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Clinical Rejection Is Distinguished from Subclinical Rejection by Increased Infiltration by a Population of Activated Macrophages

PAUL C. GRIMM^*,,¶, RACHEL MCKENNA^,, PETER NICKERSON^,, MARY E. RUSSELL^||, JIM GOUGH^§, ELZBIETA GOSPODAREK^*, BIN LIU^*, JOHN JEFFERY and DAVID N. RUSH

^* Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada
Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada
Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
^§ Department of Pathology, University of Manitoba, Winnipeg, Manitoba, Canada
^|| Harvard School of Public Health, Boston, Massachusetts
^¶ University of California at San Diego, San Diego, California.

Correspondence to Dr. Paul C. Grimm, Division of Pediatric Nephrology, University of California at San Diego, 9500 Gilman Drive, Mail Code 0831, La Drive, Jolla, CA 92093-0831. Phone: 619-543-5218; Fax: 619-543-3575; E-mail: pgrimm{at}ucsd.edu

Abstract. It has been reported previously that one-third of protocol renal biopsies in asymptomatic, biochemically stable renal transplant recipients in the first 6 mo show unsuspected subclinical graft rejection (both infiltrate and tubulitis) and that subclinical rejection is a risk factor for chronic renal dysfunction. This study was performed to determine whether differences in phenotype or activation status of graft-infiltrating cells underlie these different manifestations of acute rejection. Biopsies with normal histology (n = 10), subclinical rejection (n = 13), and clinical rejection (n = 9) were studied using immunohistochemistry and computerized image analysis. Subclinical and clinical rejections had similar histologic Banff scores. Univariate analysis showed a trend for a higher infiltration with CD8+ (P = 0.053) and CD68+ (P = 0.06) cells in clinical rejection. Of the activation markers studied (CD25, perforin, tumor necrosis factor-), only allograft inflammatory factor-1 +-activated macrophages were significantly (P = 0.014) increased in the infiltrate of clinical rejection biopsies. These data suggest that activated macrophages or their products are responsible for acute renal dysfunction associated with clinical rejection episodes.

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