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

Yukio Yuzawa, Naoki Aoi, Atsushi Fukatsu, Shizunori Ichida, Futoshi Yoshida, Yoshiki Akatsuka, Saburo Minami, Yoshinao Kodera, Seiichi Matsuo

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Abstract

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 patient 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.

Original languageEnglish
Pages (from-to)67-72
Number of pages6
JournalTransplantation
Volume55
Issue number1
Publication statusPublished - 01-01-1993
Externally publishedYes

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Homologous Transplantation
Antigen-Antibody Complex
Bone Marrow Transplantation
Acute Kidney Injury
Adenoviridae
Complement Membrane Attack Complex
Viral Antibodies
Adenoviridae Infections
Kidney
Cystitis
Viral Antigens
Nephrons
Needle Biopsy
HLA-DR Antigens
Cell Nucleus
Basement Membrane
Acute Myeloid Leukemia
Fluorescent Antibody Technique
Immunoglobulins
Electron Microscopy

All Science Journal Classification (ASJC) codes

  • Transplantation

Cite this

Yuzawa, Yukio ; Aoi, Naoki ; Fukatsu, Atsushi ; Ichida, Shizunori ; Yoshida, Futoshi ; Akatsuka, Yoshiki ; Minami, Saburo ; Kodera, Yoshinao ; Matsuo, Seiichi. / Acute renal failure and degenerative tubular lesions associated with in situ formation of adenovirus immune complexes in a patient with allogeneic bone marrow transplantation. In: Transplantation. 1993 ; Vol. 55, No. 1. pp. 67-72.
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Acute renal failure and degenerative tubular lesions associated with in situ formation of adenovirus immune complexes in a patient with allogeneic bone marrow transplantation. / Yuzawa, Yukio; Aoi, Naoki; Fukatsu, Atsushi; Ichida, Shizunori; Yoshida, Futoshi; Akatsuka, Yoshiki; Minami, Saburo; Kodera, Yoshinao; Matsuo, Seiichi.

In: Transplantation, Vol. 55, No. 1, 01.01.1993, p. 67-72.

Research output: Contribution to journalArticle

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N2 - 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 patient 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.

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