Abstract
Objective: The mechanisms of contrast-induced nephropathy are not fully understood and sensitive biomarkers of contrast-induced nephropathy are yet to be found. We investigated whether urinary fibrinogen could be a potential biomarker for contrast-induced nephropathy. Methods: To create a contrast-induced nephropathy model, mice received a prostaglandin synthesis inhibitor (indomethacin) and a nitric oxide synthase inhibitor (Nω-Nitro-L-arginine methyl ester) intraperitoneally followed by a different dose of iodixanol. In the control group, normal saline was administered. Urinary fibrinogen and serum creatinine were analyzed using enzyme-linked immunosorbent assay. Kidneys were used to quantify fibrinogen using qRT-PCR and Western blot and for histopathological examination. Results: Histopathological examination demonstrated mild renal injury in the low-dose group, and moderate renal injury in the high-dose group. Urinary fibrinogen levels were significantly increased in an iodixanol dose-dependent manner (control vs. low-dose group, P < 0.05; control vs. high-dose group P < 0.01). Serum creatinine levels were only increased in the high-dose group (P < 0.01 compared to control), but not in the low-dose group. For fibrinogen-gene expression, in the low-dose group, Fgγ increased (qRT-PCR, Western blot, P < 0.05) in the high-dose group, Fgβ and Fgγ decreased (qRT-PCR, P < 0.01; Western blot, P < 0.05), and Fgα increased (qRT-PCR, P < 0.05; Western blot, P < 0.05). Conclusions: We propose that urinary fibrinogen could be used as a potential biomarker for early contrast-induced nephropathy diagnosis.
Original language | English (US) |
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Pages (from-to) | 273-278 |
Number of pages | 6 |
Journal | Vascular |
Volume | 24 |
Issue number | 3 |
DOIs | |
State | Published - Jun 2016 |
Externally published | Yes |
Keywords
- Acute kidney injury
- contrast-induced nephropathy
- fibrinogen
- renal failure
ASJC Scopus subject areas
- Surgery
- Radiology Nuclear Medicine and imaging
- Cardiology and Cardiovascular Medicine