Predictors for Irreversibility of Contrast-Induced Acute Kidney Injury in Patients with Obesity After Contrast-Enhanced Computed Tomography Coronary Angiography

Overview

Journal Adv Ther

Date 2024 Nov 11

PMID 39527336

Authors

Tetiana A Berezina

Oleksandr O Berezin

Michael Lichtenauer

Alexander E Berezin

Affiliations

Soon will be listed here.

Abstract

Introduction: Although contrast-induced (CI) acute kidney injury (AKI) is a common complication in high-risk individuals requiring evaluation with contrast-enhanced angiography, the possible predictors of CI-AKI in patients with obesity are not fully understood. The aim of this study was to elucidate plausible factors associated with the irreversibility of CI-AKI in individuals with obesity undergoing contrast-enhanced computed tomography coronary angiography.

Methods: A total of 96 adult patients with obesity and the KDIGO criteria of CI-AKI (increase of serum levels of creatinine ≥ 25% or ≥ 500 µmol/L at 48 h after procedure) were retrospectively screened from the cohort of 1833 patients who underwent iodine contrast medium (ICM)-enhanced computed tomography coronary angiography, and were included in the study. The patients were divided into two cohorts: 96 adult patients with obesity and recovery of CI-AKI in 7 days after initiating of the event, and 57 individuals with irreversibility of CI-AKI. Serum concentrations of conventional biochemistry and urine biomarkers [i.e., hemoglobin, creatinine, high-sensitivity C-reactive protein, urinary albumin/creatinine ratio (UACR)] as well as natriuretic peptide, adropin, apelin, irisin, tumor necrosis factor-alpha (TNF-alpha), were determined at baseline. The levels of creatinine were measured at baseline, at the event, and in 7 days after the event.

Results: We identified 12 variables, which were associated with irreversibility of CI-AKI: age > 75 years [odds ratio (OR) = 1.22. P = 0.001], male gender (OR = 1.03, P = 0.042), stable coronary artery disease (OR = 1.06, P = 0.048), chronic kidney disease (CKD) 1-3 grade (OR = 1.60, P = 0.001), heart failure with preserved ejection fraction (HFpEF) (OR = 1.07, P = 0.046), baseline estimated GFR < 80 mL/min/1.73 m (OR = 1.10, P = 0.040), UACR > 17.5 mg/g Cr (OR = 1.05, P = 0.048), TNF-alpha > 3.11 pg/mL (OR = 1.12, P = 0.001), and adropin < 2.43 ng/mL (OR = 1.18, P = 0.001). After adjustment for CKD and UACR > 17.5 mg/g Cr, only HFpEF (OR = 1.06, P = 0.042) and adropin < 2.43 ng/mL (OR = 1.11, P = 0.001) remained independent predictors of CI-AKI irreversibility. Yet, adropin < 2.43 ng/mL at baseline exerted sufficiently better predictive ability than both HFpEF and preexisting CKD 1-3 grade.

Conclusion: In a multivariate prediction model adjusted for CKD and urinary albumin/creatinine ratio > 17.5 mg/g Cr, low levels of adropin (< 2.43 ng/mL) in individuals with non-morbid obesity together with the presence of HFpEF were independent predictors of CI-AKI irreversibility after ICM-enhanced computed tomography coronary angiography.

References

Mehta R, Cerda J, Burdmann E, Tonelli M, Garcia-Garcia G, Jha V . International Society of Nephrology's 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): a human rights case for nephrology. Lancet. 2015; 385(9987):2616-43. DOI: 10.1016/S0140-6736(15)60126-X. View

Haq M, Yip C, Arora P . The conundrum of contrast-induced acute kidney injury. J Thorac Dis. 2020; 12(4):1721-1727. PMC: 7212164. DOI: 10.21037/jtd.2019.12.88. View

Kimachi M, Ikenoue T, Fukuma S . Prevalent and new use of common drugs for the incidence of community-acquired acute kidney injury: cohort and case-crossover study. Sci Rep. 2024; 14(1):17906. PMC: 11297046. DOI: 10.1038/s41598-024-66532-w. View

Ma M, Wan X, Gao M, Pan B, Chen D, Sun Q . Renin-angiotensin-aldosterone system blockade is associated with higher risk of contrast-induced acute kidney injury in patients with diabetes. Aging (Albany NY). 2020; 12(7):5858-5877. PMC: 7185147. DOI: 10.18632/aging.102982. View

Lee S, Zhuo H, Zhang Y, Dahl N, Dardik A, Ochoa Chaar C . Risk factors and safe contrast volume thresholds for postcontrast acute kidney injury after peripheral vascular interventions. J Vasc Surg. 2019; 72(2):603-610.e1. DOI: 10.1016/j.jvs.2019.09.059. View

Li Y, Wang J . Contrast-induced acute kidney injury: a review of definition, pathogenesis, risk factors, prevention and treatment. BMC Nephrol. 2024; 25(1):140. PMC: 11034108. DOI: 10.1186/s12882-024-03570-6. View

Kabeer M, Cross J, Hamilton G, Rashid S . Obesity as a Risk Factor for Radiographic Contrast-Induced Nephropathy. Angiology. 2020; 72(3):274-278. PMC: 7859667. DOI: 10.1177/0003319720969536. View

Mironova O, Staroverov I, Sivakova O, Deev A, Fomin V . [Contrast-induced acute kidney injury in chronic coronary artery disease patients with diabetes mellitus and obesity]. Ter Arkh. 2020; 92(10):29-33. DOI: 10.26442/00403660.2020.10.000753. View

Safley D, Salisbury A, Tsai T, Secemsky E, Kennedy K, Rogers R . Acute Kidney Injury Following In-Patient Lower Extremity Vascular Intervention: From the National Cardiovascular Data Registry. JACC Cardiovasc Interv. 2021; 14(3):333-341. PMC: 8076888. DOI: 10.1016/j.jcin.2020.10.028. View

10.

Jaipaul N, Manalo R, Sadjadi S, McMillan J . Obesity is not associated with contrast nephropathy. Ther Clin Risk Manag. 2010; 6:213-7. PMC: 2878954. DOI: 10.2147/tcrm.s10198. View

11.

Prasad A, Ortiz-Lopez C, Khan A, Levin D, Kaye D . Acute kidney injury following peripheral angiography and endovascular therapy: A systematic review of the literature. Catheter Cardiovasc Interv. 2016; 88(2):264-73. DOI: 10.1002/ccd.26466. View

12.

Kusirisin P, Chattipakorn S, Chattipakorn N . Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches. J Transl Med. 2020; 18(1):400. PMC: 7576747. DOI: 10.1186/s12967-020-02574-8. View

13.

Heyman S, Rosen S, Khamaisi M, Idee J, Rosenberger C . Reactive oxygen species and the pathogenesis of radiocontrast-induced nephropathy. Invest Radiol. 2010; 45(4):188-95. DOI: 10.1097/RLI.0b013e3181d2eed8. View

14.

Andreucci M, Faga T, Pisani A, Sabbatini M, Russo D, Michael A . Prevention of contrast-induced nephropathy through a knowledge of its pathogenesis and risk factors. ScientificWorldJournal. 2014; 2014:823169. PMC: 4266998. DOI: 10.1155/2014/823169. View

15.

Kawai T, Autieri M, Scalia R . Adipose tissue inflammation and metabolic dysfunction in obesity. Am J Physiol Cell Physiol. 2020; 320(3):C375-C391. PMC: 8294624. DOI: 10.1152/ajpcell.00379.2020. View

16.

An S, Cho S, Yoon J . Adipose Tissue and Metabolic Health. Diabetes Metab J. 2023; 47(5):595-611. PMC: 10555533. DOI: 10.4093/dmj.2023.0011. View

17.

Marcelin G, Silveira A, Martins L, Ferreira A, Clement K . Deciphering the cellular interplays underlying obesity-induced adipose tissue fibrosis. J Clin Invest. 2019; 129(10):4032-4040. PMC: 6763252. DOI: 10.1172/JCI129192. View

18.

Crewe C, An Y, Scherer P . The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. J Clin Invest. 2017; 127(1):74-82. PMC: 5199684. DOI: 10.1172/JCI88883. View

19.

Berezina T, Fushtey I, Berezin A, Pavlov S, Berezin A . Predictors of Kidney Function Outcomes and Their Relation to SGLT2 Inhibitor Dapagliflozin in Patients with Type 2 Diabetes Mellitus Who Had Chronic Heart Failure. Adv Ther. 2023; 41(1):292-314. PMC: 10796534. DOI: 10.1007/s12325-023-02683-y. View

20.

Maak S, Norheim F, Drevon C, Erickson H . Progress and Challenges in the Biology of FNDC5 and Irisin. Endocr Rev. 2021; 42(4):436-456. PMC: 8284618. DOI: 10.1210/endrev/bnab003. View