The following article requires a subscription:



(Format: HTML, PDF)

Objective: To identify hemostatic abnormalities in dogs with protein-losing nephropathies (PLN) that represent risk factors for pathologic thrombosis.

Design: Cross-sectional observational study of client-owned dogs with PLN, nonprotein losing renal failure (RF), and systemic illness (SI) exclusive of primary renal disease.

Setting: Urban University Referral Center.

Animals: A total of 29 dogs (n=11 PLN, n=7 RF, n=11 SI) were enrolled between January 2001 and July 2002. Samples were also collected from 20 clinically normal dogs to serve as hemostasis assay controls.

Interventions: None.

Hemostasis Testing: Citrate anticoagulated blood was collected for point-of-care testing with a viscoelastic monitor (thromboelastograph [TEG]) and citrate plasma was prepared for coagulation screening tests and specific assay of the following hemostatic proteins: antiplasmin, antithrombin, D-dimer, Factor VIII, fibrinogen, plasminogen, protein C, and von Willebrand factor.

Results: Dogs with PLN and RF demonstrated TEG abnormalities consistent with hypercoagulability (eg, short clotting time, high clot amplitude) and both groups had significantly lower antithrombin than the SI group. The PLN dogs had significantly higher protein C than either the RF or SI group. Hyperfibrinogenemia was a consistent finding among all 3 disease groups, and the coagulation index a measure of hypercoagulability derived from TEG parameters, directly correlated with fibrinogen values of all study dogs.

Conclusions: Hemostatic abnormalities consistent with systemic hypercoagulability are common in dogs with RF and PLN, however, no prothrombotic factors unique to PLN were identified in our study. The thrombotic tendency of PLN may therefore involve parameters we did not directly assess such as platelet reactivity, fibrinolysis, perturbations in blood flow, and/or endothelial dysfunction. High protein C is a novel finding in PLN dogs of unknown clinical relevance.

Copyright (C) 2011 John Wiley & Sons, Inc.