title: Monocyte-mediated acute renal rejection after combined treatment with preoperative Campath-1H (alemtuzumab) and postoperative immunosuppression.
abstract: Campath-1H (alemtuzumab), a humanized monoclonal antibody against CD52, can cause more profound depletion of lymphocytes than monocytes. The resultant imbalance of lymphocytes and monocytes after Campath-1H treatment of a renal-transplant recipient may lead to an acute rejection dominated by monocytes. We report such a case of acute transplant rejection in a 49-yr-old man who received a living non-related kidney transplant and was treated with preoperative Campath-1H and postoperative immunosuppression. An initial post-transplant renal biopsy showed diffuse mild acute rejection with 95% CD68-positive monocytes, but only 5% CD3-positive T lymphocytes. Inflammatory cells in the renal biopsy were negative for CD34 and CD1a stains, suggesting non-involvement of CD34-derived dendritic cells in the acute rejection. After steroid treatment for 2 wk, the patient's serum creatinine concentration diminished to 1.5 mg/dl. The histopathological features of acute rejection were absent in a second biopsy of the transplanted kidney. In summary, this case is an instance of monocyte-mediated acute rejection of a transplanted kidney.
authors.affiliation: Division of Laboratory Medicine, Geisinger Medical Center, Danville, Pennsylvania 17822, USA. plzhang@geisinger.edu
authors.forename: Ping L
authors.initials: PL
authors.lastname: Zhang
authors.forename: Sayeed K
authors.initials: SK
authors.lastname: Malek
authors.forename: Jeffery W
authors.initials: JW
authors.lastname: Prichard
authors.forename: Fan
authors.initials: F
authors.lastname: Lin
authors.forename: Taher M
authors.initials: TM
authors.lastname: Yahya
authors.forename: Michael S
authors.initials: MS
authors.lastname: Schwartzman
authors.forename: Ruth P
authors.initials: RP
authors.lastname: Latsha
authors.forename: Marybess
authors.initials: M
authors.lastname: Skaletsky
authors.forename: Evan R
authors.initials: ER
authors.lastname: Norfolk
authors.forename: Robert E
authors.initials: RE
authors.lastname: Brown
authors.forename: James E
authors.initials: JE
authors.lastname: Hartle
authors.forename: Santosh
authors.initials: S
authors.lastname: Potdar
mesh_terms: D000328:Adult; D000074323:Alemtuzumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm / Q000627:therapeutic use*; D015703:Antigens, CD / Q000097:blood / Q000276:immunology; D018952:Antigens, CD34 / Q000097:blood / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000097:blood / Q000276:immunology; D000951:Antigens, Neoplasm / Q000097:blood / Q000276:immunology; D000074301:CD52 Antigen; D004359:Drug Therapy, Combination; D006023:Glycoproteins / Q000097:blood / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000502:physiology; D009173:Mycophenolic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D011182:Postoperative Care; D011241:Prednisone / Q000627:therapeutic use; D011300:Preoperative Care; D000097382:CD68 Molecule
chemical_list: D000074323:Alemtuzumab; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D015703:Antigens, CD; D018952:Antigens, CD34; D015214:Antigens, Differentiation, Myelomonocytic; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; D006023:Glycoproteins; D007166:Immunosuppressive Agents; D009173:Mycophenolic Acid; D011241:Prednisone; C000613862:CD52 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule