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Review
. 2024 Aug 29;37(6):938-944.
doi: 10.1080/08998280.2024.2395765. eCollection 2024.

Current updates in radiocontrast-associated acute kidney injury

Affiliations
Review

Current updates in radiocontrast-associated acute kidney injury

Mohammed Mahgoub et al. Proc (Bayl Univ Med Cent). .

Abstract

Contrast-associated acute kidney injury (CA-AKI) is an abrupt decline in kidney function occurring after a recent exposure to iodinated radiocontrast media. CA-AKI presents as elevated serum creatinine level or decreased urine output. CA-AKI is the third leading cause of inpatient AKI. The incidence of CA-AKI varies according to patient population characteristics, ranging from 5% in the general population to as high as 30% in special populations with preexisting comorbidities such as diabetes mellitus, cardiovascular disease, and chronic kidney disease. The development of CA-AKI places a heavy toll on patients and the healthcare system secondary to increased patient morbidity, mortality, hospital length of stay, readmission risk, and healthcare cost. Patients undergoing cardiac catheterization are of special interest, since they have higher risk of developing CA-AKI and its associated complications. The recognition, prevention, and management of CA-AKI has improved over the past few years with the introduction of fluid management guidelines, using less nephrotoxic radiocontrast media, and preprocedural CA-AKI risk assessment. Future advancements in patients' CA-AKI risk stratification and early detection will facilitate prompt initiation of mitigation treatment plans and decrease associated complications.

Keywords: Acute kidney injury; contrast media; contrast tubular injury; urine tubular biomarkers.

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Conflict of interest statement

The authors report no funding or conflicts of interest.

Figures

Figure 1.
Figure 1.
An x-ray nephrogram obtained 24 hours after contrast administration, showcasing the persistence of contrast within the kidneys due to the accumulation of contrast media in the renal parenchyma.
Figure 2.
Figure 2.
Proposed radiocontrast-mediated nephron injury sites and mechanisms.

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