1. ¹Department of Nephrology, University of Vienna, Austria
2. ²Department of Pathology, University of Vienna, Austria
3. ³Department of Transplant Surgery, University of Vienna, Austria
4. ⁴Department of Nephrology, University of Innsbruck, Austria
5. ⁵Emergentec Data Analytics, Vienna, Austria
6. ⁶Department of Nephrology, Stanford University, Stanford, CA, USA

Correspondence: Rainer Oberbauer, Universitätsklinik für Innere Medizin III, Abteilung für Nephrologie und Dialyse, Währinger Gürtel 18-20, A-1090 Vienna, Austria. E-mail: rainer.oberbauer@akh-wien.ac.at

Received 5 June 2003; Revised 11 August 2003; Accepted 13 November 2003; Published online 29 December 2003.

Abstract

Roughly 25% of cadaveric, but rarely living donor renal transplant recipients, develop postischemic acute renal failure, which is a main risk factor for reduced long-term allograft survival. An accurate prediction of recipients at risk for ARF is not possible on the basis of donor kidney morphology or donor/recipient demographics. We determined the genome-wide gene-expression pattern using cDNA microarrays in three groups of 36 donor kidney wedge biopsies: living donor kidneys with primary function, cadaveric donor kidneys with primary function and cadaveric donor kidneys with biopsy proven acute renal failure. The descriptive genes were characterized in gene ontology terms to determine their functional role. The validation of microarray experiments was performed by real-time PCR. We retrieved 132 genes after maxT adjustment for multiple testing that significantly separated living from cadaveric kidneys, and 48 genes that classified the donor kidneys according to their post-transplant course. The main functional roles of these genes are cell communication, apoptosis and inflammation. In particular, members of the complement cascade were activated in cadaveric, but not in living donor kidneys. Thus, suppression of inflammation in the cadaveric donor might be a cheap and promising intervention for postischemic acute renal failure.