Hematological and Hemostatic Alterations Associated With a Single Extracorporeal Renal Replacement Therapy in Dogs With Acute Kidney Injury Associated Leptospirosis: A Pilot Study.

Extracorporeal renal replacement therapy (ERRT) used in dogs with acute kidney injury (AKI) may be associated with hematological and hemostatic disorders. However, its characteristics are not fully described in dogs. The purpose of this pilot study was to characterize the impact of ERRT on hematological, hemostatic, and thromboelastometric parameters in dogs with AKI. We conducted a prospective observational single cohort study in 10 client-owned dogs with AKI associated leptospirosis undergoing ERRT. Results from the CBC, coagulation tests (prothrombin and activated partial thromboplastin times [aPTT]) and rotational thromboelastometry (TEM; intrinsic TEM [inTEM] and heparinase-based TEM [hepTEM]) were recorded before and after the first ERRT session. Blood abnormalities observed before the ERRT session included thrombocytopenia (10/10), anemia (8/10), leukocytosis (4/10), prolonged aPTT (4/10) and leukopenia (1/10). After ERRT, the platelet count decreased (-25%; P = .012) whereas leukocytes (+15%; P = .046) and aPTT (+24%; P = .006) increased. The clotting time (CT) on inTEM assay and the relative variation of CT based on inTEM and hepTEM profiles increased after the ERRT session (P = .037 and P = .048, respectively). Seven dogs, 2 dogs, and 1 dog were defined as having a normal, hypocoagulable, and hypercoagulable inTEM profile after ERRT, respectively. After ERRT, no hepTEM parameter was significantly different from before treatment. Platelet count, leukocytes, aPTT and CT were altered after the first ERRT session. Beyond the hemostatic abnormalities expected by the use of UFH, thrombocytopenia appears as the only hemostatic change after a single ERRT session in dogs with AKI.

Presumptive Glucocorticoid-Induced Refractory Hypocalcemia in a Dog with Idiopathic Immune-Mediated Hypoparathyroidism, Thrombocytopenia, and Hemolytic Anemia.

Clinically relevant hypocalcemia is a well-documented complication of glucocorticoid administration in people with hypoparathyroidism. The current report describes the phenomenon in a dog. A 7 yr old neutered male Pomeranian was diagnosed with immune-mediated thrombocytopenia, immune-mediated hemolytic anemia, and primary hypoparathyroidism. This dog required long-term parenteral calcium gluconate to prevent clinical hypocalcemia despite appropriate doses of oral calcitriol and calcium carbonate. This is the first description of clinically significant presumptive glucocorticoid induced hypocalcemia in a dog with primary hypoparathyroidism.

Serum Thymidine Kinase 1, Canine-C-Reactive Protein, Haptoglobin, and Vitamin D Concentrations in Dogs with Immune-Mediated Hemolytic Anemia, Thrombocytopenia, and Polyarthropathy.

BACKGROUND: Relapses of immune-mediated hemolytic anemia (IMHA), thrombocytopenia (ITP), or polyarthropathy (IMPA) occur despite normal hematologic and cytologic parameters. Thymidine kinase 1 (TK1), canine C-reactive protein (c-CRP), haptoglobin (HPT), and 25-Hydroxyvitamin-D (25(OH)D) might be adjunct to current monitoring strategies. HYPOTHESIS/OBJECTIVES: Compare serum concentrations of TK1, c-CRP, HPT, and 25(OH)D in dogs with well- and poorly controlled primary IMHA, ITP, or IMPA. ANIMALS: Thirty-eight client-owned dogs. METHODS: Prospective descriptive study. Dogs diagnosed with IMHA, ITP, or IMPA had serum biomarker concentrations measured commercially. Disease control was assessed by hematocrit/PCV and reticulocyte count, platelet count, and synovial fluid cytology for IMHA, ITP, and IMPA, respectively. Statistical analysis performed by Mann-Whitney rank-sum tests and receiver operating characteristic curves. RESULTS: TK1 and c-CRP, but not HPT significantly decreased with well- versus poorly controlled IMHA (P = 0.047, P = 0.028, P = 0.37). C-CRP, but not TK or HPT was significantly lower with well- versus poorly controlled IMPA (P = 0.05, P = 0.28, P = 0.84). Sensitivity and specificity of TK and c-CRP (simultaneously) for detecting dogs with poorly controlled IMHA were 88 and 100%, respectively. Sensitivity and specificity of c-CRP for detecting poorly controlled dogs with IMPA were 13 and 100%, respectively. 92% of dogs were vitamin D insufficient (<100 ng/mL) regardless of disease control. CONCLUSIONS AND CLINICAL IMPORTANCE: Combining TK1 and c-CRP might act markers of disease control in dogs with IMHA. Canine-CRP cannot be recommended as an independent marker of disease control in IMPA. 25(OH)D insufficiency in immune-mediated disorders might benefit from further study to determine if supplementation could improve therapeutic response or reduce disease risk.

Comparison of platelet clumping and complete blood count results with Sysmex XT-2000iV in feline blood sampled on EDTA or EDTA plus CTAD (citrate, theophylline, adenosine and dipyridamole).

False thrombocytopenia may result from platelet aggregation, especially in feline ethylenediamine tetra-acetic acid (EDTA) blood specimens. Citrate, theophylline, adenosine and dipyridamole (CTAD) was added to 46 feline EDTA specimens to test its anti-aggregation action. Platelet aggregation was estimated from blood films and a complete blood count was performed with a Sysmex XT-2000iV analyser. Platelet aggregation score was >2 in 11/46 EDTA tubes and only in one EDTA+CTAD specimen. The platelet count was higher in all CTAD-supplemented tubes except one, medians measured by cytometry being 225.5 × 10(9)/l and 249.0 × 10(9)/l in EDTA and EDTA+CTAD, respectively (P = 0.007). Adding CTAD had statistically and analytically significant but moderate effects on other blood variables, the most intense variations being observed for reticulocytes (about 3% higher in EDTA specimens) and reticulocyte indexes. Addition of CTAD to EDTA when sampling feline blood is a useful option to reduce platelet clumping.

Ulcerative dermatitis, thrombocytopenia, and neutropenia in neonatal foals.

This report describes transient ulcerative dermatitis, severe thrombocytopenia, and mild neutropenia in 6 foals from 4 mares from geographically diverse regions of the United States. The foals presented at <4 days of age with oral and lingual ulcers, and crusting and erythema around the eyes, muzzle, and perineal, inguinal, axillary, trunk, and neck regions. There was a severe thrombocytopenia (0-30,000 platelets/microL), leukopenia (1900-3200 white blood cells/microL), and mild neutropenia (500-1800 neutrophils/microL). Four of the 6 foals had petechiae and ecchymotic hemorrhages and 3 had bleeding tendencies. Results of examination of a bone marrow biopsy from 1 foal were normal and results of a platelet surface immunoglobulin test in another were negative. Histopathology of the skin in all foals showed subepidermal clefting with subjacent vascular dilation, dermal hemorrhage, and superficial papillary necrosis. The foals were treated supportively with broad-spectrum antibiotics (5/6), corticosteroids (3/6), gastric ulcer prophylaxis (6/6), whole-blood transfusion (4/6), and platelet-rich plasma (1/6). The skin lesions and thrombocytopenia (>50,000 platelets/microL) improved in 2 weeks (4/6). Two foals had a decline in their platelet counts when the steroids were decreased and needed protracted treatment. All foals survived and were healthy as yearlings. Two mares that had 2 affected foals each, upon subsequent pregnancies to different stallions, had healthy foals when an alternate source of colostrum was given. The findings in the cases in this report suggest a possible relationship between colostral antibodies or some other factor in the colostrum and the thrombocytopenia and skin lesions, although further investigation is warranted to confirm or refute this hypothesis.

Thrombocytopenia in lambs fed with bovine colostrum.

Artificially reared lambs, fed with bovine colostrum, died within 48 hours after birth, showing thrombocytopenia and extensive haemorrhages on autopsy. The mechanism behind was not fully understood, but experimental immunization of young cattle against sheep red blood cells, carried out five years earlier on the same farm, may have played a role.

Reproduction of acute bracken poisoning in a calf with ptaquiloside, a bracken constituent.

Acute bracken fern toxicity in a calf was reproduced with ptaquiloside, a norsesquiterpene glucoside, isolated from the boiling water extract of bracken fern. Ptaquiloside was dissolved in 500 ml of saline and administered by drench at increasing dosages for six days out of every seven for the following periods: 400 mg/day for 24 days, 800 mg/day for 14 days and 1600 mg/day for four days. Neutrophilic granulocytes began to decrease markedly around 50 days after the start of the experiment, and granulocytopenia continued for a further 35 days until the autopsy, despite the discontinuance of ptaquiloside administration. Thrombocytes showed a relatively slow depression and reached 1 X 10(5)/mm3 at the lowest level. The calf was autopsied 86 days after the start of administration of ptaquiloside. Sternal bone marrow was found to be mostly replaced with fat marrow and only small foci of erythropoietic cells and a small number of megakaryocytes remained.