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Prediction of Acute Renal Allograft Rejection by Urinary Monokine Induced by IFN- (MIG)

Ingeborg A. Hauser^*, Sandra Spiegler, Eva Kiss, Stefan Gauer^*, Olaf Sichler^*, Ernst H. Scheuermann^*, Hanns Ackermann, Josef M. Pfeilschifter, Helmut Geiger^*, Hermann-Josef Gröne and Heinfried H. Radeke

^* Medical Clinic IV, Nephrology; The pharmazentrum frankfurt, Dr. Hans Schleussner Foundation, Immune Pharmacology; Department of Medical Informatics and Biomathematics, Clinic of the J.W. Goethe University, Frankfurt, Germany; and Institute of Pathology, German Cancer Research Center (DKFZ), Heidelberg, Germany

Address correspondence to: Dr. Ingeborg A. Hauser, Medical Clinic IV, Department of Nephrology, Clinic of the J.W. Goethe University, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany. Phone: +49-696301-7864; Fax: +49-696301-7862; E-mail: i.hauser{at}em.uni-frankfurt.de; or Dr. Heinfried Radeke, Pharmazentrum Frankfurt, Dr. Hans Schleussner Foundation of Immune Pharmacology, Building 75, Room 103, Clinic of the J.W. Goethe University, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany. Phone: +49-696-3018-3104; Fax: +49-696-3018-3202; radeke{at}em.uni-frankfurt.de

Received for publication October 8, 2004. Accepted for publication March 14, 2005.

Early diagnosis of acute allograft rejection (AR) is still decisive for long-term renal allograft survival. The aim of this study was to define the role of the chemokine monokine induced by IFN- (MIG) (CXCL9) and IFN-–inducible protein 10 (IP-10) (CXCL10) as early markers of AR in renal transplantation (NTX). In a prospective study, 69 de novo renal transplant recipients were monitored and urine samples were collected after NTX for a median of 29 d. In pH-adjusted urine, MIG and IP-10 were determined by modified ELISA. AR was clinically diagnosed in 15 of 69 recipients and confirmed by biopsy in 14 of 15 AR patients (Banff classification). Corresponding to CXCR3-positive infiltrates in renal tissue, urinary MIG was elevated in 14 of 15 AR patients with a median of 2809 pg/ml (quartile 25% and 75% = 870 and 13,000; n = 15), being significantly (P < 0.0001) different from both nonrejecting allograft patients (NO-AR) (median, 25%, and 75%: 96, 1.0, and 161, n = 54) and healthy controls (median, 25%, and 75%: 144, 19, and 208, n = 13). Urinary MIG predicted AR with a sensitivity of 93% and a specificity of 89%. In AR and NO-AR groups, MIG values correlated well with IP-10 (P < 0.001). MIG values indicated both imminent rejection and response to successful antirejection therapy. MIG was not related to intercurrent infections or other causes for impairment of renal function. In a multivariate analysis, MIG correlated best (P < 0.001) with AR from all AR-associated parameters. In conclusion, urinary MIG serves as a very sensitive and specific predictor for AR, mirrors response to antirejection therapy, and thus may contribute to improved long-term renal allograft survival.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673