Incidences of and risk factors for clinical and subclinical contrast-associated acute kidney injury in patients who underwent neuroendovascular surgery

Author:

Mitaka Chieko1ORCID,Teranishi Kohsuke2,Wakita Mitsuru3,Misawa Shigeki4,Nojiri Shuko5,Satoh Daizoh1,Hayashida Masakazu1

Affiliation:

1. Department of Anesthesiology and Pain Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan

2. Department of Neurosurgery, Juntendo University Graduate School of Medicine, Tokyo, Japan

3. Department of Clinical Laboratory, Juntendo University Hospital, Tokyo, Japan

4. Department of Clinical Laboratory Technology, Faculty Medical Science, Juntendo University, Tokyo, Japan

5. Medical Technology Innovation Center, Juntendo University, Tokyo, Japan

Abstract

Background Contrast-associated acute kidney injury (CA-AKI) can develop after intravascular administration of iodinated contrast media. Neutrophil gelatinase-associated lipocalin (NGAL) is an early marker for AKI that helps to detect subclinical CA-AKI. We investigated the incidence of and risk factors for clinical and subclinical CA-AKI in patients who underwent neuroendovascular surgery. Methods We retrospectively investigated 228 patients who underwent neuroendovascular surgery in 2020. Changes in serum creatinine and urine output were used to detect clinical CA-AKI. Urine NGAL concentration was used to detect subclinical CA-AKI in 67 out of 228 patients. Results In 228 patients, serum creatinine, hemoglobin, hematocrit, total protein, and blood urea nitrogen (BUN) decreased significantly ( p < 0.001) after surgery. However, serum creatinine decreased less significantly ( p < 0.05) than hemoglobin, hematocrit, total protein, and BUN on postoperative Day 3. Two patients out of 228 developed clinical CA-AKI, and seven patients out of 67 with urine NGAL measurements developed subclinical CA-AKI. Multivariate regression analysis revealed that diabetes mellitus and carotid artery stenosis were significantly ( p < 0.05) associated with the development of clinical and/or subclinical CA-AKI. Conclusion There was a large difference between the incidences of clinical CA-AKI (0.88%) and subclinical CA-AKI (10.4%). The difference might have primarily resulted from the different sensitivities between serum creatinine and urine NGAL and possibly from underestimation of the incidence of clinical AKI due to a postoperative decrease in serum creatinine caused by hemodilution. In addition to diabetes mellitus, carotid artery stenosis could also be a risk factor for CA-AKI.

Publisher

SAGE Publications

Subject

Neurology (clinical),Radiology, Nuclear Medicine and imaging,General Medicine

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