CASE REPORT Necrotizing Glomerulonephritis Caused by Bartonella henselae Endocarditis Ian Bookman, MD, James W. Scholey, MD, Sarbjit V. Jassal, MD, Ginette Lajoie, MD, and Andrew M. Herzenberg, MD ● Glomerulonephritis secondary to endocarditis is uncommon and usually associated with valvular infection by blood culture–positive bacteria. We report 3 cases of necrotizing glomerulonephritis associated with culture- negative endocarditis caused by Bartonella henselae. Two of the patients presented with renal abnormalities and were investigated for endocarditis after results of renal biopsy. All 3 patients had an immune complex–mediated necrotizing and crescentic glomerulonephritis with mesangial and capillary wall deposition of immunoglobulin M (IgM), IgG, and C3. Electron microscopy showed immune-type electron-dense deposits in the mesangium and segmental subendothelial (2 cases) or subepithelial (1 case) deposits. Patients were treated with antibiotics, including azithromycin or doxycycline and ceftriaxone or tobramycin. In addition, 2 patients were administered steroids and 2 patients underwent valve replacement surgery. The 2 patients who underwent cardiac surgery were discharged from the hospital with stable renal function. The third patient died 4 months after hospital admission of renal failure. In conclusion, glomerulonephritis caused by B henselae endocarditis is an immune complex– mediated disease characterized by segmental necrotizing and crescentic glomerular lesions that can respond to aggressive medical and surgical therapy. Am J Kidney Dis 43:E8. © 2004 by the National Kidney Foundation, Inc. INDEX WORDS: Immune complex; crescentic glomerulonephritis; culture-negative endocarditis; renal pathology; electron microscopy; immunofluorescence; antibiotic therapy. A NTIBIOTIC TREATMENT has reduced the morbidity and mortality associated with bacterial endocarditis, but the diagnosis of cul- ture-negative endocarditis often is delayed, and treatment is suboptimal. 1 Glomerulonephritis sec- ondary to endocarditis is an uncommon diagno- sis. 2,3 We describe 3 patients with culture- negative endocarditis caused by Bartonella henselae, each of whom developed abnormal urinalysis results that led to a renal biopsy. B henselae is one of the most common causes of culture-negative endocarditis, 4 but histological characteristics of glomerulonephritis associated with B henselae have not been well character- ized. 5 Accordingly, we also describe light, immu- nofluorescent, and electron microscopic features of glomerulonephritis complicating B henselae endocarditis. CASE REPORTS Case 1 A 53-year-old woman presented with fatigue and general malaise. Her medical history included rheumatic heart dis- ease with severe mitral and tricuspid regurgitation, conges- tive heart failure, acquired brain injury secondary to a motor vehicle accident, and hypothyroidism. She had a pet dog, but no history of exposure to cats. Medications included furo- semide, spironolactone, cilazapril, and levothyroxine. On admission, she had atrial fibrillation with an uncontrolled ventricular response and mild congestive heart failure. There were no stigmata of endocarditis, and she was afebrile. Serum creatinine level was 1.2 mg/dL (106 mol/L; Table 1). The patient was admitted to the hospital and treated with digoxin. A 2-dimensional echocardiogram showed 2 small vegetations on the anterior and posterior leaflets of the mitral valve, both of which had been documented previously. Blood culture results were negative, and antibiotic therapy was not started. Seven days after admission, her creatinine level increased to 2.2 mg/dL (194 mol/L), and a urinalysis showed 3 + blood and 3 + protein. Microscopy showed red blood cells, granular casts, and red blood cell casts. Serologi- cal tests for atypical pathogens, including B henselae and Q fever, were ordered. Serum creatinine level increased to 3.5 mg/dL (309 mol/L), and a renal biopsy was performed 2 weeks after admission. Based on renal biopsy findings, the patient was treated with methylprednisolone, 250 mg/d intravenously for 3 From the Departments of Medicine and Pathology and Laboratory Medicine, University Health Network; and De- partment of Pathology, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada. Received July 28, 2003; accepted in revised form October 30, 2003. Supported in part by a Canada Institute for Health Re- search New Emerging Team Grant (J.W.S. and A.M.H.). Address reprint requests to Andrew M. Herzenberg, MD, Department of Pathology and Laboratory Medicine, Univer- sity Health Network and University of Toronto, 610 Univer- sity Ave, Toronto, Ontario, Canada M5G 2M9. E-mail: andrew.herzenberg@uhn.on.ca © 2004 by the National Kidney Foundation, Inc. 0272-6386/04/4302-0016$30.00/0 doi:10.1053/j.ajkd.2003.10.027 American Journal of Kidney Diseases, Vol 43, No 2 (February), 2004: E8 e25