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21 May 2009

Pentoxifylline augments fasting induced nephroprotection in ischemic model of acute kidney injury in rats

A Wystrychowski, W Wystrychowski, P Król, E Obuchowicz, L Cierpka, A Więcek

Ann Transplant 2009; 14(1): 60-60 :: ID: 880418


Background: Ischemic acute kidney injury (iAKI) activates also general inflammatory reaction. Prolonged fasting exerts anti-inflammatory effects through increased secretion of ghrelin - an orexigenic hormone produced in the gastrointestinal system that inhibits NF-B activation and induces IL-10 release. PTX has similar immunomodulating and anti-inflammatory properties. The aim of this study was to assess and compare the influence of feeding status and PTX administration on the course of iAKI.
Material/Methods: 44 male Sprague-Dawley rats, 14 days after right nephrectomy and 7 days before renal ischemia were placed in individual cages preventing feaces consumption with ad libitum water access. Rats of groups Ia and Ib were fed with no limitations as opposed to groups IIa and IIb, starved for 32 hours prior to renal ischemia. 90 min before left kidney vascular pedicle clamping (for 45 min) rats of groups Ib/IIb and Ia/IIa were given PTX (100 mg/kg body weight in 1ml 0.9% NaCl, s.c.) or 0.9% NaCl only, respectively. Creatinine clearance (CrCl; ml/min/kg bw), fractional excretion of sodium (FENa; %) and proteinuria to creatinine clearance ratio (PUrea/ClCrea) were estimated 24 hours after ischemia.
Results: As shown in the table, both fasting and PTX administration diminished the degree of ischemia-induced impairment of renal function. Their combined effects were additive.
Conclusions: Fasting and treatment with pentoxifylline in the periischemic period exert additive nephroprotective effects in the setting of ischemic acute kidney injury. These findings may be useful in the studies and future practice of preservation of kidney transplant function.

Keywords: Ischemia reperfusion injury, Kidney Transplantation

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Annals of Transplantation eISSN: 2329-0358
Annals of Transplantation eISSN: 2329-0358