INTERNE GENEESKUNDE Randomized trial of short-course high-dose erythropoietin in donation after cardiac death kidney transplant recipients. Aydin Z, Mallat MJ, Schaapherder AF, van Zonneveld AJ, van Kooten C, Rabelink TJ, de Fijter JW. Am J Transplant 2012;12 (7):1793-800. PMID: 22429395. Eryhropoiesis-stimulating agents have demonstrated tissue-protective effects in experimental models of ischemia-reperfusion injury. PROTECT was a 12-month, randomized, double-blind, placebo-controlled, single center study with high-dose recombinant human erythropoietin-β (Epoetin) in 92 donation after cardiac death (DCD) kidney transplant recipients. Patients were randomized to receive an intravenous bolus of Epoetin (3.3 × 10(4) international unit (IU); n = 45) or placebo (saline 0.9% solution; n = 47) on 3 consecutive days, starting 3-4 h before the transplantation and 24 h and 48 h after reperfusion. The immunosuppressive regimen included an anti-CD25 antibody, steroids, mycophenolate mofetil and delayed introduction of cyclosporine. Primary end point was a composite of the incidence of primary nonfunction and delayed graft function, either defined by spontaneous functional recovery or need for dialysis in the first week. Secondary objectives included duration of delayed function, renal function and proteinuria up to 1 year and thrombotic adverse events. Results showed no differences in the incidence or duration of delayed graft function and/or primary nonfunction (Epoetin 77.8 vs. placebo 78.7%, p = 1.00). Epoetin treatment significantly increased the risk of thrombotic events at 1 month and 1 year (Epoetin 24.4% vs. placebo 6.4%, p = 0.02). Pitfalls in urinary complement measurements. Van der Pol P, de Vries DK, van Gijlswijk DJ, van Anken GE, Schlagwein N, Daha MR, Aydin Z, de Fijter JW, Schaapherder AF, van Kooten C. Transpl Immunol 2012;27(1):55-8. PMID: 22709941. Local activation of the complement system has been associated with ischemia/reperfusion injury following kidney transplantation and tubular injury under proteinuric conditions. The soluble terminal complement complex sC5b-9 is a stable end-product of the complement cascade, and as such a promising urinary biomarker. In the early post-transplant period we found high urinary levels of sC5b-9, significantly correlating with the degree of proteinuria, suggesting activation of filtered complement components at the tubular epithelial surface of the kidney. However, when mimicking proteinuria in vitro by exposing serum (or blood) to urine (both negative for sC5b-9), we found extensive generation of sC5b-9 in urine. This process was inhibited by EDTA, confirming activation of the complement system. In conclusion, although sC5b-9 is an attractive urinary biomarker, one should be aware of the risk of extra-renal complement activation independent of a renal contribution. This may be of special interest when measuring urinary sC5b-9 following kidney transplantation in which procedure-related (microscopic) hematuria and proteinuria are common. 37 WETENSCHAPPELIJK jaarverslag 2012 Pagina 36
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