Patients with Different Stages of Chronic Kidney Disease Undergoing Intravenous Contrast-Enhanced Computed Tomography-The Incidence of Contrast-Associated Acute Kidney Injury

Ming-Ju Wu, Shang-Feng Tsai, Ming-Ju Wu, Shang-Feng Tsai

Abstract

Introduction: Iodinated contrast medium (CM) is the third most common cause of acute kidney injury (AKI). However, the association is poorly known between the definitions of AKI between different stages of chronic kidney disease after intravenous CM administration. Methods: The dataset, covering a period of ~15 years (1 June 2008 to 31 March 2015), consisted of 20,018 non-dialytic adult patients who had received intravenous injections of non-ionic iso-osmolar CM, iodixanol, for enhanced computed tomography imaging. Contrast-associated AKI (CA-AKI), dialysis-required AKI, and mortality were analyzed. Results: A total of 12,271 participants were enrolled. CA-AKI increased significantly starting from stage 3A onward (p < 0.001). In summary, incidences of CA-AKI against different levels of chronic kidney disease were as follows: stage 1 (8.3%) = stage 2 (6.7%) < stage 3A (9.9%) < stage 3B (14.3%) < stage 4 (20.5%) = stage 5 (20.4%). The incidences of dialysis within 30 days were as follows: stage 1 (1%) = stage 2 (1.4%) = stage 3A (2.7%) < stage 3B (5.7%) < stage 4 (18%) < stage 5 (54.1%). The prediction of dialysis was good based on the baseline serum creatinine > 1.5 mg/dL (72.78% of sensitivity, 86.07% of specificity, 0.851 of area under curve) or baseline estimated glomerular filtration rate ≤ 38.49 mL/min/1.732 m2 (70.19% of sensitivity, 89.08% of specificity, 0.853 of area under curve). In multivariate Cox regression analysis model for CA-AKI, independent risk factors were stage 4 chronic kidney disease (p = 0.001) and shock (p = 0.001). Conclusion: Baseline serum creatinine and estimated glomerular filtration rate were good predictors for dialysis-required AKI. CA-AKI increased significantly since stage 3A chronic kidney disease. Stage 4 and 5 chronic kidney disease have the same risk for CA-AKI, but stage 5 chronic kidney disease has markedly higher risk for dialysis.

Keywords: acute kidney injury; chronic kidney disease; computed tomography; dialysis; intravenous contrast medium; mortality.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Patients selection flow chart.
Figure 2
Figure 2
Outcomes of renal function outcomes according to baseline stages of CKD. All the three renal outcomes are significantly worse beyond the baseline renal function of stage IIIA. (A) Incidences of acute kidney injury after CCT according to baseline stages of CKD. Incidences are significant (p < 0.001) between stages I and IIIB–V; between stages II and IIIA to V; between stages IIIA and IIIB to V; and between stages IIIB and V. The increases in incidence are statistically significant starting from stage IIIA onward. Acute kidney injury after contrast computed tomography shown according to baseline stages of CKD; post hoc analysis showed p < 0.001 in I vs. IIIB, I vs. IV, I vs. V, II vs. IIIA, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IIIB, IIIA vs. IV, IIIA vs. V, and IIIB vs. IV. (B) Incidences of dialysis within 30 days after CCT shown according to baseline stages of CKD. The incidence was significantly different (p < 0.001) between stages I and IIIA to V; between stages II and IIIB to V; between stages IIIA and IIIB to V; between stages IIIB and IV to V; between stages IV and V. The incidence significantly increased from stage IIIA onward. Dialysis within 30 days after contrast computed tomography shown according to baseline stages of CKD, Post hoc analysis showed p < 0.001 in I vs. IIIA, I vs. IIIB, I vs. IV, I vs. V, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IIIB, IIIA vs. IV, IIIA vs. V, IIIB vs. IV, IIIB vs. V, and IV vs. V. (C) Incidences of death within 30 days after CCT shown according to baseline stages of CKD. The incidence was significantly different (p < 0.001) between stages I and IIIA to V; between stages II and s IIIA to V; between stages IIIA and IV to V; and between stages IIIB and IV. The incidence significantly increased from stage IIIA onward. Deaths within 30 days after contrast computed tomography shown according to baseline stages of CKD. Post hoc analysis showed p < 0.001 in I vs. IIIA, I vs. IIIB, I vs. IV, I vs. V, II vs. IIIA, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IV, IIIA vs. V, and IIIB vs. IV; chi-square test, ** p < 0.01.
Figure 2
Figure 2
Outcomes of renal function outcomes according to baseline stages of CKD. All the three renal outcomes are significantly worse beyond the baseline renal function of stage IIIA. (A) Incidences of acute kidney injury after CCT according to baseline stages of CKD. Incidences are significant (p < 0.001) between stages I and IIIB–V; between stages II and IIIA to V; between stages IIIA and IIIB to V; and between stages IIIB and V. The increases in incidence are statistically significant starting from stage IIIA onward. Acute kidney injury after contrast computed tomography shown according to baseline stages of CKD; post hoc analysis showed p < 0.001 in I vs. IIIB, I vs. IV, I vs. V, II vs. IIIA, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IIIB, IIIA vs. IV, IIIA vs. V, and IIIB vs. IV. (B) Incidences of dialysis within 30 days after CCT shown according to baseline stages of CKD. The incidence was significantly different (p < 0.001) between stages I and IIIA to V; between stages II and IIIB to V; between stages IIIA and IIIB to V; between stages IIIB and IV to V; between stages IV and V. The incidence significantly increased from stage IIIA onward. Dialysis within 30 days after contrast computed tomography shown according to baseline stages of CKD, Post hoc analysis showed p < 0.001 in I vs. IIIA, I vs. IIIB, I vs. IV, I vs. V, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IIIB, IIIA vs. IV, IIIA vs. V, IIIB vs. IV, IIIB vs. V, and IV vs. V. (C) Incidences of death within 30 days after CCT shown according to baseline stages of CKD. The incidence was significantly different (p < 0.001) between stages I and IIIA to V; between stages II and s IIIA to V; between stages IIIA and IV to V; and between stages IIIB and IV. The incidence significantly increased from stage IIIA onward. Deaths within 30 days after contrast computed tomography shown according to baseline stages of CKD. Post hoc analysis showed p < 0.001 in I vs. IIIA, I vs. IIIB, I vs. IV, I vs. V, II vs. IIIA, II vs. IIIB, II vs. IV, II vs. V, IIIA vs. IV, IIIA vs. V, and IIIB vs. IV; chi-square test, ** p < 0.01.
Figure 3
Figure 3
Once patients had developed post-CCT AKI, they more likely died (33.3% vs. 7.9%, p < 0.001). Similarly, once patients started with dialysis after CCT, they more likely died (32.7% vs. 9.3%, p < 0.001). The association between mortality within 30 days and AKI or dialysis within 30 days. Chi-square test, ** p < 0.01.
Figure 4
Figure 4
The predictive value of baseline serum creatinine (SCr) and eGFR to acute kidney injury and dialysis within 30 days after CCT. (A) The baseline serum creatinine (SCr) (>1.3 mg/dL) to predicting post-CCT AKI showed rather low sensitivity (36.73%) and high specificity (78.92%). The AUC was only 0.555. (B) The baseline eGFR (≤57.18 mL/min/1.732 m2) in predicting post-CCT AKI showed rather low sensitivity (43.17%) and high specificity (73.69%). The AUC was only 0.563. The baseline eGFR in predicting post-CCT AKI. (C) The baseline serum creatinine (SCr) (>1.5 mg/dL) in predicting dialysis within 30 days after CCT showed high sensitivity (72.78%) and high specificity (86.07%). The AUC was up to 0.851. The baseline serum creatinine (Scr) in predicting dialysis within 30 days after CCT. (D) The baseline eGFR (≤38.49 mL/min/1.732 m2) in predicting dialysis within 30 days after CCT showed high sensitivity (70.19%) and high specificity (89.08%). The AUC was up to 0.853. The baseline eGFR in predicting dialysis within 30 days after CCT.
Figure 4
Figure 4
The predictive value of baseline serum creatinine (SCr) and eGFR to acute kidney injury and dialysis within 30 days after CCT. (A) The baseline serum creatinine (SCr) (>1.3 mg/dL) to predicting post-CCT AKI showed rather low sensitivity (36.73%) and high specificity (78.92%). The AUC was only 0.555. (B) The baseline eGFR (≤57.18 mL/min/1.732 m2) in predicting post-CCT AKI showed rather low sensitivity (43.17%) and high specificity (73.69%). The AUC was only 0.563. The baseline eGFR in predicting post-CCT AKI. (C) The baseline serum creatinine (SCr) (>1.5 mg/dL) in predicting dialysis within 30 days after CCT showed high sensitivity (72.78%) and high specificity (86.07%). The AUC was up to 0.851. The baseline serum creatinine (Scr) in predicting dialysis within 30 days after CCT. (D) The baseline eGFR (≤38.49 mL/min/1.732 m2) in predicting dialysis within 30 days after CCT showed high sensitivity (70.19%) and high specificity (89.08%). The AUC was up to 0.853. The baseline eGFR in predicting dialysis within 30 days after CCT.
Figure 4
Figure 4
The predictive value of baseline serum creatinine (SCr) and eGFR to acute kidney injury and dialysis within 30 days after CCT. (A) The baseline serum creatinine (SCr) (>1.3 mg/dL) to predicting post-CCT AKI showed rather low sensitivity (36.73%) and high specificity (78.92%). The AUC was only 0.555. (B) The baseline eGFR (≤57.18 mL/min/1.732 m2) in predicting post-CCT AKI showed rather low sensitivity (43.17%) and high specificity (73.69%). The AUC was only 0.563. The baseline eGFR in predicting post-CCT AKI. (C) The baseline serum creatinine (SCr) (>1.5 mg/dL) in predicting dialysis within 30 days after CCT showed high sensitivity (72.78%) and high specificity (86.07%). The AUC was up to 0.851. The baseline serum creatinine (Scr) in predicting dialysis within 30 days after CCT. (D) The baseline eGFR (≤38.49 mL/min/1.732 m2) in predicting dialysis within 30 days after CCT showed high sensitivity (70.19%) and high specificity (89.08%). The AUC was up to 0.853. The baseline eGFR in predicting dialysis within 30 days after CCT.
Figure 4
Figure 4
The predictive value of baseline serum creatinine (SCr) and eGFR to acute kidney injury and dialysis within 30 days after CCT. (A) The baseline serum creatinine (SCr) (>1.3 mg/dL) to predicting post-CCT AKI showed rather low sensitivity (36.73%) and high specificity (78.92%). The AUC was only 0.555. (B) The baseline eGFR (≤57.18 mL/min/1.732 m2) in predicting post-CCT AKI showed rather low sensitivity (43.17%) and high specificity (73.69%). The AUC was only 0.563. The baseline eGFR in predicting post-CCT AKI. (C) The baseline serum creatinine (SCr) (>1.5 mg/dL) in predicting dialysis within 30 days after CCT showed high sensitivity (72.78%) and high specificity (86.07%). The AUC was up to 0.851. The baseline serum creatinine (Scr) in predicting dialysis within 30 days after CCT. (D) The baseline eGFR (≤38.49 mL/min/1.732 m2) in predicting dialysis within 30 days after CCT showed high sensitivity (70.19%) and high specificity (89.08%). The AUC was up to 0.853. The baseline eGFR in predicting dialysis within 30 days after CCT.

References

    1. Mohammed N.M., Mahfouz A., Achkar K., Rafie I.M., Hajar R. Contrast-induced Nephropathy. Heart Views. 2013;14:106–116. doi: 10.4103/1995-705X.125926.
    1. Hsu C.Y., Ordonez J.D., Chertow G.M., Fan D., McCulloch C.E., Go A.S. The risk of acute renal failure in patients with chronic kidney disease. Kidney Int. 2008;74:101–107. doi: 10.1038/ki.2008.107.
    1. Gansevoort R.T., Matsushita K., van der Velde M., Astor B.C., Woodward M., Levey A.S., de Jong P.E., Coresh J. Lower estimated GFR and higher albuminuria are associated with adverse kidney outcomes. A collaborative meta-analysis of general and high-risk population cohorts. Kidney Int. 2011;80:93–104. doi: 10.1038/ki.2010.531.
    1. Patschan D., Muller G.A. Acute Kidney Injury, AKI-Update 2018. Dtsch. Med. Wochenschr. 2018;143:1094–1096. doi: 10.1055/a-0523-4571.
    1. McDonald J.S., McDonald R.J., Tran C.L., Kolbe A.B., Williamson E.E., Kallmes D.F. Postcontrast Acute Kidney Injury in Pediatric Patients: A Cohort Study. Am. J. Kidney Dis. Off. J. Natl. Kidney Found. 2018;72:811–818. doi: 10.1053/j.ajkd.2018.05.014.
    1. Hossain M.A., Costanzo E., Cosentino J., Patel C., Qaisar H., Singh V., Khan T., Cheng J.S., Asif A., Vachharajani T.J. Contrast-induced nephropathy: Pathophysiology, risk factors, and prevention. Saudi J. Kidney Dis. Transplant. Off. Publ. Saudi Cent. Organ Transplant. Saudi Arab. 2018;29:1–9. doi: 10.4103/1319-2442.225199.
    1. Pistolesi V., Regolisti G., Morabito S., Gandolfini I., Corrado S., Piotti G., Fiaccadori E. Contrast medium induced acute kidney injury: A narrative review. J. Nephrol. 2018;31:797–812. doi: 10.1007/s40620-018-0498-y.
    1. Pannu N. In patients with CKD having CT with contrast media, no prehydration and prehydration did not differ for AKI. Ann. Intern. Med. 2020;173:Jc8. doi: 10.7326/ACPJ202007210-009.
    1. Rudnick M.R., Wahba I.M., Leonberg-Yoo A.K., Miskulin D., Litt H.I. Risks and Options with Gadolinium-Based Contrast Agents in Patients with CKD: A Review. Am. J. Kidney Dis. 2021;77:517–528. doi: 10.1053/j.ajkd.2020.07.012.
    1. Hinson J.S., Ehmann M.R., Fine D.M., Fishman E.K., Toerper M.F., Rothman R.E., Klein E.Y. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann. Emerg. Med. 2017;69:577–586.e574. doi: 10.1016/j.annemergmed.2016.11.021.
    1. Stacul F., van der Molen A.J., Reimer P., Webb J.A., Thomsen H.S., Morcos S.K., Almen T., Aspelin P., Bellin M.F., Clement O., et al. Contrast induced nephropathy: Updated ESUR Contrast Media Safety Committee guidelines. Eur. Radiol. 2011;21:2527–2541. doi: 10.1007/s00330-011-2225-0.
    1. Okusa M.D., Davenport A. Reading between the (guide)lines–the KDIGO practice guideline on acute kidney injury in the individual patient. Kidney Int. 2014;85:39–48. doi: 10.1038/ki.2013.378.
    1. van der Molen A.J., Reimer P., Dekkers I.A., Bongartz G., Bellin M.F., Bertolotto M., Clement O., Heinz-Peer G., Stacul F., Webb J.A.W., et al. Post-contrast acute kidney injury-Part 1: Definition, clinical features, incidence, role of contrast medium and risk factors: Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur. Radiol. 2018;28:2845–2855. doi: 10.1007/s00330-017-5246-5.
    1. Luk L., Steinman J., Newhouse J.H. Intravenous Contrast-Induced Nephropathy-The Rise and Fall of a Threatening Idea. Adv. Chronic Kidney Dis. 2017;24:169–175. doi: 10.1053/j.ackd.2017.03.001.
    1. Goldfarb S., Spinler S., Berns J.S., Rudnick M.R. Low-osmolality contrast media and the risk of contrast-associated nephrotoxicity. Investig. Radiol. 1993;28((Suppl. S5)) doi: 10.1097/00004424-199311001-00003.
    1. Thomsen H.S., Morcos S.K. Contrast media and the kidney: European Society of Urogenital Radiology (ESUR) guidelines. Br. J. Radiol. 2003;76:513–518. doi: 10.1259/bjr/26964464.
    1. van der Molen A.J., Reimer P., Dekkers I.A., Bongartz G., Bellin M.F., Bertolotto M., Clement O., Heinz-Peer G., Stacul F., Webb J.A.W., et al. Post-contrast acute kidney injury. Part 2: Risk stratification, role of hydration and other prophylactic measures, patients taking metformin and chronic dialysis patients: Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur. Radiol. 2018;28:2856–2869. doi: 10.1007/s00330-017-5247-4.
    1. McDonald J.S., McDonald R.J., Lieske J.C., Carter R.E., Katzberg R.W., Williamson E.E., Kallmes D.F. Risk of Acute Kidney Injury, Dialysis, and Mortality in Patients with Chronic Kidney Disease After Intravenous Contrast Material Exposure. Mayo Clin. Proc. 2015;90:1046–1053. doi: 10.1016/j.mayocp.2015.05.016.
    1. Mitchell A.M., Jones A.E., Tumlin J.A., Kline J.A. Incidence of contrast-induced nephropathy after contrast-enhanced computed tomography in the outpatient setting. Clin. J. Am. Soc. Nephrol. CJASN. 2010;5:4–9. doi: 10.2215/CJN.05200709.
    1. Nyman U., Aspelin P., Jakobsen J., Bjork J. Controversies in Contrast Material-induced Acute Kidney Injury: Propensity Score Matching of Patients with Different Dose/Absolute Glomerular Filtration Rate Ratios. Radiology. 2015;277:633–637. doi: 10.1148/radiol.2015151341.
    1. Levey A.S., Coresh J., Greene T., Stevens L.A., Zhang Y.L., Hendriksen S., Kusek J.W., Van Lente F., Chronic Kidney Disease Epidemiology C. Using standardized serum creatinine values in the modification of diet in renal disease study equation for estimating glomerular filtration rate. Ann. Intern. Med. 2006;145:247–254. doi: 10.7326/0003-4819-145-4-200608150-00004.
    1. Davenport M.S., Khalatbari S., Cohan R.H., Dillman J.R., Myles J.D., Ellis J.H. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: Risk stratification by using estimated glomerular filtration rate. Radiology. 2013;268:719–728. doi: 10.1148/radiol.13122276.
    1. McDonald J.S., McDonald R.J., Carter R.E., Katzberg R.W., Kallmes D.F., Williamson E.E. Risk of intravenous contrast material-mediated acute kidney injury: A propensity score-matched study stratified by baseline-estimated glomerular filtration rate. Radiology. 2014;271:65–73. doi: 10.1148/radiol.13130775.
    1. Rich M.W., Crecelius C.A. Incidence, risk factors, and clinical course of acute renal insufficiency after cardiac catheterization in patients 70 years of age or older. A prospective study. Arch. Intern. Med. 1990;150:1237–1242. doi: 10.1001/archinte.1990.00390180067011.
    1. Rudnick M.R., Berns J.S., Cohen R.M., Goldfarb S. Nephrotoxic risks of renal angiography: Contrast media-associated nephrotoxicity and atheroembolism--a critical review. Am. J. Kidney Dis. 1994;24:713–727. doi: 10.1016/S0272-6386(12)80235-6.
    1. Abe M., Morimoto T., Akao M., Furukawa Y., Nakagawa Y., Shizuta S., Ehara N., Taniguchi R., Doi T., Nishiyama K., et al. Relation of contrast-induced nephropathy to long-term mortality after percutaneous coronary intervention. Am. J. Cardiol. 2014;114:362–368. doi: 10.1016/j.amjcard.2014.05.009.
    1. Kroneberger C., Enzweiler C.N., Schmidt-Lucke A., Ruckert R.I., Teichgraber U., Franiel T. Contrast-induced nephropathy in patients with chronic kidney disease and peripheral arterial disease. Acta Radiol. Open. 2015;4:815–821. doi: 10.1177/2058460115583034.
    1. Modi K., Gupta M. StatPearls. StatPearls Publishing LLC; Treasure Island, FL, USA: 2019. Contrast-Induced Nephropathy.
    1. Aycock R.D., Westafer L.M., Boxen J.L., Majlesi N., Schoenfeld E.M., Bannuru R.R. Acute Kidney Injury After Computed Tomography: A Meta-analysis. Ann. Emerg. Med. 2018;71:44–53.e44. doi: 10.1016/j.annemergmed.2017.06.041.
    1. Bruce R.J., Djamali A., Shinki K., Michel S.J., Fine J.P., Pozniak M.A. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am. J. Roentgenol. 2009;192:711–718. doi: 10.2214/AJR.08.1413.
    1. Murakami R., Hayashi H., Sugizaki K., Yoshida T., Okazaki E., Kumita S., Owan C. Contrast-induced nephropathy in patients with renal insufficiency undergoing contrast-enhanced MDCT. Eur. Radiol. 2012;22:2147–2152. doi: 10.1007/s00330-012-2473-7.
    1. McDonald R.J., McDonald J.S., Carter R.E., Hartman R.P., Katzberg R.W., Kallmes D.F., Williamson E.E. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology. 2014;273:714–725. doi: 10.1148/radiol.14132418.
    1. Tublin M.E., Murphy M.E., Tessler F.N. Current concepts in contrast media-induced nephropathy. AJR Am. J. Roentgenol. 1998;171:933–939. doi: 10.2214/ajr.171.4.9762972.
    1. Chaudhury P., Armanyous S., Harb S.C., Ferreira Provenzano L., Ashour T., Jolly S.E., Arrigain S., Konig V., Schold J.D., Navaneethan S.D., et al. Intra-Arterial versus Intravenous Contrast and Renal Injury in Chronic Kidney Disease: A Propensity-Matched Analysis. Nephron. 2019;141:31–40. doi: 10.1159/000494047.
    1. Poston J.T., Koyner J.L. Sepsis associated acute kidney injury. Bmj. 2019;364:k4891. doi: 10.1136/bmj.k4891.
    1. Cook A.M., Hatton-Kolpek J. Augmented Renal Clearance. Pharmacotherapy. 2019;39:346–354. doi: 10.1002/phar.2231.
    1. Goldstein S.L. Medication-induced acute kidney injury. Curr. Opin. Crit. Care. 2016;22:542–545. doi: 10.1097/MCC.0000000000000355.
    1. Yang B., Xie Y., Guo M., Rosner M.H., Yang H., Ronco C. Nephrotoxicity and Chinese Herbal Medicine. Clin. J. Am. Soc. Nephrol. CJASN. 2018;13:1605–1611. doi: 10.2215/CJN.11571017.
    1. Parikh C.R., Liu C., Mor M.K., Palevsky P.M., Kaufman J.S., Thiessen Philbrook H., Weisbord S.D. Kidney Biomarkers of Injury and Repair as Predictors of Contrast-Associated AKI: A Substudy of the PRESERVE Trial. Am. J. Kidney Dis. 2020;75:187–194. doi: 10.1053/j.ajkd.2019.06.011.
    1. Eftekhari A., Maleki Dizaj S., Ahmadian E., Przekora A., Hosseiniyan Khatibi S.M., Ardalan M., Zununi Vahed S., Valiyeva M., Mehraliyeva S., Khalilov R., et al. Application of Advanced Nanomaterials for Kidney Failure Treatment and Regeneration. Materials. 2021;14:2939. doi: 10.3390/ma14112939.

Source: PubMed

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