1. ¹Universidade Federal do Rio de Janeiro: Nefrologica, HUCFF, Rio de Janeiro, Brazil
2. ²Universidade Federal do Rio de Janeiro Histologia/Embriologia-ICB. Rio de Janeiro, Brazil
3. ³Universidade Federal do Rio de Janeiro NPPN, Rio de Janeiro, Brazil
4. ⁴Universidade Federal do Rio de Janeiro: Faculdade de Medicina, HUCFF, Rio de Janeiro, Brazil

Correspondence: LR Cardoso, Rua Candido Gaffree # 27 apto. 302, Rio de Janeiro, RJ, CEP – 22291-080, Brazil. E-mail: lcardoso@hucff.ufrj.br

Received 28 December 2004; Revised 14 June 2005; Accepted 14 July 2005.

Abstract

Cold ischemia time is a risk factor for the development of acute renal failure in the immediate post-transplant period. In this study, we aimed to determine if intravenous fructose-1,6-diphosphate (FDP), given before nephrectomy, attenuates renal cell injury in a cold ischemia model. Male adult Wistar rats were subjected to infusion of either FDP 350 mg/kg (group F, n=6), an equal volume of 0.9% NaCl (group S, n=6), an equal volume/osmolality of mannitol (group M, n=6) or no infusion (group C, n=7). Kidneys were then perfused in situ with Collins solution and nephrectomy was performed. Other kidney slices were stored in Collins solution at 4°C. Adenosine triphosphate (ATP) levels and lactate dehydrogenase (LDH) release were examined at 0, 24, 48 and 72 h. Other slices, obtained after 50 min immersion in Collins solution at 37°C, were frozen for characterization of cytoskeletal preservation using phalloidin-FITC staining. Apical fluorescence intensity of proximal tubule cells, indicative of the F-actin concentration, was measured in a fluorescence microscope interfaced with computer image analysis system. Adenosine triphosphate levels, after up to 72 h of tissue incubation, were higher (P<0.05) in the FDP group when compared to other groups. In addition, LDH release was smaller (P<0.0001) in the FDP group. The F-actin concentration of proximal tubule cells cells was greater in the FDP group (P<0.0001). Results indicate that FDP is a useful tool to increase tissue viability in a rat kidney subjected to cold ischemia, by maintaining ATP cell content, decreasing LDH release and preventing microfilament disruption of proximal tubule cells.