title: Inflammation and oxidative stress markers by pentoxifylline treatment in rats with chronic renal failure and high sodium intake.
abstract: BACKGROUND
  Inflammation 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.
  
  
  METHODS
  CRF was 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 alpha (TNF-alpha), nitrites, thiols, malondialdehyde (MDA), and advanced oxidation protein products (AOPP) were measured.
  
  
  RESULTS
  Higher 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-alpha 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 microg/mL. MDA was not modified by sodium intake. PF treatment decreased serum TNF-alpha (151.7 pg/mL, p < 0.5) and AOPP (49.83 micromol/L, p < 0.03), and increased nitrites and thiols levels when compared with HNa rats.
  
  
  CONCLUSIONS
  High sodium intake increases the serum concentration of inflammation and oxidative stress markers; these changes are prevented by PF treatment.
authors.affiliation: Unidad de Investigación Médica en Enfermedades Nefrológicas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, México, DF, México. jmgallardo2salud.gob.mx
authors.forename: Juan M
authors.initials: JM
authors.lastname: Gallardo
authors.forename: María
authors.initials: M
authors.lastname: de Carmen Prado-Uribe
authors.forename: Dante
authors.initials: D
authors.lastname: Amato
authors.forename: Ramón
authors.initials: R
authors.lastname: Paniagua
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D003404:Creatinine / Q000097:blood; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D007249:Inflammation / Q000517:prevention & control*; D007676:Kidney Failure, Chronic / Q000188:drug therapy*; D008315:Malondialdehyde / Q000097:blood; D009573:Nitrites / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects; D010431:Pentoxifylline / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000037:antagonists & inhibitors* / Q000633:toxicity; D013438:Sulfhydryl Compounds / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D016166:Free Radical Scavengers; D009573:Nitrites; D012982:Sodium, Dietary; D013438:Sulfhydryl Compounds; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D003404:Creatinine; D010431:Pentoxifylline