OBJECTIVE To investigate the effects of bilirubin in a rat model of pyelonephritis.METHODS Experimental pyelonephritis was induced in 32 wistar rats and 4 groups were formed: group 1 (no treatment), group 2 (antibiotic), group 3 (bilirubin), and group 4 (antibiotic + bilirubin). Antibiotic was given on days 3 to 8, and bilirubin was administered between days 0 and 8 of bacterial inoculation. Half of the rats were killed on the 9th day (early period) and histopathological parameters, immunohistochemical renal fibrosis markers, apoptosis, and oxidant/antioxidant system activities were evaluated. The rest of the rats were killed at the 6th week of the study and evaluated for histopathological parameters and renal fibrosis markers.RESULTS Inflammatory activity was significantly lower in rats treated with antibiotic + bilirubin vs no treatment group both in the early and late periods. In the late period, inflammatory cell intensity was lower in rats treated with bilirubin vs no treatment and the antibiotic + bilirubin groups. Interstitial fibrosis/tubular atrophy was lower in the antibiotic + bilirubin group vs the no treatment and antibiotic groups, and in bilirubin vs antibiotic group. Tissue inhibitor of metalloproteinase-1 expression was lower in the bilirubin vs antibiotic group. Terminal deoxynucleotidyl transferase mediated 2'-deoxyuridine, 5'-triphosphate nick end labeling(+) cells were significantly lower in bilirubin and antibiotic + bilirubin groups vs no treatment group. Malondialdehyde levels were significantly lower in the antibiotic + bilirubin vs the no treatment group and superoxide dismutase activity was significantly higher in the antibiotic and antibiotic + bilirubin groups vs the no treatment group.CONCLUSION Bilirubin may have protective effects on pyelonephritis-associated inflammation in both early and late periods in addition to fibrosis and apoptosis when applied with antibiotics. When used alone, bilirubin may also prevent inflammation (in the late period) and apoptosis. UROLOGY 80: 1389.e17-1389.e22, 2012. (C) 2012 Elsevier Inc.