Prospects and applicability of molecular diagnosis of allograft rejection.
We believe that changes in blood urea nitrogen and plasma creatinine are, at best, surrogate markers for rejection. It seems certain that rejection, an immunologic process must precede deterioration in renal function. We suggest that the efforts to prevent chronic rejection should include an effective means to diagnose rejection before the advent of fixed renal injury. Through an analysis of transcription for a series of genes that are expressed by activated, but not resting, cytotoxic lymphocytes, eg, granzyme B, a remarkably accurate tool for assessing the presence of rejection has emerged. Although our methods first centered on analysis of kidney transplant biopsy specimens, noninvasive surveillance using transcriptional profiling analysis circulating blood or urine sediment cells has proven equally informative.
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Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02255, USA.
Suthanthiran
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D000818:Animals; D005786:Gene Expression Regulation; D006084:Graft Rejection / Q000175:diagnosis / Q000235:genetics*; D053804:Granzymes; D006801:Humans; D016030:Kidney Transplantation / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012697:Serine Endopeptidases / Q000235:genetics; D014158:Transcription, Genetic
C509213:GZMB protein, human; D053804:Granzymes; D012697:Serine Endopeptidases