Evaluation of Renal Medulla Injury After Cold Preservation and Transplantation: Noninvasive Determination of Medullar Damage by Proton Nuclear Magnetic Resonance Spectroscopy of Urine and Plasma J.P. Richer, T.H. Baumer, H. Gibelin, I. Ben Amor, W. Hebrard, M. Carretier, M. Eugene, and T. Hauet P RIMARY and early allograft dysfunction remains a challenge for the nephrologist. Usually, the assess- ment of renal graft dysfunction following transplantation is based on nonspecific measurement of renal function or an invasive method such as transplant biopsy. A rapid diagno- sis is necessary because a delay in treating early rejection deteriorates the prognosis of the allograft function. In addition, the antirejection treatment based on a mere clinical diagnosis of rejection could improve delayed graft function caused by acute tubular necrosis or cyclosporine damage through possible side effects of antirejection treat- ment. In the present study, we wanted to assess whether proton nuclear magnetic resonance ( 1 HNMR) spectroscopy can detect ischemic damage and predict acute tubular necrosis after pig kidney preservation in two preservation solutions (Euro-Collins: EC and University of Wisconsin: UW). MATERIALS AND METHODS Three experimental groups were studied: control group (sham operated, n = 4, group EC: 48-h cold preservation [CP] in EC, n = 7; group UW, 48-h CP, n = 7). Glomerular filtration rate (GFR) was assessed after autotransplantation, and renal medulla damage was assessed by trimethylamine-N-oxide (TMAO) and dimethyl- amine (DMA) excretion in urine during reperfusion at day 1, 3, 5, 7, 11, and 14 (D1–14). The ratios of TMAO and DMA to creatinine (Ct) levels were determined by 1 HNMR spectroscopy. RESULTS At D14, in the EC group, three of seven pigs survived and four of seven in the UW group. GFR was not significantly different from D1 to D11 between EC and UW preserved groups. GFR was significantly different at D14. However, TMAO and DMA to Ct ratios were improved in EC group. TMAO was detected in plasma in EC group (Fig 1). From the Laboratoire de Transplantation Expe ´ rimentale, INRA Le Magneraud, Surge ` res and Centre Hospitalo Universitaire and Faculte ´ de Me ´ decine (EA 2426), Poitiers, France. Supported by grants from the Ministe ` re de la Recherche, the Conseil Re ´ gional Poitou Charente, and the Association pour le De ´ veloppement de l’Auto-dialyse a ` domicile en Charente Mari- time (ADA 17). Address reprint requests to Dr T. Hauet, INRA, Laboratorie de Transplantation Experimentale, 17700 Surgeres BP 52, France. Fig 1. A and B: Changes in TMAO and DMA excretion in urine and C: change in TMAO in plasma °°P .01, °P .05. © 2000 by Elsevier Science Inc. 0041-1345/00/$–see front matter 655 Avenue of the Americas, New York, NY 10010 PII S0041-1345(99)00871-4 Transplantation Proceedings, 32, 47–48 (2000) 47