Diesel exhaust particles in the lung aggravate experimental acute renal failure

Inhaled particles are associatedwithpulmonary andextrapulmonary effects. Also, acute renal failure (ARF) is associated with increased mortality, related to pulmonary complications. Here, we tested the possible potentiating effect of diesel exhaust particles (DEP) inananimal modelofARF induced byasingleipinjectionof cisplatin (CP, 6 mg/kg) in rats. Six days later, the rats were intratracheally instilled with either DEP (0.5 or 1 mg/kg) or saline (control) and renal,systemic, and pulmonary variables were studied 24 h thereafter. CP increased the serum concentrations of urea and creatinine and reduced glutathione (GSH) concentration and superoxide dismutase activity in renal cortex. CP caused renal tubular necrosis; increased urine volume, protein concentrations, and N-acetyl-b-D-glucosaminidase (NAG) activity; and decreased urine osmolality. The combination of DEP and CP aggravated the CP-induced effects on serum urea and creatinine, urine NAG activity, and renal GSH. The arterial O2 saturation and PO2 were significantly decreased in CP 1 DEP versus CP 1 saline and CP 1 DEP versus DEP. The number of platelets was reduced in DEP comparedtosaline-treated ratsandCP 1DEPversus DEPaloneor CP 1 saline. Increases in macrophage and neutrophils numbers in bronchoalveolar lavage were found in DEP versus saline group and CP 1 DEP versus CP. Histopathological changes in lungs of DEPtreated rats were aggravated by the combination of CP 1 DEP. These included marked interstitial cell infiltration and congestion. We conclude that the presence of DEP in the lung aggravated the renal, pulmonary, and systemic effects of CP-induced ARF.