ArticleBMC nephrology2026
Indirect bilirubin mitigates tubular vacuolization and injury in experimental contrast nephropathy.
Article in BMC nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.