CASE REPORT Hemolytic Uremic Syndrome Due to Capnocytophaga canimorsus Bacteremia After a Dog Bite Tom J.M. Tobe ´, MD, Casper F.M. Franssen, MD, Jan G. Zijlstra, MD, Paul E. de Jong, MD, and Coen A. Stegeman, MD ● The hemolytic uremic syndrome (HUS) is known to have several causes, including infectious diseases, drugs, pregnancy, and malignant disease. We report a patient who developed acute renal failure attributable to HUS in the course of Capnocytophaga canimorsus bacteremia. Acute tubular necrosis as well as HUS should be considered as a cause of acute renal failure in the setting of Capnocytophaga canimorsus bacteremia.  1999 by the National Kidney Foundation, Inc. INDEX WORDS: Hemolytic uremic syndrome; Capnocytophaga canimorsus bacteremia; acute renal failure. T HE HEMOLYTIC uremic syndrome (HUS) is characterized by the presence of microan- giopathic hemolytic anemia, thrombocytopenia, fever, and acute renal failure. It can be caused by various underlying infectious and noninfectious factors. 1 If an underlying factor can be identified, then treatment aiming at the correction of that factor may improve outcome in addition to therapy directed toward HUS itself (eg, plasma exchange). 2-4 In this report, we describe an adult patient who developed HUS after Capnocyto- phaga canimorsus bacteremia. CASE REPORT A 50-year-old man presented elsewhere with fever and arthralgias. He had been bitten by his pet dog 1 day before presentation. His blood pressure was 130/80 mm Hg, his heart rate was 100 beats/min, and his temperature was 39°C. He had a small puncture on his left hand, without signs of active infection or lymphangitis. No purpura, rash, gan- grene, or lymphadenopathy was found. Results of neurologi- cal examination were unremarkable. Initial hematology tests included the following: hematocrit, 45%; platelet count, 77,000/μL; white cell count, 3,700/μL; 80% neutrophils; 1% band forms. Serum creatinine was 1.5 mg/dL; lactate dehy- drogenase (LDH) was 514 U/L. Despite the absence of circulatory problems or documented hypotension, the pa- tient remained oliguric and was transferred to our hospital because of progressive renal failure requiring dialysis (uri- nary output, 150 mL/24 hours). On admission (3 days after the initial presentation), his blood pressure was 145/60 mm Hg, his heart rate was 60 beats/min, and his temperature was 37°C. Hematology tests showed a hematocrit of 30%; reticulocytes, 0.6%; white blood cell count, 15,900 cells/μL; and progressive thrombo- cytopenia with a platelet count of 9,000 cells/μL. Microan- giopathic hemolysis was documented by schistocytes (13%), increased lactate dehydrogenase (LDH) (3,102 U/L), in- creased bilirubin (total and conjugated, 3.2 and 1.3 mg/dL, respectively). Alkaline phosphatase was 102 U/L (normal, 13 to 120), alanine transaminase, 83 U/L (normal, 40); aspartate transaminase, 91 U/L (normal, 30). The prothrom- bin time was 12.4 seconds (normal value, 11 to 16 seconds), activated partial thromboplastin time was 19.3 seconds (nor- mal, 26 to 36 seconds), antithrombin III was 71% (normal, 80% to 120%), fibrinogen was 468 mg/dL (normal, 170 to 350 mg/dL), and fibrinogen-fibrin degradation products were 8 to 16 mg/L (normal, 0.01 mg/L). Serum creatinine was 10.9 mg/dL, and urea was 143 mg/dL. Urinalysis showed 15 to 20 leukocytes and 15 to 20 erythrocytes per high-power field, but no casts. Proteinuria was 2.3 g/24 hours. Blood culture grew Capnocytophaga canimorsus, and treatment with amoxycillin/potassium clavulanate was started. Inotro- pic support was never necessary. Urine and stool culture were negative (including verocytotoxin producing Esch- erichia coli strains). A diagnosis of HUS was made on the basis of microangio- pathic hemolytic anemia, normal clotting times, thrombocy- topenia, and acute oliguric renal failure. Two days after the start of antibiotic therapy (platelets at that time were 24,000/ μL, LDH was 1,386 U/L), plasma exchange using fresh frozen plasma was added to the therapeutic regimen. 2-4 The serum LDH level started to decrease after the start of antibiotic therapy (before plasma exchange was started) (Fig 1). Because renal function showed no tendency to improve notwithstanding full normalization of the hematologic param- eters characteristic for HUS, a renal biopsy was performed on day 13. It showed mesangiolysis, tubular necrosis, and interstitial inflammation, but no thrombotic microangio- pathic changes nor vasculitis. However, at day 14, an in- crease in urinary output occurred (300 mL/24 hours), and after a phase of polyuria, recovery of renal function was From the Department of Nephrology and Intensive and Respiratory Care Unit, University Hospital Groningen, Gro- ningen, The Netherlands. Received October 26, 1998; accepted in revised form February 26, 1999. Address reprint requests to Tom J.M. Tobe ´, MD, Depart- ment of Intensive Care I, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands. E-mail: m.koller@digd.azu.nl  1999 by the National Kidney Foundation, Inc. 1523-6838/99/3306-0037$3.00/0 American Journal of Kidney Diseases, Vol 33, No 6 (June), 1999: E5 1