclinical phases of myxomatous mitral valve disease (MMVD) in dogs relies heavily on echocardiography. Focused cardiac ultrasonography (FCU) is a point‐of‐care technique that can assess heart size. Hypothesis/Objectives Veterinary students trained in FCU can differentiate dogs with subclinical MMVD based on left ventricular (LV) and left atrial (LA) dimensions. Animals Forty‐eight dogs with subclinical MMVD. Methods Veterinary students were trained to measure LV dimension and LA‐to‐aortic root dimension ratio (LA : Ao) using FCU. Dogs were categorized into 2 cohorts based on whether or not the LV normalized internal diastolic dimension was ≥1.7 and LA : Ao was ≥1.6. Agreement between FCU and echocardiographic studies performed by cardiologists was evaluated. Results One‐hundred and forty‐six FCU examinations were performed by 58 veterinary students on 48 dogs. Overall agreement between students and cardiologists was moderate (Fleiss' kappa, 0.54; 95% confidence interval [CI], 0.39‐0.69; P < .001). Percentage accuracy in observations with heart dimensions less than the cutoffs (86/89, 97%) was significantly higher than in observations in with larger hearts (31/57, 54%; P < .001). Agreement increased from moderate to good as heart sizes became more extreme. Degree of confidence by students in performing FCU was significantly higher at the end vs start of the study. Conclusions and Clinical Importance Categorization of dogs with subclinical MMVD by veterinary students using FCU was associated with moderate to good agreement with echocardiography. Focused cardiac ultrasonography is a point‐of‐care method that can help assess clinical stage in dogs with subclinical MMVD.
Abstract Background and aims The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress. Hypertrophic cardiomyopathy (HCM) is a common heart condition, affecting approximately 15% of the general cat population. Feline HCM shares phenotypical and genotypical similarities with human HCM, but the disease mechanisms for both species are incompletely understood. Our goal was to characterize global changes in metabolome between healthy control cats and cats with different stages of HCM. Methods Serum samples from 83 cats, the majority (70/83) of which were domestic shorthair and included 23 healthy control cats, 31 and 12 preclinical cats with American College of Veterinary Internal Medicine (ACVIM) stages B1 and B2, respectively, and 17 cats with history of clinical heart failure or arterial thromboembolism (ACVIM stage C), were collected for untargeted metabolomic analysis. Multiple linear regression adjusted for age, sex and body weight was applied to compare between control and across HCM groups. Results Our study identified 1253 metabolites, of which 983 metabolites had known identities. Statistical analysis identified 167 metabolites that were significantly different among groups (adjusted P < 0.1). About half of the differentially identified metabolites were lipids, including glycerophospholipids, sphingolipids and cholesterol. Serum concentrations of free fatty acids, 3‐hydroxy fatty acids and acylcarnitines were increased in HCM groups compared with control group. The levels of creatine phosphate and multiple Krebs cycle intermediates, including succinate, aconitate and α‐ketoglutarate, also accumulated in the circulation of HCM cats. In addition, serum levels of nicotinamide and tryptophan, precursors for de novo NAD+ biosynthesis, were reduced in HCM groups versus control group. Glutathione metabolism was altered. Serum levels of cystine, the oxidized form of cysteine and cysteine‐glutathione disulfide, were elevated in the HCM groups, indicative of heightened oxidative stress. Further, the level of ophthalmate, an endogenous glutathione analog and competitive inhibitor, was increased by more than twofold in HCM groups versus control group. Finally, several uremic toxins, including guanidino compounds and protein bound putrescine, accumulated in the circulation of HCM cats. Conclusions Our study provided evidence of deranged energy metabolism, altered glutathione homeostasis and impaired renal uremic toxin excretion. Altered lipid metabolism suggested perturbed structure and function of cardiac sarcolemma membrane and lipid signalling.
Abstract Background Poor natriuresis is a potential marker of diuretic resistance in dogs with acute congestive heart failure (CHF) but little is known about the relationship between urine sodium concentration (uNa) and frequency of successful decongestion. Supplemental O 2 is a common treatment in dogs with severe CHF. The time from start to discontinuation of supplemental O 2 therapy (DCSO 2 ) typically reflects the time course and ease of decongestion. Hypothesis/Objectives Urine Na concentration after IV administration of furosemide will be correlated with duration of treatment with supplemental O 2 (time O2 ) and the cumulative frequency of successful DCSO 2 during hospitalization. Animals Fifty‐one dogs with acute CHF. Methods Retrospective observational single center study. Results Dogs with low uNa had significantly longer mean time O2 than dogs with high uNa (uNa <87 mmol/L, 24.2 ± 2.6 hours vs uNa ≥87 mmol/L, 16.6 ± 1.7 hours; P = .02). Low uNa was correlated with lower cumulative frequency of DCSO 2 (12 hour, 28%; 24 hour, 42%; 36 hour, 73%) compared to high uNa (12 hour, 28%; 24 hour, 88%; 36 hour, 96%; P = .005). History of PO loop diuretics, low serum chloride concentration (sCl), and high PCV were associated with low uNa. Urine Na concentration outperformed other metrics of diuretic responsiveness including weight loss. Conclusions and Clinical Importance Urine Na concentration after IV furosemide predicted time O2 and cumulative frequency of DCSO 2 in dogs with acute CHF, which likely reflects important aspects of diuretic responsiveness. Urine Na can assess diuretic responsiveness and treatment efficacy in dogs with CHF.
Abstract Background Reliability of echocardiographic calculations for stroke volume and mitral regurgitant fraction (RF MR ) are affected by observer variability and lack of a gold standard. Variability is used to calculate critical change values (CCVs) that are thresholds representing real change in a measure not associated with observer variability. Hypothesis Observed intra‐ and interobserver accuracy and variability in healthy dogs help model CCV for RF MR . Animals Reliability cohort of 34 healthy dogs; allometric scaling cohort of 99 dogs with heart disease and 25 healthy dogs. Methods Accuracy, variability, and CCV of 2 observers using geometric and flow‐based echocardiography were prospectively compared against a standard of RF MR = 0% and extrapolated across a range of expected RF MR values in the reliability cohort partly derived from cardiac dimensions predicted by the allometric cohort. Results Accuracy of methods to determine RF MR in descending order was 4‐chamber bullet (Bullet 4CH ), mitral inflow, cube formula, and Simpson's method of disks. Intraobserver variability was relatively high. The CCV for RF MR ranged from 28% to 88% and was inversely related to RF MR when extrapolated for use in affected dogs. For both observers, the Bullet 4CH method had the lowest intraobserver CCV (Operator 1:28%, Operator 2:41%). Interobserver strength of agreement was low with intraclass correlation coefficients ranging from 0.210 to 0.413. Conclusions and Clinical Importance Echocardiographic volumetric methods used to calculate stroke volume and RF MR have low accuracy and high variability in healthy dogs. Extrapolation of observed CCV to a range of expected RF MR suggests observers and methods are not interchangeable and variability might hinder routine clinical usage. Individual observers should be aware of their own variability and CCV.
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