Delayed type III hypersensitivity reaction with acute kidney injury in two dogs following administration of concentrated human albumin during treatment for hypoalbuminemia secondary to septic peritonitis.

OBJECTIVE: To describe 2 dogs with acute kidney injury secondary to type III hypersensitivity reaction to 25% human serum albumin (HSA). CASE SERIES SUMMARY: Two dogs were presented with evidence of septic peritonitis. The dogs were hospitalized following definitive surgical correction of a jejunal laceration following routine ovariohysterectomy, and removal of a jejunal foreign body. In the postoperative period, both dogs developed hypoalbuminemia and received 25% HSA. At the time of initial discharge, both dogs were doing well clinically and had normal renal parameters. Eleven and 18 days after HSA infusion, respectively, both dogs were re-presented with clinical signs of inappetence, vomiting, and lameness that progressed to urticaria, peripheral and angioedema, and petechiae, consistent with a delayed type III hypersensitivity reaction. Treatment for the type III hypersensitivity reaction to HSA included administration of diphenhydramine and glucocorticoids. Despite partial resolution of edema and joint swelling, both dogs developed progressive azotemia together with hypoalbuminemia and proteinuria. One dog developed an anuric acute kidney injury (AKI). Both dogs were humanely euthanized. Histopathology of the kidneys of both dogs was consistent with immune complex deposition and vasculitis. NEW OR UNIQUE INFORMATION: Severe type III hypersensitivity reactions have been documented in healthy dogs and clinical patients following the administration of HSA. This report describes the first documented delayed type III hypersensitivity reaction in 2 dogs with septic peritonitis that resulted in AKI, glomerulonephritis, and oligo- to anuria in clinical patients following administration of 25% HSA.

Evaluation of the relationship between clinical variables and thromboelastographic findings in dogs with protein-losing nephropathy.

OBJECTIVE: To determine whether hypercoagulability in proteinuric dogs, defined by thromboelastography (TEG), is related to the degree of proteinuria, presence of systemic arterial hypertension, presence of hypoalbuminemia, or reduced antithrombin activity. DESIGN: Prospective study of client-owned dogs. Data collected from each patient included signalment, body weight, urine protein-to-creatinine ratio (UPC), serum albumin concentration, TEG values, noninvasive arterial blood pressure, and AT activity. Hypercoagulability was diagnosed by TEG and odds ratios for other measurements were assessed by univariate logistic regression. SETTING: Urban referral center and teaching hospital. ANIMALS: Seventy-six dogs with protein-losing nephropathy (PLN) based on UPC, diagnosed between Oct 2009 and Oct 2012. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The prevalence of hypercoagulability was 89%. No statistically significant associations were detected between hypercoagulability and UPC, serum albumin, noninvasive blood pressure, or AT activity (all P > 0.05). The prevalence of thromboembolism was 6.6%. CONCLUSIONS: Hypercoagulability was prevalent in dogs with PLN but could not be predicted based upon the presence or degree of proteinuria, systemic arterial hypertension, hypoalbuminemia, or low AT activity. The prevalance of thromboembolism was low in this population with PLN.

Clinical management of canine babesiosis.

OBJECTIVE: To review and summarize current information regarding epidemiology, pathogenesis, and pathophysiology leading to the various clinical syndromes associated with canine babesiosis. Diagnosis, treatment, preventative strategies, and zoonotic implications are discussed. ETIOLOGY: Babesiosis is caused by hemoprotozoa of the genus Babesia. Numerous species of Babesia exist worldwide. An increased incidence of babesiosis is described, especially in North America. The babesial organism spends the majority of its life cycle within the erythrocyte of the definitive host, resulting in hemolysis, with or without systemic complications. DIAGNOSIS: Definitive diagnosis depends on direct visualization of the organism on blood smear or polymerase chain reaction. A positive serologic antibody test indicates exposure with or without active infection. THERAPY: Antiprotozoal drugs, antimicrobials, and supportive care are the mainstays of babesiosis therapy. PROGNOSIS: Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Clinical syndromes associated with a poorer prognosis include red biliary syndrome, acute renal failure, acute respiratory distress syndrome, neurologic dysfunction, acute pancreatitis, cardiac dysfunction, and hypoglycemia.

Feline babesiosis.

OBJECTIVE: To review and summarize current information regarding the etiology, clinical presentation, diagnosis, treatment, and prognosis of feline babesiosis, especially with regard to features distinct from canine babesiosis. ETIOLOGY: Babesiosis is caused by hemoprotozoa of the genus Babesia. Numerous species of Babesia exist worldwide. The babesial organism spends the majority of its life cycle within the erythrocyte of the definitive host, resulting in hemolysis, with or without systemic complications. DIAGNOSIS: Definitive diagnosis depends on direct visualization of the organism on blood smear or a positive polymerase chain reaction. Positive serologic tests indicate only exposure, with or without active infection. THERAPY: Antiprotozoal drugs and supportive care are the mainstays of therapy. Primaquine phosphate is considered the treatment of choice in cats. PROGNOSIS: Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Mortality rates of 15-20% are reported.

Therapeutic percutaneous ultrasound-guided cholecystocentesis in three dogs with extrahepatic biliary obstruction and pancreatitis.

Three dogs were examined because of acute pancreatitis. In all 3, distension of the gallbladder was seen ultrasonographically, and extrahepatic biliary tract obstruction (EHBO) was diagnosed on the basis of ultrasonographic findings and serum biochemical abnormalities (i.e., high serum bilirubin and cholesterol concentrations and increased hepatic enzyme activities). In all 3 dogs, percutaneous ultrasound-guided cholecystocentesis (PUCC) was used to decompress the gallbladder, with cholecystocentesis performed multiple times in 1 dog. Serum bilirubin concentration was substantially decreased following the procedure in all 3 dogs. Two of the 3 dogs did not require surgery to resolve the obstruction. In the third dog, an exploratory laparotomy was performed because of concerns about development of abdominal effusion following the procedure. Bile staining of the mesenteric fat was seen during the laparotomy, but no defect in the gallbladder wall could be identified. In most dogs with EHBO secondary to pancreatitis, the obstruction resolves spontaneously as the acute pancreatitis improves so that surgery is not required. In those few dogs in which EHBO does not resolve or in which EHBO results in complications, therapeutic PUCC may be useful in relieving gallbladder distension.