Immunoadsorption in a dog with severe immune mediated hemolytic anemia.

Immune mediated hemolytic anemia (IMHA) is a life-threatening disease with severe, acute hemolysis as a result of an autoimmune response directed against erythrocyte surface antigens. In veterinary medicine, IMHA is usually treated with immunosuppressants and often multiple blood transfusions. In human medicine, immunoadsorption (IA) is an established therapy for antibody removal in immune-mediated diseases. A female, spayed, five-year-old, 28 kg Entlebucher Mountain dog was presented with regenerative anemia and positive autoagglutination diagnosed as immune-mediated hemolytic anemia to the veterinary emergency service. Conventional treatment consisting immunosuppression with prednisolone and mycophenolate failed to improve hemolysis. As hematocrit dropped daily, multiple blood transfusions of blood group DEA 1 negative were required. IA was initiated at day 3 with COM.TEC and ADAsorb platforms and a LIGASORBstaphylococcus antitoxin A column. IA with citrate anticoagulation was performed over the treatment time of 77 minutes with a blood flow of 50 mL/min. Total plasma volume of 1.6 L was processed. Complications consisted of vomitus and lid swelling, shivering, excessive clotting in the tubing after a calcium bolus and hypotension. After IA, hemolysis stopped immediately, plasma concentrations of immunoglobulin G, immunoglobulin M and bilirubin decreased, and hematocrit remained stable. The dog was discharged without further hemolysis 4 days after immunoadsorption with immunosuppressive therapy. IA is a promising adjunctive therapy in severe cases of canine IMHA, but it cannot be concluded to which degree IA or concurrent immunosuppression contributed to cessation of hemolysis in the present case.

Hemostatic and thromboelastographic parameters in dogs with renal azotemia.

Background and Aim: Humans and dogs with azotemia can develop coagulation disorders. Therefore, this study aimed to evaluate the coagulation profiles and thromboelastographic parameters in dogs with acute kidney injury (AKI) and chronic kidney disease (CKD). Materials and Methods: In this prospective study, 31 client-owned dogs with renal azotemia (creatinine >220 µmol/L) were enrolled. Clinical signs of hemostatic disorders, complete blood count, coagulation profile, D-dimers, thromboelastography, and 28-day survival data were obtained and analyzed using the t-test, Mann-Whitney U test, and Chi-square test. Statistical significance was set at p < 0.05. Results: Seventeen dogs with AKI, 10 with CKD, and four with acute-on-chronic kidney injury (AoC) were enrolled. Ten dogs (AKI, 8/17; CKD, 2/10) had thrombocytopenia. Prothrombin time was prolonged in four dogs with AKI and longer in dogs with AKI than in dogs with CKD (p = 0.004). The activated partial thromboplastin time was prolonged in 23 dogs (AKI, 14/17; CKD, 7/10; AoC, 3/4) and was longer in azotemic dogs than in healthy control dogs (p = 0.003). Thromboelastographic tracings were hypocoagulable in three dogs with AKI and hypercoagulable in 16 dogs (AKI 4/17, CKD 9/10, AoC 3/4). The thromboelastographic values for maximum amplitude (p < 0.001) and global clot strength (p < 0.001) were lower in dogs with AKI than in those with CKD. Conclusion: Hypercoagulable thromboelastographic tracings were observed in dogs with CKD, whereas coagulation times were prolonged in dogs with AKI. However these findings should be validated by further studies.