BackgroundF2‐isoprostanes, a biomarker of oxidant injury, increase with advancing chronic kidney disease (CKD) in humans. In cats, the relationship between CKD and oxidative stress is poorly understood.ObjectivesTo determine whether cats with advancing CKD have increasing urinary F2‐isoprostanes.AnimalsControl cats without evidence of CKD (≥6 years old; n = 11), and cats with IRIS stage 1 (n = 8), 2 (n = 38), 3 (n = 21), and 4 (n = 10) CKD.MethodsThis was a prospective observational study. Urinary F2‐isoprostanes (specifically free 15‐F2t‐isoprostanes) normalized to urine creatinine (IsoPs) were compared among groups and tested for correlations with blood pressure, proteinuria, serum creatinine concentration, and urine specific gravity. The IsoPs also were compared between cats with and without hypertension or proteinuria, and in cats fed predominantly standard versus renal diets.ResultsUrinary IsoPs were increased, but not significantly, in cats with stage 1 CKD (median 263 pg/mg creatinine; range, 211–380) compared to controls (182 pg/mg; range, 80–348) and decreased significantly from stage 1 through advancing CKD (stage 2, 144 pg/mg; range, 49–608; stage 3, 102 pg/mg; range, 25–158; stage 4, 67 pg/mg; range, 26–117; P < .01). Urinary IsoPs were inversely correlated with serum creatinine (r = −0.66, P < .0001).Conclusion and Clinical ImportanceUrinary IsoPs are significantly higher in early CKD (stage 1) compared to cats with more advanced CKD. Additional studies are warranted to characterize oxidative stress in cats with stage 1 CKD and determine whether early antioxidant treatments have a protective effect on CKD progression.

BackgroundHyperthyroidism, the most common endocrine disorder in cats, has been associated with low serum cobalamin concentrations. Whether this is a functional cobalamin deficiency of clinical importance has not been assessed.Hypothesis/ObjectivesCats with hyperthyroidism experience a functional cobalamin deficiency which correlates with their clinical catabolic state and is reversible with return of the euthyroid state.AnimalsThirty‐nine client‐owned hyperthyroid cats.MethodsProspective observational study. Serum cobalamin, methylmalonic acid, and clinical scores were determined in each hyperthyroid cat at enrollment and when euthyroid (60 days after radioiodine treatment).ResultsFive of the 39 hyperthyroid cats (13%) had a low serum cobalamin concentration ranging from <150 to 290 ng/L. Serum cobalamin concentrations normalized to >350 ng/L in 2 of the hypocobalaminemic cats once euthyroid. None of the hyperthyroid/hypocobalaminemic cats had increased serum methylmalonic acid concentrations (175–601 nmol/L). In cats with clinical and biochemical hyperthyroidism, there was no correlation between serum cobalamin concentrations with total T4 concentration (P = .12) or clinical scores including body weight (P = .11) and BCS (P = .54).Conclusions and Clinical ImportanceIn this population of hyperthyroid cats, the prevalence of hypocobalaminemia was low. Specifically, hyperthyroid cats, in which concurrent gastrointestinal disease is unlikely. Hypocobalaminemia is not a functional deficiency requiring supplementation in hyperthyroid cats without gastrointestinal disease.

A 9-y-old, castrated male, domestic medium-hair cat diagnosed previously with chronic kidney disease developed anorexia and vomiting. Ultrasonography revealed abdominal effusion and a left renal perihilar mass. Cytologic evaluation of the peritoneal fluid and mass identified atypical epithelioid cells suspected to be of renal epithelial or possible mesothelial origin. Immunohistochemical (IHC) evaluation of a formalin-fixed, paraffin-embedded peritoneal fluid cell block indicated both pancytokeratin and vimentin expression in the atypical epithelioid cell population. With scanning electron microscopic evaluation, similar epithelioid cells lacked the cell-surface microvilli expected of mesothelium, supporting an antemortem diagnosis of probable carcinoma. On postmortem examination, the left kidney was effaced by an infiltrative neoplasm with myriad similar nodules throughout the peritoneum. The neoplasm was composed primarily of polygonal-to-spindle-shaped cells with strong vimentin and weak pancytokeratin cytoplasmic immunolabeling. Further IHC characterization with PAX8, CK18, KIT, napsin A, SMA, desmin, CD18, and claudin 5 was performed. Histologic and IHC findings supported a diagnosis of sarcomatoid renal cell carcinoma with peritoneal carcinomatosis. An in vitro cell culture line of neoplastic cells harvested from the primary tumor was successfully established for future research endeavors.

Veterinarians diagnose marijuana toxicity based on clinical signs and history, or in conjunction with an over-the-counter (OTC) human urine drug screen. With the legalization of recreational marijuana use becoming more prevalent in the United States, a more accurate test to aid in the diagnosis of canine marijuana toxicity is needed. We collected urine and serum samples from 19 dogs with confirmed or suspected marijuana toxicosis from multiple veterinary hospitals and analyzed them with a novel UPLC-MS/MS method. Calibrations from 0.1 to 100 ng/mL and QC materials were prepared. Samples were extracted, purified, and eluted with solid-phase extraction. Urine samples were tested with an OTC human urine drug screen. The limit of detection (LOD) and lower limit of quantification (LLOQ) ranges for marijuana metabolites in serum were 0.05–0.25 ng/mL and 0.1–0.5 ng/mL, respectively. In urine, the LOD and LLOQ ranges for the metabolites were 0.05–0.1 ng/mL and 0.1–0.5 ng/mL, respectively. In serum, median and range of metabolite concentrations (ng/mL) detected included: THC, 65.0 (0.14–160); 11-OH-Δ9-THC, 4.78 (1.15–17.8); 11-nor-9-carboxy-Δ9-THC, 2.18 (0.71–7.79); CBD, 0.28 (0.11–82.5); and THC-glucuronide, 2.05 (0.72–18.3). In the 19 urine samples, metabolite: creatinine (ng: mg) values detected included: THC, 0.22 (0.05–0.74); 11-OH-Δ9-THC, 0; 11-nor-9-carboxy-Δ9-THC, 1.32 (0.16–11.2); CBD, 0.19 (0.12–0.26); THC-COOH-glucuronide, 0.08 (0.04–0.11); and THC-glucuronide, 0.98 (0.25–10.7). Twenty of 21 urine samples tested negative for THC on the urine drug screen. All 19 serum samples contained quantifiable concentrations of THC using our novel UPLC-MS/MS method. Utilizing a UPLC-MS/MS method can be a useful aid in the diagnosis of marijuana toxicosis in dogs, whereas using an OTC human urine drug test is not a useful test for confirming marijuana exposure in dogs because of the low concentration of THC-COOH in urine.

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The evidence for use of some of these medications is limited due to their novelty. Known mechanisms of action, pharmacokinetic and pharmacodynamics data, adverse effects and clinical uses are reviewed where possible, with clinical recommendations made based on the evidence of data available.

OBJECTIVE To determine if left ventricular systolic function on echocardiography, systemic blood pressure, and electrocardiography change with a clinically accepted intravenous (IV) diltiazem constant rate infusion (CRI) compared to a control. ANIMALS 10 healthy client-owned adult dogs. PROCEDURES Prospective, masked, crossover study from May 27, 2021, to August 22, 2021. Dogs were randomized to receive diltiazem (loading dose of 240 μg/kg, IV followed by a CRI of 6 μg/kg/min for 300 minutes) or the same volume of 5% dextrose in water (D5W) administered IV followed by the opposite intervention after a 7-day washout. Blood pressure was monitored during each CRI, and echocardiographic and electrocardiographic studies were performed immediately before the CRI and during the last hour of the CRI. RESULTS Postdiltiazem systolic time interval (STI) (median, 0.30; range, 0.16 to 0.34) was significantly lower than post-D5W STI (median, 0.32; range, 0.22 to 0.40; P = .046). All other echocardiographic parameters did not differ significantly between each of the groups after receiving diltiazem or D5W. Systemic blood pressure did not change significantly with either diltiazem (P = .450) or D5W (P = .940), and none of the dogs became hypotensive at any point in the study. Expectedly, negative dromotropy was observed with diltiazem. CLINICAL RELEVANCE A significant decrease in left ventricular systolic function was not appreciated in healthy dogs receiving diltiazem at a clinically accepted intravenous infusion rate at this dosing regimen. Further studies are needed in dogs with cardiac disease.

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