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A 7-year-old mixed breed dog was evaluated for erythrocytosis with an initial hematocrit of 82.3%. Abdominal ultrasound revealed a 6 cm mass on the cranial pole of the right kidney. Daily therapeutic phlebotomies were performed, reducing the hematocrit to 54%. The dog underwent a right nephroureterectomy, recovered without complications, and was discharged 3 days after surgery. Histopathologic evaluation revealed a completely excised grade II soft tissue sarcoma. The preoperative erythropoietin level was 7.00 mU/mL (RI 1.90-22.90 mU/mL) and the 3-day postoperative erythropoietin level was 0.99 mU/mL, supporting a diagnosis of inappropriate secondary erythrocytosis due to the renal tumor. Secondary erythrocytosis resulting from renal soft tissue sarcoma is rare. Confirmatory testing with erythropoietin levels can assist in the diagnosis of secondary erythrocytosis. Erythropoietin levels that are normal or increased in the face of erythrocytosis indicate a source of inappropriate erythropoietin production., (Copyright © 2019 Elsevier Inc. All rights reserved.)

OBJECTIVE To assess pharmacokinetics of tranexamic acid (TXA) in dogs and assess antifibrinolytic properties of TXA in canine blood by use of a thromboelastography-based in vitro model of hyperfibrinolysis. ANIMALS 6 healthy adult dogs. PROCEDURES Dogs received each of 4 TXA treatments (10 mg/kg, IV; 20 mg/kg, IV; approx 15 mg/kg, PO; and approx 20 mg/kg, PO) in a randomized crossover-design study. Blood samples were collected at baseline (time 0; immediately prior to drug administration) and predetermined time points afterward for pharmacokinetic analysis and pharmacodynamic (thromboelastography) analysis by use of an in vitro hyperfibrinolysis model. RESULTS Maximum amplitude (MA [representing maximum clot strength]) significantly increased from baseline at all time points for all treatments. The MA was lower at 360 minutes for the 10-mg/kg IV treatment than for other treatments. Percentage of clot lysis 30 minutes after MA was detected was significantly decreased from baseline at all time points for all treatments; at 360 minutes, this value was higher for the 10-mg/kg IV treatment than for other treatments and higher for the 20-mg/kg IV treatment than for the 20-mg/kg PO treatment. Maximum plasma TXA concentrations were dose dependent. At 20 mg/kg, IV, plasma TXA concentrations briefly exceeded concentrations suggested for complete inhibition of fibrinolysis. Oral drug administration resulted in a later peak antifibrinolytic effect than did IV administration. CONCLUSIONS AND CLINICAL RELEVANCE Administration of TXA improved clot strength and decreased fibrinolysis in blood samples from healthy dogs in an in vitro hyperfibrinolysis model. Further research is needed to determine clinical effects of TXA in dogs with hyperfibrinolysis.