Acute renal failure and degenerative tubular lesions associated with in situ formation of adenovirus immune complexes in a patient with allogeneic bone marrow transplantation

• Published in: Transplantation Vol. 55; no. 1; p. 67
• Main Authors: Yuzawa, Y, Aoi, N, Fukatsu, A, Ichida, S, Yoshida, F, Akatsuka, Y, Minami, S, Kodera, Y, Matsuo, S
• Format: Journal Article
• Language: English
• Published: United States 01.01.1993
• Subjects: Acute Kidney Injury - etiology; Adenoviruses, Human - immunology; Adult; Antibodies, Viral - analysis; Antigen-Antibody Complex - analysis; Antigens, Viral - analysis; Bone Marrow Transplantation; Cystitis - etiology; Hemorrhage - etiology; Humans; Kidney Tubules, Distal - pathology; Kidney Tubules, Distal - ultrastructure; Leukemia, Myeloid, Acute - surgery; Male; Microscopy, Electron; Necrosis; Transplantation, Homologous
• ISSN: 0041-1337
• DOI: 10.1097/00007890-199301000-00013

We describe the development of acute renal failure and degenerative tubular lesions associated with local immune deposits in a patient with allogeneic bone marrow transplantation. A 21-year-old man with an acute myelocytic leukemia received a bone marrow graft from a cousin mismatched for a single HLA-DR locus antigen. Hemorrhagic cystitis due to adenovirus type 11 infection occurred 26 days after transplantation, and 17 days later the patients developed acute renal failure. A study of renal tissue obtained by needle biopsy showed degenerative and necrotic lesions, especially in the distal part of the nephron. By electron microscopy adenovirus type 11 particles were found in the nuclei of tubular cells and in cellular debris in tubular lumina. By immunofluorescence technique, granular immune deposits containing adenovirus type 11 related antigen(s), immunoglobulins, C3, and membrane attack complex (MAC) C5b-9 of the complement system were detected along the tubular basement membranes but not in glomeruli. The patient's IgG did not bind to normal human kidneys. These findings suggest that adenovirus type 11 directly induced acute tubular damage, and that the tubular immune deposits were formed "in situ" by viral antigens and circulating viral antibody.