Table A1.
Article | Codes | Summary | Subthemes/ Themes |
Themes |
---|---|---|---|---|
(Kene et al., 2021) [20] |
High incidence of CIN: 13.2% | With reference to the pooled CIN incidence of 4.96% reported in the meta-analysis by Moos et al. (2013), values above 4.96% were categorized as high incidence of CIN. | Overall CIN Incidence | |
(Hinson et al., 2019) [23] |
High incidence of CIN: 7.2% | |||
(Mitchell & Kline, 2007) [34] | High incidence of CIN: 12% | |||
(Brito et al., 2020) [21] |
High incidence of CIN: 6.2% | |||
(Hong et al., 2016) [18] |
High incidence of CIN: 7.5% | |||
(Sinert et al., 2012) [31] |
High incidence of CIN: 5.69% | |||
(Mitchell et al., 2010 [32] |
High incidence of CIN: 11% and 6% | |||
(Cho et al., 2019) [24] |
High incidence of CIN: 6.49% | |||
(Mitchell et al., 2012) [30] |
High incidence of CIN: 14% | |||
(Huang et al., 2013) [28] |
High incidence of CIN: 8.6% | |||
(Traub et al., 2013) [29] |
High incidence of CIN: 7% | |||
(Hinson et al., 2017) [27] |
High incidence of CIN: 6.8% and 10.6% | |||
(Hsu et al., 2019) [25] |
High incidence of CIN: 12.4% | |||
(Puchol et al., 2019) [26] |
High incidence of CIN: 7.15% and 7.72% | |||
(Akman & Bakirdogen, 2020) [22] | High incidence of CIN: 36.9% | |||
(McGillicuddy et al., 2010) [13] | Low incidence of CIN: 1.9% | With reference to the pooled CIN incidence of 4.96% reported in the meta-analysis by Moos et al. (2013), values below 4.96% were categorized as low incidence of CIN. | ||
(Hopyan et al., 2008) [33] |
Low incidence of CIN: 2.9% | |||
(Dağar et al., 2020) [12] |
Low incidence of CIN: 4.9% | |||
(Kene et al., 2021 [20]; Brito et al., 2020 [21]; Hinson et al., 2019 [23]) | Absolute sCr increase of ≥0.3 mg/dL or ≥1.5-fold increase over baseline sCr | The different serum creatinine (sCr) measurements used in the definition of nephropathy | sCr Measurement | CIN Definitions in various studies |
(Akman & Bakirdogen, 2020 [22]; Dağar et al., 2020 [12]; Puchol et al., 2019 [26]; Hinson et al., 2017 [27]; Hong et al., 2016 [18]; Traub et al., 2013 [29]; Mitchell et al., 2012 [30]; Sinert et al., 2012 [31]; McGillicuddy et al., 2010 [13]; Mitchell et al., 2010 [32]; Mitchell & Kline, 2007 [34]) | Absolute increase of ≥0.5 mg/dL or ≥25% increase over baseline sCr | |||
(Mitchell et al., 2010) [32] |
An absolute rise in sCr of ≥0.3 mg/dL | |||
(Cho et al., 2019 [24]; Hinson et al., 2017 [27]) | Increase in sCr ≥0.3 mg/dL or ≥1.5 to 1.9-fold increase from baseline sCr | |||
(Hopyan et al., 2008) [33] |
≥25% increase in baseline sCr | |||
(Huang et al., 2013) [28] |
Increase in sCr ≥ 0.5 mg/dL | |||
(Hsu et al., 2019) [25] |
Absolute increase of 0.5 mg/dL or >50% increase in baseline sCr | |||
(Puchol et al., 2019) [26] |
Absolute increase of ≥0.3 mg/dL or 1.3 times greater than baseline sCr | |||
(Kene et al., 2021 [20]; Puchol et al., 2019 [26]) | 24 to 72 h | The different timings of sCr follow-ups after CECT used in the definition of nephropathy | Post-CECT sCr Collection Time | |
(Dağar et al., 2020 [12]; Cho et al., 2019 [24]; Hinson et al., 2019 [23]; Hsu et al., 2019 [25]; Hinson et al., 2017 [27]; Hong et al., 2016 [18]; Huang et al., 2013 [28]; Sinert et al., 2012 [31]) | 48 to 72 qh | |||
(Akman & Bakirdogen, 2020 [22]; Brito et al., 2020 [21]; McGillicuddy et al., 2010 [13]; Hopyan et al., 2008 [33]) | Within 72 h | |||
(Mitchell et al., 2012, [30], 2010 [32]; Mitchell & Kline, 2007 [34]) | 2 to 7 days | |||
(Traub et al., 2013) [29] |
48 to 96 h | |||
(Sinert et al., 2012 [31]; Hopyan et al., 2008 [33]; Mitchell and Kline, 2007 [34]) | No dialysis was required | Complications of CIN include adverse renal events such as dialysis, chronic kidney disease, end-stage renal disease, and renal transplantation. | CIN-induced Complications | |
(Kene et al., 2021 [31]; Brito et al., 2020 [21]; Dağar et al., 2020 [12]; Huang et al., 2013 [28]; McGillicuddy et al., 2010 [13]; Hinson et al., 2017 [27]) | Low incidence of dialysis | |||
(Hsu et al., 2019) [25] |
High incidence of dialysis | |||
(Brito et al., 2020 [21]; Dağar et al., 2020 [12]; Hsu et al., 2019 [25]; Huang et al., 2013 [28]) | Temporary haemodialysis only, none required permanent dialysis | |||
(McGillicuddy et al., 2010) [13] | Require permanent dialysis | |||
(Cho et al., 2019) [24] |
Renal replacement therapy required for 5 patients | |||
(Hsu et al., 2019 [25]; Hinson et al., 2017 [27]) | IV administration of contrast does not increase the risk of emergent dialysis | |||
(Hinson et al., 2019) [23] |
IV administration of contrast does not increase the risk of diagnosis of CKD and renal transplantation at 6 months | |||
(Mitchell et al., 2010 [32], 2012 [30]) | Association between CIN development and higher risk of severe renal failure within 45 days | |||
(Kene et al., 2021 [20]; Hsu et al., 2019 [25]; Huang et al., 2013 [28]; Mitchel et al., 2012 [30]; McGillicuddy et al., 2010 [13]) | CIN is associated with an increased risk of death | Mortality is another complication of CIN | ||
(Hsu et al., 2019 [25]; Hong et al., 2016 [18]; Sinert et al., 2012 [31]) | No significant differences in mortality rates between the CECT and non-CECT groups | |||
(Hong et al., 2016) [18] |
No association between CIN and LOS | Increased length of stay (LOS) is also a complication of CIN | ||
(McGillicuddy et al., 2010) [13] | CIN was associated with an increased LOS | |||
(Hinson et al., 2019 [23]; Hinson et al., 2017 [27]; Traub et al., 2013 [29]) | Congestive heart failure was associated with development of CIN | Congestive heart failure, acute hypotension, liver diseases, and illness severity of patients are associated with development of CIN in the ED. | Positive Findings | Validity of Classical Risk factors for CIN in ED settings |
(Brito et al., 2020) [21] |
Congestive heart failure was not a predictor of CIN | |||
(Dağar et al., 2020 [12]; Hong et al., 2016 [18]; Huang et al., 2013 [28]) | Patients with acute hypotension are at a higher risk for CIN | |||
(Hong et al., 2016 [18]; Traub et al., 2013 [29]) | Patients with liver diseases such as liver cirrhosis are at a higher risk of CIN | |||
(Hinson et al., 2019 [23]; Puchol et al., 2019 [26]) | CIN was associated with patients that were more severely ill | |||
(Dağar et al., 2020 [12]; Puchol et al., 2019 [26]; Hinson et al., 2017 [27]) | Age is associated with an increased likelihood of CIN development | Age, gender, eGFR, diabetes, vascular disease, anaemia, and smoking habits were not associated with CIN development in the ED. | Negative Findings | |
(Brito et al., 2020 [21]; Hong et al., 2016 [18]; Traub et al., 2013 [29]; Sinert et al., 2012 [31]) | Age is not associated with risk of developing CIN | |||
(Puchol et al., 2019 [26]; Hong et al., 2016 [18]) | Gender is not associated with CIN development | |||
(Akman & Bakirdogen, 2020) [22] | Older females associated with higher risk of CIN, compared to males who are younger | |||
(Brito et al., 2020 [21]; Cho et al., 2019 [24]; Hinson et al., 2019 [23]; Hinson et al., 2017 [27]; Hong et al., 2016 [18]; Sinert et al., 2012 [31]) | No association between eGFR and CIN | |||
(Mitchell et al., 2012) [30] |
eGFR < 60 mL/min/1.73 m2 may be an insensitive predictor of CIN after CTPA | |||
(Brito et al., 2020) [21] |
eGFR < 60 mL/min/1.73 m2 is a predictor of CIN | |||
(Kene et al., 2021) [20] |
Patients with CKD stage 3 at higher risk of AKI, but not for CKD 4–5 patients | |||
(Hinson et al., 2017) [27] |
Pre-existing diagnosis of CKD was associated with increased likelihood of CIN by multivariable logistic regression modelling | |||
(Brito et al., 2020 [21]; Sinert et al., 2012 [31] Hopyan et al., 2008 [33]) | No association between CIN and diabetes | |||
(Huang et al., 2013 [28]; Traub et al., 2013 [29]) | Diabetes mellitus was a risk factor for CIN | |||
(Mitchell & Kline, 2007) [34] |
A relatively high AKI frequency among those with coronary artery disease | |||
(Brito et al., 2020 [21]; Traub et al., 2013 [29]) | History of vascular disease failed to predict CIN | |||
(Traub et al., 2013) [29] |
Anaemia was not a risk factor of CIN | |||
(Brito et al., 2020) [21] |
Smoking habits was not a predictor of CIN. | |||
(Brito et al., 2020 [21]; Akman & Bakirdogen, 2020 [22]; Puchol et al., 2019 [26]) | Baseline sCr was associated with a higher risk of developing CIN | There was inconclusive evidence to conclude if sCr levels and hypertension were risk factors for CIN development after receiving iodinated contrast in the ED. | Inconclusive Findings | |
(Huang et al., 2013) [28] |
Pre-contrast sCr of more than 1.5 mg/dL was a risk factor for CIN | |||
(Traub et al., 2013) [29] |
Pre-contrast creatinine level > 2.0 mg/dL is an independent predictor of CIN, but not for creatinine > 1.5 mg/dL | |||
(Hinson et al., 2017 [27]; Hong et al., 2016 [18]; Sinert et al., 2012 [31]) | sCr level is not associated with risk of CIN | |||
(Mitchell et al., 2012) [30] |
Elevated sCr measurement was not associated with an increased risk of CIN following CTPA | |||
(Mitchell & Kline, 2007) [34] |
Laboratory-defined CIN occurred at a lower than expected frequency among those with an elevated baseline sCr concentration (6% vs. 15% among those with normal baseline sCr). | |||
(Traub et al., 2013) [29] |
Hypertension was a predictor of CIN | |||
(Brito et al., 2020) [21] |
Hypertension is not a predictor of AKI | |||
(Kene et al., 2021) [20] |
Administration of iodinated contrast is associated with increased risk of CIN development | The relationship between iodinated contrast media (ICM) and development of acute kidney injury (AKI). | ICM Administration and AKI Development | |
(Brito et al., 2020 [21]; Hinson et al., 2019 [23]; Puchol et al., 2019 [26]; Hsu et al., 2019 [25]; Hinson et al., 2017 [27]; McGillicuddy et al., 2010 [13]; Hopyan et al., 2008 [33]) | No association between administration of iodinated contrast and development of CIN |