Inflammation and Oxidative Stress Markers by Pentoxifylline Treatment in Rats with Chronic Renal Failure and High Sodium Intake

Background mation is a risk factor for mortality in patients with chronic renal failure (CRF). Prevention of extracellular fluid volume expansion and the use of certain drugs such as pentoxifylline (PF) may reduce inflammation and oxidative stress. The aim of this study is to analyze the effect of dietary sodium and PF treatment on the levels of inflammation and oxidative stress markers in rats with CRF. s s induced in rats by 5/6 nephrectomy. Different groups of rats with CRF received low sodium (LNa, 0.01% sodium chloride [NaCl] in the diet), normal sodium (NNa, 0.05% NaCl in the diet), or high sodium diet (HNa, as in NNa plus 0.015% NaCl in the drinking water). An additional group received HNa plus PF treatment (25 mg/kg in the drinking water) for 60 days. Circulating creatinine, tumor necrosis factor α (TNF-α), nitrites, thiols, malondialdehyde (MDA), and advanced oxidation protein products (AOPP) were measured. s sodium intake was associated with higher serum creatinine levels (median; interquartile range), LNa, 1.255; 0.715, NNa, 1.305; 0.495, HNa, 2.015; 1.115 mg/dL (p <0.05), TNF-α levels, LNa, 2.7; 23.6, NNa, 36.7; 47.7, HNa, 263.7; 126.5 pg/mL, and AOPP, LNa, 31.72; 7.55, NNa, 45.89; 9.38, HNa, 60.41; 37.42 μg/mL. MDA was not modified by sodium intake. PF treatment decreased serum TNF-α (151.7 pg/mL, p <0.5) and AOPP (49.83 μmol/L, p <0.03), and increased nitrites and thiols levels when compared with HNa rats. sions odium intake increases the serum concentration of inflammation and oxidative stress markers; these changes are prevented by PF treatment.