TY - JOUR
T1 - Postangiography increases in serum creatinine and biomarkers of injury and repair
AU - Liu, Caroline
AU - Mor, Maria K.
AU - Palevsky, Paul M.
AU - Kaufman, James S.
AU - Philbrook, Heather Thiessen
AU - Weisbord, Steven D.
AU - Parikh, Chirag R.
N1 - Funding Information:
M. Mor reports receiving grants from the National Institutes of Health during the conduct of the study. P. Palevsky receives consulting fees and advisory committee fees from Durect, Health-Span Dx, and Novartis; serves on the Data and Safety Monitoring Board of Baxter; serves as a member of an end point adjudication committee from GE Healthcare; and reports receiving grants from BioPorto and Dascena outside the submitted work. C. Parikh has received consulting fees from Renalytix; serves on the Data and Safety Monitoring Board of Genfit; reports receiving consulting fees from Akebia Therapeutics, Inc.; reports receiving grants from the National Institute of Diabetes and Digestive and Kidney Diseases and grants from the National Heart, Lung, and Blood Institute; and reports receiving consulting fees from Renaltix AI outside the submitted work. S. Weisbord has received consulting fees and advisory fees from Durect and Saghmos Therapeutics and reports receiving personal fees from Cytokinetics and Saghmos Therapeutics outside the submitted work. All remaining authors have nothing to disclose.
Funding Information:
This study was supported by United States Department of Veterans Affairs Office of Research and Development grant VA CSP #578 PRESERVE Trial (Principal Investigator: S.D. Weisbord; co-Principal Investigator: P.M. Palevsky), National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK098214 Biomarker Collection and Analysis in the PRESERVE Trial Cohort (Multiple Principal Investigators: S.D. Weisbord, P.M. Palevsky, and C.R. Parikh), and National Health and Medical Research Council of Australia grant 1011387. C.R. Parikh was additionally supported by George M. O?Brien Kidney Center grant P30DK079310 and National Institutes of Health grant R01HL085757. Acknowledgments Parts of this study were presented in poster form at the American Society of Nephrology Kidney Week in San Diego, California from October 23?28, 2018. The funding sourcehad no rolein the studydesign, data collection, analysis, reporting, or decision to submit for publication.
Funding Information:
This study was supported by United States Department of Veterans Affairs Office of Research and Development grant VA CSP #578 PRESERVE Trial (Principal Investigator: S.D. Weisbord; co-PrincipalInvestigator:P.M.Palevsky),NationalInstituteofDiabetes and Digestive and Kidney Diseases grant R01DK098214 Biomarker Collection and Analysis in the PRESERVE Trial Cohort (Multiple Principal Investigators: S.D. Weisbord, P.M. Palevsky, and C.R. Parikh), and National Health and Medical Research Council of Australia grant 1011387. C.R. Parikh was additionally supported by George M. O’Brien Kidney Center grant P30DK079310 and National Institutes of Health grant R01HL085757.
Publisher Copyright:
© 2020 by the American Society of Nephrology.
PY - 2020/9/7
Y1 - 2020/9/7
N2 - Background and objectives It is unknown whether iodinated contrast causes kidney parenchymal damage. Biomarkers that are more specific to nephron injury than serum creatinine may provide insight into whether contrast-associated AKI reflects tubular damage. We assessed the association between biomarker changes after contrast angiography with contrast-associated AKI and 90-day major adverse kidney events and death. Design, setting, participants, & measurements We conducted a longitudinal analysis of participants from the biomarker substudy of the Prevention of Serious Adverse Events following Angiography trial. We measured injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, IL-18) and repair (monocyte chemoattractant protein-1, uromodulin, YKL-40) proteins from plasma and urine samples at baseline and 2–4 hours postangiography. We assessed the associations between absolute changes and relative ratios of biomarkers with contrast-associated AKI and 90-day major adverse kidney events and death. Results Participants (n=922) were predominately men (97%) with diabetes (82%). Mean age was 70±8years,and eGFR was 48±13 ml/min per 1.73 m2; 73 (8%) and 60 (7%) participants experienced contrast-associated AKI and 90-day major adverse kidney events and death, respectively. No postangiography urine biomarkers were associated with contrast-associated AKI. Postangiography plasma kidney injury molecule-1 and IL-18 were significantly higher in participants with contrast-associated AKI compared with those who did not develop contrast-associated AKI: 428 (248, 745) versus 306 (179, 567) mg/dl; P=0.04 and 325 (247, 422) versus 280 (212, 366) mg/dl; P=0.009, respectively. The majority of patients did not experience an increase in urine or plasma biomarkers. Absolute changes in plasma IL-18 were comparable in participants with contrast-associated AKI (-30 [-71,-9] mg/dl) and those without contrast-associated AKI (-27 [-53,-10] mg/dl; P=0.62). Relative ratios of plasma IL-18 were alsocomparable in participants with contrast-associated AKI (0.91; 0.86, 0.97) and those without contrast-associated AKI (0.91; 0.85, 0.96; P=0.54). Conclusions The lack of significant differences in the absolute changes and relative ratios of injury and repair biomarkers by contrast-associated AKI status suggests that the majority of mild contrast-associated AKI cases may be driven by hemodynamic changes at the kidney.
AB - Background and objectives It is unknown whether iodinated contrast causes kidney parenchymal damage. Biomarkers that are more specific to nephron injury than serum creatinine may provide insight into whether contrast-associated AKI reflects tubular damage. We assessed the association between biomarker changes after contrast angiography with contrast-associated AKI and 90-day major adverse kidney events and death. Design, setting, participants, & measurements We conducted a longitudinal analysis of participants from the biomarker substudy of the Prevention of Serious Adverse Events following Angiography trial. We measured injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, IL-18) and repair (monocyte chemoattractant protein-1, uromodulin, YKL-40) proteins from plasma and urine samples at baseline and 2–4 hours postangiography. We assessed the associations between absolute changes and relative ratios of biomarkers with contrast-associated AKI and 90-day major adverse kidney events and death. Results Participants (n=922) were predominately men (97%) with diabetes (82%). Mean age was 70±8years,and eGFR was 48±13 ml/min per 1.73 m2; 73 (8%) and 60 (7%) participants experienced contrast-associated AKI and 90-day major adverse kidney events and death, respectively. No postangiography urine biomarkers were associated with contrast-associated AKI. Postangiography plasma kidney injury molecule-1 and IL-18 were significantly higher in participants with contrast-associated AKI compared with those who did not develop contrast-associated AKI: 428 (248, 745) versus 306 (179, 567) mg/dl; P=0.04 and 325 (247, 422) versus 280 (212, 366) mg/dl; P=0.009, respectively. The majority of patients did not experience an increase in urine or plasma biomarkers. Absolute changes in plasma IL-18 were comparable in participants with contrast-associated AKI (-30 [-71,-9] mg/dl) and those without contrast-associated AKI (-27 [-53,-10] mg/dl; P=0.62). Relative ratios of plasma IL-18 were alsocomparable in participants with contrast-associated AKI (0.91; 0.86, 0.97) and those without contrast-associated AKI (0.91; 0.85, 0.96; P=0.54). Conclusions The lack of significant differences in the absolute changes and relative ratios of injury and repair biomarkers by contrast-associated AKI status suggests that the majority of mild contrast-associated AKI cases may be driven by hemodynamic changes at the kidney.
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U2 - 10.2215/CJN.15931219
DO - 10.2215/CJN.15931219
M3 - Article
C2 - 32839195
AN - SCOPUS:85090505069
SN - 1555-9041
VL - 15
SP - 1240
EP - 1250
JO - Clinical Journal of the American Society of Nephrology
JF - Clinical Journal of the American Society of Nephrology
IS - 9
ER -