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<p>Contrast-associated acute kidney injury (CA-AKI) remains a clinically relevant complication of intravascular contrast media use, involving complex and incompletely understood mechanisms including oxidative stress, inflammation, apoptosis, and vasomotor dysregulation. Indirect bilirubin has been proposed as a potential cytoprotective molecule due to its antioxidant and anti-inflammatory properties. In this experimental study, twenty-four male Wistar albino rats were randomized into three groups: sham, contrast nephropathy (CN), and contrast nephropathy treated with indirect bilirubin (CNIB). CA-AKI was induced using indomethacin, Nω-Nitro-L-Arginin-Methylester (L-NAME), and iodinated contrast media. Indirect bilirubin (30&#xa0;mg/kg, intraperitoneal [i.p.]) was administered after injury induction. Renal function was assessed using serum creatinine (SCR), blood urea nitrogen (BUN), and urinary parameters. Histopathological injury was evaluated using semi-quantitative tubular damage scoring, and molecular analyses included inflammatory, apoptotic, and anti-apoptotic markers. Contrast media administration induced significant impairment in renal function and marked tubular injury compared with sham animals. Indirect bilirubin administration was associated with a reduction in histological tubular damage and vacuolization compared to untreated CA-AKI animals. However, improvements in Scr, BUN, and urinary indices did not reach statistical significance. In addition, expression patterns of inflammatory and apoptotic markers were inconsistent between functional, histological, and molecular outcomes, and did not uniformly support a classical anti-inflammatory or anti-apoptotic mechanism. Indirect bilirubin was associated with attenuation of histological renal injury in an experimental model of contrast-associated acute kidney injury; however, this effect was not accompanied by consistent functional improvement or coherent modulation of inflammatory and apoptotic pathways. These findings suggest a potential structural protective signal of indirect bilirubin in renal tissue, while highlighting the need for further studies to clarify underlying mechanisms and functional relevance.</p>

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Indirect bilirubin mitigates tubular vacuolization and injury in experimental contrast nephropathy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月5日

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  • Fatih Ünal,
  • Mehmet Timur Selçuk,
  • Samet Ece,
  • Şefika Karabulut,
  • Candan Altuntaş,
  • Sevil Atalay Vural

摘要

Contrast-associated acute kidney injury (CA-AKI) remains a clinically relevant complication of intravascular contrast media use, involving complex and incompletely understood mechanisms including oxidative stress, inflammation, apoptosis, and vasomotor dysregulation. Indirect bilirubin has been proposed as a potential cytoprotective molecule due to its antioxidant and anti-inflammatory properties. In this experimental study, twenty-four male Wistar albino rats were randomized into three groups: sham, contrast nephropathy (CN), and contrast nephropathy treated with indirect bilirubin (CNIB). CA-AKI was induced using indomethacin, Nω-Nitro-L-Arginin-Methylester (L-NAME), and iodinated contrast media. Indirect bilirubin (30 mg/kg, intraperitoneal [i.p.]) was administered after injury induction. Renal function was assessed using serum creatinine (SCR), blood urea nitrogen (BUN), and urinary parameters. Histopathological injury was evaluated using semi-quantitative tubular damage scoring, and molecular analyses included inflammatory, apoptotic, and anti-apoptotic markers. Contrast media administration induced significant impairment in renal function and marked tubular injury compared with sham animals. Indirect bilirubin administration was associated with a reduction in histological tubular damage and vacuolization compared to untreated CA-AKI animals. However, improvements in Scr, BUN, and urinary indices did not reach statistical significance. In addition, expression patterns of inflammatory and apoptotic markers were inconsistent between functional, histological, and molecular outcomes, and did not uniformly support a classical anti-inflammatory or anti-apoptotic mechanism. Indirect bilirubin was associated with attenuation of histological renal injury in an experimental model of contrast-associated acute kidney injury; however, this effect was not accompanied by consistent functional improvement or coherent modulation of inflammatory and apoptotic pathways. These findings suggest a potential structural protective signal of indirect bilirubin in renal tissue, while highlighting the need for further studies to clarify underlying mechanisms and functional relevance.