Contrast-induced Acute Kidney Injury Group Research Articles

Correlation between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury and the establishment of machine-learning-based predictive models

Objective To explore the correlation between neutrophil-to-lymphocyte ratio (NLR) and contrast-induced acute kidney injury (CI-AKI). To develop machine-learning (ML) methods based on NLR and other relevant high-risk factors to establish new and effective predictive models of CI-AKI. Methods: The data of 2230 patients, who underwent elective vascular intervention, coronary angiography and percutaneous coronary intervention were retrospectively collected. The patients were divided into a CI-AKI group and a non-CI-AKI group. Logistic regression was used to analyze the correlation of NLR with CI-AKI and high-risk factors for CI-AKI, and logistic regression (LR), random forest (RF), gradient boosting decision tree (GBDT), extreme gradient boosting (XGBoost), and naïve Bayes (NB) models based on NLR and the high-risk factors were established. Results A high NLR(>2.844) was an independent risk factor for CI-AKI (odds ratio = 2.304, p < 0.001). The area under the ROC curve (AUC) of the NB model was the largest (0.774), indicating that it had the best performance. NLR, serum creatinine concentration, fasting plasma glucose concentration, and use of β-blocker all accounted for a large proportion of the predictive performance of each model and were the four most important factors affecting the occurrence of CI-AKI. Conclusions There was a significant correlation between NLR and CI-AKI The NB model exhibited the best predictive performance out of the five ML models based on NLR exhibited the best predictive performance out of the five ML models.

Delivery of recombinant sestrin2 ameliorates oxidative stress, mitochondrial damage and renal dysfunction in contrast-induced acute kidney injury

Although the use of iodinated contrast agents is sometimes unavoidable for accurate diagnosis, contrast-induced acute kidney injury (CI-AKI) is a possible complication of its administration. The pathogenesis of CI-AKI has not been fully elucidated, but oxidative stress is thought to be a major factor. Sestrin2 plays an important role in cellular and mitochondrial homeostasis by regulating oxidative stress. In this study, we aimed to investigate whether recombinant adenovirus containing sestrin2 (RS) can attenuate CI-AKI by reducing oxidative stress in a CI-AKI mice model. Our results showed that RS decreases oxidative stress, pro-inflammatory cytokines (TNF-α, IL-1α, IL-1β and IL-6) and apoptosis (Bax/Bcl2 and cleaved caspase-3) in the CI-AKI model. Additionally, RS alleviated mitochondrial damage, as evidenced by morphological changes, are restored ATP synthesis. Furthermore, RS administration resulted in a decrease in mitochondrial fission marker (Drp1) that was increased in the CI-AKI model, while the mitochondrial fusion marker (Mfn2) increased, indicating a restoration of mitochondrial dynamics. Decreased relative blood volume, as evaluated on computed tomography (CT), significantly increased compared to the CI-AKI group after RS administration. Finally, renal injury markers such as Kim-1, Ngal, IL-18 also decreased and kidney function was preserved with RS. These results suggested that RS can mitigate the deterioration of renal function in CI-AKI model.

Association Between Inflammatory Biomarkers and Contrast-induced Acute Kidney Injury in ACS Patients Undergoing Percutaneous Coronary Intervention: A Cross-sectional Study.

The present study aimed to evaluate the predictive role of inflammatory biomarkers in the development of contrast-induced acute kidney injury (CI-AKI) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). The inflammatory biomarkers assessed were: platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), derived neutrophil-to-lymphocyte ratio (dNLR), neutrophil-to-lymphocyte*platelet ratio (NLPR), systemic inflammatory index (SII), and systemic inflammation response index (SIRI). Overall, 950 patients undergoing PCI were enrolled. The frequency of CI-AKI was 15.2% (n = 144). The levels of NLR, MLR, NLPR, SII, and SIRI were higher in the CI-AKI group than in the Non-CI-AKI group (P < .05). The addition of NLR ≥2.96, dNLR ≥2.08, NLPR ≥.012, SII ≥558.04, and SIRI ≥1.13 to the Mehran score model significantly increased the area under the curve (P < .05). Multivariable logistic regression analyses indicated that inflammatory biomarkers were significantly associated with CI-AKI, including NLR ≥2.96 (OR = 1.588, P = .017), dNLR ≥2.08 (OR = 1.686, P = .007), SII ≥558.04 (OR = 1.521, P = .030), and SIRI ≥1.13 (OR = 1.601, P = .017). Therefore, inflammation is associated with the development of CI-AKI, and preoperative hematological inflammatory markers could predict the risk of CI-AKI in ACS patients undergoing PCI.

NGAL as Biomarker of Clinical and Subclinical Damage of Kidney Function after Coronary Angiography.

Contrast-induced acute kidney injury (CI-AKI) is a serious complication after angiographic examinations in cardiology. Diagnosis may be delayed based on standard serum creatinine, and subclinical forms of kidney damage may not be detected at all. In our study, we investigate the clinical use in these directions of a "damage"-type biomarker-neutrophil gelatinase-associated lipocalin (NGAL). Among patients with a high-risk profile undergoing scheduled coronary angiography and/or angioplasty, plasma NGAL was determined at baseline and at 4th and 24th h after contrast administration. In the CI-AKI group, NGAL increased significantly at the 4th hour (Me 109.3 (IQR 92.1-148.7) ng/mL versus 97.6 (IQR 69.4-127.0) ng/mL, p = 0.006) and at the 24th hour (Me 131.0 (IQR 81.1-240.8) ng/mL, p = 0.008). In patients with subclinical CI-AKI, NGAL also increased significantly at the 4th hour (Me 94.0 (IQR 75.5-148.2) ng/mL, p = 0.002) and reached levels close to those in patients with CI-AKI. Unlike the new biomarker, however, serum creatinine did not change significantly in this group. The diagnostic power of NGAL is extremely good-AUC 0.847 (95% CI: 0.677-1.000; p = 0.001) in CI-AKI and AUC 0.731 (95% CI: 0.539-0.924; p = 0.024) in subclinical CI-AKI. NGAL may be a reliable biomarker for the early diagnosis of clinical and subclinical forms of renal injury after contrast angiographic studies.

Predictive Value of Neutrophil to High-Density Lipoprotein Ratio for Contrast-Induced Acute Kidney Injury for Patients with Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Background: To investigate the incidence of contrast-induced acute kidney injury (CI-AKI) in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) in relation to the neutrophil to high-density lipoprotein cholesterol ratio (NHR), and to further compare the predictive value of NHR and the neutrophil to lymphocyte ratio (NLR) for CI-AKI. Methods: We retrospectively analyzed 1243 AMI patients undergoing PCI from January 2019 to December 2021, and collected creatinine within 72 h after PCI. All patients were divided into a CI-AKI group and non-CI-AKI group according to the definition of CI-AKI, and the clinical information of the two groups was compared. Potential risk factors for CI-AKI in AMI patients undergoing primary PCI were screened by using logistic regression analysis, and receiver operating characteristic (ROC) curves were used to compare the predictive value of NHR and NLR. Results: A high NHR and high NLR were correlated with a high incidence of CI-AKI in AMI patients undergoing primary PCI, and NHR (odds ratio (OR): 1.313, 95% confidence interval (CI): 1.199–1.438) and NLR (OR: 1.105, 95% CI: 1.041–1.174) were independent risk factors for CI-AKI (p &lt; 0.05). Compared with NLR, the area under the curve (AUC) of NHR was larger (AUC = 0.668, 95% CI: 0.641–0.694 vs. AUC = 0.723, 95% CI: 0.697–0.748), and the difference was significant (p &lt; 0.05), with higher sensitivity (61.67% vs. 70.83%) and specificity (64.91% vs. 66.10%). Conclusions: Compared with the NLR, the NHR is more valuable in predicting the incidence of CI-AKI in AMI patients undergoing primary PCI.

Exploring the effects of edaravone in rats with contrast-induced acute kidney injury

AimsOxidative stress and inflammatory response play a vital role in the pathogenesis of contrast-induced acute kidney injury (CI-AKI). This study investigated the effects of edaravone in rats with CI-AKI. Main methodsMale Sprague Dawley rats were randomly assigned into four groups (n = 11–14/group): control, edaravone (30 mg/kg/day intraperitoneally (IP)), CI-AKI, and edaravone with CI-AKI. The induction of CI-AKI was performed by dehydration and the administration of contrast media (iohexol) and inhibitors of prostaglandin (indomethacin) and nitric oxide synthesis (L-NAME: N-nitro L-arginine methyl ester). Edaravone was administered for two weeks before the induction of CI-AKI. Serum creatinine and urea, renal oxidative stress and inflammatory biomarkers, and histopathological alterations were evaluated after 48 h of contrast exposure. Key findingsRats with CI-AKI showed a significant increase in serum creatinine and urea. The levels of antioxidant biomarkers including glutathione peroxidase, superoxide dismutase and reduced glutathione were significantly decreased in CI-AKI group versus control. Pre-treatment of rats with edaravone normalized kidney function and protected the kidney from oxidative damage as demonstrated by normalization of previous biomarkers. Furthermore, edaravone partially ameliorated renal histopathological alterations relative to the CI-AKI group, notably in the nephrons. No changes were observed in inflammatory biomarkers including tumour necrosis factor-alpha and interleukin-6 among all groups. SignificanceThe current findings suggest that edaravone could be a potential strategy to ameliorate developing CI-AKI possibly by improving renal antioxidant capacity. Further studies are warranted to expand the current understanding of the use of edaravone in the various models of AKI.

Urinary NGAL, IGFBP-7, and TIMP-2: novel biomarkers to predict contrast medium-induced acute kidney injury in children

Background Serum creatinine (SCr) is unreliable in detecting acute changes in kidney function. Early recognition of contrast-induced acute kidney injury (CI-AKI) can provide better opportunities for preventive interventions. Therefore, the purpose of this study is to examine the value of the combined detection of urinary neutrophil gelatinase-associated lipocalin (NGAL), insulin-like growth factor binding protein-7 (IGFBP-7), and tissue inhibitor of metalloproteinase-2 (TIMP-2) in the early diagnosis of children with CI-AKI. Methods A prospective, single-center clinical trial was performed and included 172 children aged 0–18 years. The dynamic changes of urinary NGAL, IGFBP-7, and TIMP-2 levels in children with intravascular injection of contrast medium were investigated to determine whether they can diagnose CI-AKI early. Results CI-AKI occurred in 20 of 137 enrolled patients, and the incidence was 14.59%. In the CI-AKI group, urinary levels of NGAL, IGFBP-7, TIMP-2, and [IGFBP-7]*[TIMP-2] were significantly increased 2 h after angiography and remained at high levels at 6 h. Using a cutoff value of 36.274 ng/mL, the specificity was 70.0%, and the sensitivity was 68.4% for the prediction of CI-AKI, which was excellent for urinary NGAL. When both urinary IGFBP-7 and TIMP-2 were used together, urinary [IGFBP-7]*[TIMP-2] at 0.417(ng/mL)2/1000 was regarded as the cutoff value. The specificity was 80.0%, and the sensitivity was 81.2%. Conclusions NGAL, IGFBP-7, and TIMP-2 concentrations in the urine of children after receiving injections of contrast medium increased faster than SCr and had good clinical value for the early diagnosis of CI-AKI in children. The combination of IGFBP-7 and TIMP-2 was better than either analyte alone.

Association of plasma free triiodothyronine levels with contrast-induced acute kidney injury and short-term survival in patients with acute myocardial infarction.

ObjectivePost-treatment contrast-induced acute kidney injury (CI-AKI) is associated with poor outcomes in patients with acute myocardial infarction (AMI). A lower free triiodothyronine (FT3) level predicts a poor prognosis of AMI patients. This study evaluated the effect of plasma FT3 level in predicting CI-AKI and short-term survival among AMI patients.MethodsCoronary arteriography or percutaneous coronary intervention was performed in patients with AMI. A 1:3 propensity score (PS) was used to match patients in the CI-AKI group and the non-CI-AKI group.ResultsOf 1480 patients enrolled in the study, 224 (15.1%) patients developed CI-AKI. The FT3 level was lower in CI-AKI patients than in non-CI-AKI patients (3.72 ± 0.88 pmol/L vs 4.01 ± 0.80 pmol/L, P < 0.001). Compared with those at the lowest quartile of FT3, the patients at quartiles 2–4 had a higher risk of CI-AKI respectively (P for trend = 0.005). The risk of CI-AKI increased by 17.7% as FT3 level decreased by one unit after PS-matching analysis (odds ratio: 0.823; 95% CI: 0.685–0.988, P = 0.036). After a median of 31 days of follow-up (interquartile range: 30–35 days), 78 patients died, including 72 cardiogenic deaths and 6 non-cardiogenic deaths, with more deaths in the CI-AKI group than in the non-CI-AKI group (53 vs 25, P < 0.001). Kaplan–Meier survival analysis showed that patients at a lower FT3 quartile achieved a worse survival before and after matching.ConclusionLower FT3 may increase the risk of CI-AKI and 1-month mortality in AMI patients.

Preprocedural SII Combined with High-Sensitivity C-Reactive Protein Predicts the Risk of Contrast-Induced Acute Kidney Injury in STEMI Patients Undergoing Percutaneous Coronary Intervention.

ObjectiveTo investigate the relationship between the incidence of contrast-induced acute kidney injury (CI-AKI) and the levels of the systemic immune-inflammatory index (SII, platelet × neutrophil/lymphocyte ratio) and high-sensitivity C-reactive protein (hsCRP) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), to analyze further the predictive value of the combination of SII and hsCRP for CI-AKI.MethodsRetrospectively analyze the clinical data of STEMI patients who underwent PCI in our cardiology department from November 2019 to March 2021. Restricted cubic splines were used to determine the correlation between SII and hsCRP and the risk of CI-AKI. Patients were divided into the CI-AKI group (n=71) and the non-CI-AKI group (n=344) according to postoperative creatinine changes. Logistic regression was used to analyze the factors influencing CI-AKI. ROC curves were used to evaluate the predictive value of SII, hsCRP, and their combined levels on CI-AKI.ResultsRestricted cubic spline analysis showed that when SII>653.73×109/L and hsCRP>5.52mg/dl, there was a positive correlation with the incidence of CI-AKI. And the incidence of CI-AKI rose with the inflammation status. The receiver operating characteristic curve of SII combined with hsCRP was 0.831, which was higher than SII or hsCRP alone. The logistic regression analysis showed that high-risk factors of CI-AKI were diabetes mellitus, platelet count, and highly elevated SII and hsCRP.ConclusionWithin a certain range, elevated inflammatory biomarkers SII and hsCRP were risk factors for CI-AKI after PCI in patients with STEMI. This study suggests that the combination of SII and hsCRP predicts the risk of CI-AKI more accurately than either biomarker alone.

Predictive value of combining the level of fibrinogen and CHA2DS2-VASC Score for contrast-induced acute kidney injury in patients with acute coronary syndromes undergoing percutaneous coronary intervention.

The present study aimed to investigate the value of preprocedural fibrinogen (FIB) combined with CHA2DS2-VASC scores in the risk prediction of contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention (PCI) in patients with acute coronary syndromes (ACS). A total of 934 patients (mean age 63.9 ± 11.5years, and 32.1% female), who were admitted to our hospital for ACS and underwent PCI, were retrospectively enrolled. The patients were divided into two groups: non-CI-AKI group (n = 787) and CI-AKI group (n = 147). Contrast-induced acute kidney injury was defined as an increase of ≥ 0.5mg/dL or ≥ 25% serum creatinine within 48-72h after PCI. Spearman correlation analysis was used to determine the relationship between FIB and CHA2DS2-VASC scores. Patients with high baseline FIB levels and high CHA2DS2-VASC scores had higher CI-AKI incidence. On spearman correlation analysis, FIB and CHA2DS2-VASC scores were positively correlated (R = 0.236, P < 0.001). The ROC statistical analysis showed that the combination had 63.3% sensitivity with 72.6% specificity for the development of CI-AKI (area under the curve: 0.727, 95% CI 0.697-0.755, P < 0.001). A total of 934 ACS patients were divided into low-risk group (404 cases), medium-risk group (383 cases) and high-risk group (147 cases) according to the cut-off values of FIB and CHA2DS2-VASC scores. The incidence of CI-AKI was higher in the high-risk group than in the low-risk and medium-risk groups (Log-rank χ2 = 104.505, 56.647. P < 0.001). Multivariate analysis revealed that albumin (OR = 0.913, 95% CI 0.867-0.962), FIB (OR = 1.451, 95% CI 1.185-1.77), CHA2DS2-VASC score (OR = 1.271, 95% CI 1.504-1.78) were the independent risk factors of CI-AKI (p < 0.05). The preprocedural fibrinogen combined with CHA2DS2-VASC score is independently associated with the risk of CI-AKI in ACS patients treated by PCI.

High mobility group box 1 and homocysteine as preprocedural predictors for contrast-induced acute kidney injury after percutaneous coronary artery intervention

High mobility group box 1 (HMGB1) and homocysteine (Hcy) play important roles in contrast-induced acute kidney injury (CI-AKI). We compared HMGB1 to Hcy as preprocedural predictors for CI-AKI in coronary artery disease (CAD) patients after percutaneous coronary artery intervention (PCI). We included 257 eligible patients who were categorized into CI-AKI ( +) and CI-AKI ( -) group. The differences in clinical characteristics and biochemical indexes between two groups were analyzed. We observed that thirty-eight (14.8%) of 257 eligible CAD patients developed CI-AKI. HMGB1 (14.65 [11.13-24.89] vs 10.88 [7.94-13.23], p < 0.001) and Hcy (14.07 [12.07-17.31] vs 12.09 [10.71-13.47], p < 0.001) increased significantly in CI-AKI ( +) group. Both age (r = 0.210, p = 0.001), serum creatinine (r = 0.509, p < 0.001), eGFR (r = - 0.459, p < 0.001) and Hcy (r = 0.531, p < 0.001) were significantly correlated with HMGB1. Among all patients, HMGB1 (OR 1.181, 95% CI 1.081-1.290, p < 0.001) and Hcy (OR 1.260, 95% CI 1.066-1.489, p = 0.007) were independent predictors for the development of CI-AKI. We built the propensity score matching (PSM) using 38 pairs of patients. After adjustment, HMGB1 (OR 1.169, 95% CI 1.035-1.322, p = 0.012) and Hcy (OR 1.457, 95% CI 1.064-1.997, p = 0.019) were also independent predictors for the development of CI-AKI. Both HMGB1 (AUC: 0.704, 95% CI: 0.588-0.819, p = 0.002) and Hcy (AUC: 0.708, 95% CI: 0.593-0.823, p = 0.002) had predictive values for CI-AKI. There is a significant positive association between HMGB1 and Hcy in CAD patients. Both HMGB1 and Hcy are potential preprocedural predictors of CI-AKI after PCI.

Preprocedural Lp(a) level and ApoB/ApoA-\u0399 ratio and the risk for contrast-induced acute kidney injury in patients undergoing emergency PCI

BackgroundHigh serum Lipoprotein(a) (Lp(a)) level and Apolipoprotein B/Apolipoprotein AΙ (ApoB/ApoA-Ι) ratio are risk factors for cardiovascular disease and kidney disease and have been found to be correlated with the prevalence and prognosis of various kidney diseases. However, it is not clear whether the serum Lp(a) level and ApoB/ApoA-Ι ratio pre-PCI are correlated with the prevalence of contrast-induced acute kidney injury (CI-AKI).MethodsA total of 931 participants undergoing emergency PCI from July 2018 to July 2020 were included. According to whether the serum creatinine concentration was higher than the baseline concentration (by ≥25% or ≥ 0.5 mg/dL) 48–72 h after contrast exposure, these participants were divided into a CI-AKI group (n = 174) and a non-CI-AKI group (n = 757). Serum Lp(a), ApoA-Ι and ApoB concentration were detected in the patients when they were admitted to hospital, and the ApoB/ApoA-Ι ratio was calculated. Logistic regression and restricted cubic spline analyses were used to explore the correlation between the Lp(a) concentration or the ApoB/ApoA-Ι ratio and the risk of CI-AKI.ResultsAmong the 931 participants undergoing emergency PCI, 174 (18.69%) participants developed CI-AKI. Compared with the non-CI-AKI group, the Lp(a) level and ApoB/ApoA-Ι ratio pre-PCI in the CI-AKI group were significantly higher (P < 0.05). The incidence of CI-AKI was positively associated with the serum Lp(a) level and ApoB/ApoA-Ι ratio pre-PCI in each logistic regression model (P < 0.05). After adjusting for all the risk factors included in this study, restricted cubic spline analyses found that the Lp(a) level and the ApoB/ApoA-Ι ratio before PCI, within certain ranges, were positively associated with the prevalence of CI-AKI.ConclusionHigh Lp(a) levels and high ApoB/ApoA-Ι ratios before PCI are potential risk factors for CI-AKI.

The Predictive Value of Soluble Urokinase-Type Plasminogen Activator Receptor in Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention.

ObjectiveSoluble urokinase-type plasminogen activator receptor (SuPAR) is a circulating protein and a novel identified promising biomarker for various renal diseases and kidney injury. However, it remains unknown on the predictive value of suPAR in contrast induced acute kidney injury (CI-AKI) in patients undergoing percutaneous coronary intervention (PCI).MethodsA total of 399 patients undergoing PCI were enrolled in the research from June 2020 to June 2021 in Zhongda Hospital. Patients were divided into CI-AKI and non-CI-AKI groups according to the preoperative and postoperative serum creatinine levels. Plasma suPAR level was detected through enzyme-linked immunosorbent assay on admission. Demographic data, hematological parameters, coronary angiography data and medications were recorded and compared between CI-AKI and non-CI-AKI groups. Logistic regression analysis and receiver operator characteristic (ROC) curve analysis were performed for identifying the independent risk factors of CI-AKI and assessment of the predictive value of suPAR for CI-AKI.ResultsCI-AKI occurred in 65 (16.3%) patients undergoing PCI. The level of suPAR in CI-AKI group was significantly higher than that in the non-CI-AKI group. Multivariate logistic regression indicated diabetes, lower LVEF, lower hydration rate, lower baseline eGFR, higher plasma suPAR (OR = 2.875, 95% CI = 2.038–3.672, P < 0.001) and volume of contrast media were all independent risk factors for CI-AKI after adjustment of the confounding factors. ROC analysis illustrated that the optimal area under the curve was 0.765, indicating plasma suPAR was a splendid predictor for CI-AKI. The corresponding cut-off value was 3.305 ng/mL, and the sensitivity and specificity were 63.1% and 82.3%, respectively.ConclusionIncreased suPAR level is independently associated with elevated risk of suffering CI-AKI, and suPAR is a strong predictor for CI-AKI in patients undergoing PCI. SuPAR might act as a novel biomarker for CI-AKI in clinical practice.

Midkine as an Early Biomarker of Contrast-induced Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndrome: A Single-center Prospective Study

Background: Contrast-induced acute kidney injury (CI-AKI), is an important complication of percutaneous coronary intervention (PCI). We aimed to study the role of serum midkine (MK) as an early biomarker of CI-AKI.&#x0D; Methods: We conducted a prospective observational cohort study. It includes 100 chronic kidney disease (CKD) patients with an estimated glomerular filtration rate (eGFR) &lt;60 ml/min/1.73m2. All patients were undergoing PCI for ACS. We measured serum midkine before, 2 and 24 hours after PCI. &#x0D; Results: The mean age of the patients was 70.32±3.62 years, 74% males. Twenty-seven patients developed CI-AKI. The CI-AKI group has a history of diabetes mellitus (DM) and/or dyslipidemia, history of diuretics, metformin and/or angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers (ACEI/ARBs) use. The CI-AKI patients have low left ventricular ejection fraction (LVEF) (EF &lt; 45%) and low Creatinine Clearance (CrCl) before PCI. The CI-AKI received more contrast volume, had a longer duration of PCI and had high Mehran risk score after PCI. Comparison between the two studied groups regarding serum MK showed that there was a statistically significant difference regarding serum MK 2 hours after PCI. Receiver operating characteristic (ROC) curve analysis for serum MK showed that serum MK measured 2 hours after PCI was statistically significant to predict CI-AKI.&#x0D; Conclusion: An early Serum MK after PCI can be used as an early predictor of CI-AKI in ACS patients.

Prognostic nutritional index and the risk of acute kidney injury in patients with acute coronary syndrome.

Recent studies have linked malnutrition with undesirable outcomes in cardiovascular diseases. However, the underlying mechanism is unknown. Contrast-induced acute kidney injury (CI-AKI) increased cardiovascular mortality after percutaneous coronary intervention (PCI). This study hypothesizes that prognostic nutritional index (PNI) plays a role in the development of CI-AKI in patients with acute coronary syndrome undergoing emergency PCI. This study enrolled 551 patients. PNI was determined as 10× serum albumin (g/dL)+0.005×total lymphocyte count (mm3). CI-AKI was characterized as the increase in serum creatinine ≥0.3 mg/dL level within 48 h after PCI. Patients were classified as either CI-AKI (+) or CI-AKI (-). CI-AKI has occurred in 72 of 551 patients (13.1%). PNI was significantly lower in the CI-AKI (+) group than in the CI-AKI (-) group (44.4±6.6 versus 47.2±5.8, p<0.001, respectively). Multivariate logistic regression analysis showed that PNI [odds ratio, OR: 1.631, 95% confidence interval (CI): 1.168-2.308, p=0.02] and estimated glomerular filtration rate (OR: 3.26, 95%CI 1.733-6.143, p<0.001) were independent risk factors for CI-AKI. PNI is an independent risk factor for CI-AKI. The development of CI-AKI may be the mechanism responsible for the relationship between poor nutritional status and adverse cardiac events.

Impact of small and dense low-density lipoprotein (sd-LDL)on contrast-induced acute kidney injury in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

To investigate the impact of serum small and dense low-density lipoprotein (sd-LDL) on contrast-induced acute kidney injury (CI-AKI) after emergency percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). From November 2019 to August 2020, 352 patients with STEMI who underwent primary PCI were recruited consecutively. Patients were divided into CI-AKI group (n = 71) and non-CI-AKI group (n = 281). CI-AKI was defined as an increase in serum creatinine (≥ 25% or ≥ 0.5mg/dL) from baseline occurring 72h after PCI. All subjects were tested for sd-LDL. In the 352 eligible patients with STEMI receiving emergency PCI, 71 patients (20.2%) developed CI-AKI. The levels of sd-LDL in CI-AKI group was higher than those in the non-CI-AKI group, and the difference was statistically significant (P < 0.05). The area under the curve (AUC) of the sd-LDL was 0.741 [95% confidence interval (CI) 0.538-0.636] in the STEMI patients receiving emergency PCI. CI-AKI model included the following five predictors: sd-LDL, NLR, Diabetes, Pre-PCI eGFR, and Log NT-proBNP. The AUC of forecast probability was 0.835 [95% confidence interval (CI) 0.786-0.883].The Hosmer-Lemeshow test has a P value of 0.519, which confirms the model's goodness of fit. Increased sd-LDL is independently associated with risk of CI-AKI in STEMI patients treated by primary PCI.

Contrast‑induced acute kidney injury in COVID-19 patients.

Forty-two COVID-19 patients who underwent emergency PCI due to the diagnosis of acute coronary syndrome were included in the study. Mean age was 63±14.76 and males accounted for 81 % (34/42). Contrast-induced acute kidney injury (CI-AKI) was defined as absolute increase in serum creatinine level by 0.3 mg/dL above baseline within 48 hours of contrast exposure. Patients were divided into two groups according to CI-AKI development following coronary angiography. CI-AKI developed in 33.3 % (14/42) of the patients. Pre-procedure e-GFR (p=0.028), serum albumin levels (p=0.021), and ejection fraction (p=0.039) were lower in the CI-AKI group. Whereas the platelet/lymphocyte ratio was significantly lower in the non-CI-AKI group (p=0.010). Our study results demonstrated that patients suffering from COVID-19 had a high risk of CI-AKI development following coronary angiography (Tab. 1, Ref. 36).

Serum neutrophil gelatinase-associated lipocalin as an early biomarker of acute kidney injury in subjects undergoing percutaneous transluminal coronary angiogram with normal EGFR

Introduction: Detecting AKI in a timely fashion with the current AKIN staging criteria is a challenge because the diagnosis of AKI is usually based on changes in serum creatinine (SCr) which is a poor marker of early renal dysfunction. Aim: To study the role of Serum Neutrophil Gelatinase-Associated Lipocalcin (NGAL) as early biomarker for the detection of Contrast induced acute kidney injury (CIAKI) in subjects undergoing Percutaneous transluminal coronary angiogram (PTCA) with normal eGFR. Materials and Methods: Prospective cohort study was conducted, where SCr and serum NGAL were serially measured in a heterogeneous group of subjects (n=60) presenting to cardiology department. Results: The study population consisted of 60 subjects. All subjects were divided into 2 groups “CIAKI group” and “no-CIAKI group” according to predefined definition. The serum NGAL increased and reached its peak at 4 hours after contrast media (CM) administration and did not returned to baseline by 24 hours while the SCr increased at 24 hours and reached peak at 48 hours respectively (P

Neutrophil Gelatinase-Associated Lipocalin (NGAL) predict higher risk of serious renal dysfunction in patients with CI-AKI

Abstract Introduction The Neutrophil Gellatinase Associated-Lipocalin (NGAL) as a biomarker for kidney damage is less investigated in terms of risk prediction. Purpose The aim of our study was to evaluate the diagnostic power of NGAL in detection of contrast-induced acute kidney injury (CI-AKI) and it's role for evaluation of the risk for serious renal dysfunction (SRD). Methods The study included high risk patients with chronic kidney disease (CKD) stage 2 and 3 undergoing coronary angiography and/or angioplasty for stable angina. Blood samples for plasma NGAL and serum creatinine (sCr) were collected baseline at the day before, at 4th and 24th hours after contrast exposure. The original risk scale as validated from Brown was used to calculate SRDcreat based on sCr and modified score was established with calculate SRDngal according to baseline levels of NGAL. Results The study enrolled 93 patients divided in control group (n=18/19%), CI-AKI group (n=18/19%), subclinical CI-AKI (n=15/16%), CKD 3a stage (n=33/36%) and CKD 3b stage (n=9/10%). The baseline level of NGAL in control group was 76.40±14.70 ng/ml and didn't change significantly after angiography. In the CI-AKI group NGAL increased early after contrast investigation (at 4th hour 139.59±65.57 ng/ml versus baseline values 121.91±59.37 ng/ml; p=0.003) and maintained this tendency until 24th hour (202.88±225.29 ng/ml; p&amp;lt;0.001). In the subclinical CI-AKI pattern of NGAL was similar to CI-AKI with estimated levels at 4th hour 128.18±99 ng/ml (vs baseline values 76.69±29.32 ng/ml, p=0,002). Groups with CKD showed significantly higher baseline level of NGAL (3a stage – 114.98±29.98 ng/ml and 3b stage – 173.30±47.66 ng/ml, p&amp;lt;0.05). The ROC analysis demonstrated AUC 0.889 (95% CI: 0.768–1.000; p&amp;lt;0.001) for diagnostic power of NGAL at 4th hour to detect CI-AKI and AUC 0.731 (95% CI: 0.539–0.924; p=0.024) at 4th hour to detect subclinical CI-AKI. Estimated risk of SRDcreat was 0.41±0.39% in control group and respectively 0.91±1.53% in CI-AKI group (p=0.20); 0.63±0.54% in subclinical CI-AKI (p=0.18), 1.33±1.29% in CKD 3a stage (p&amp;lt;0.001) and 3.0±2.63% in CKD 3b stage (p&amp;lt;0.001). According to baseline values of NGAL calculated risk of SRDngal were 0.41±0.39% in control group and 2.34±4.05% in CI-AKI group (p=0.02 compared to levels in control patients). In the rest groups SRDngal respectively was 0.99±1.28% for subclinical CI-AKI (p=0.09), 2.01±2.53% for CKD 3a stage (p=0.002), and 4.83±4.12% in CKD 3b stage (p&amp;lt;0.001). Direct comparison of the two scales SRDcreat/SRDngal demonstrated significantly higher levels with measurement of NGAL in CI-AKI group (p=0.03) and CKD 3b stage group (p=0.02). Conclusions The NGAL is not only a good predictor for clinical/subclinical CI-AKI but can also predict better the level of risk for SRD in patients with CI-AKI than the risk estimated by measurement of sCr. NGAL incorporated in risk calculator may be applied as useful assessment tool in clinical practice. Funding Acknowledgement Type of funding source: None

Elevated left ventricular end diastolic pressure is associated with increased risk of contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention

AimsTo study the correlation between intra-procedural left ventricular end-diastolic pressure (LVEDP) and the development of contrast-induced acute kidney injury (CI-AKI) in patients undergoing percutaneous coronary intervention (PCI). Methods and resultsA single center retrospective observational study compared clinical and hemodynamic characteristics of patients who developed post-PCI CI-AKI with those did not. CI-AKI was defined as an absolute increase in serum creatinine ≥0.5 mg/dl or an increase ≥25% from baseline 48–72 h after the administration of contrast medium. Among 1301 consecutive patients who underwent PCI, 125 patients (9.6%) developed CI-AKI. The CI-AKI group had a higher average LVEDP (18.4 ± 8.7 vs 14.4 ± 6.6 mm Hg; p < .0001) and higher prevalence of elevated LVEDP (≥20 mm Hg) than those without CI-AKI (47.2% vs 23.3%, p < .0001). After adjustments, elevated LVEDP remained independently associated with CI-AKI (OR 2.21; 95% CI 1.40–3.50). LVEDP predicted the development of CI-AKI with a receiver operating characteristic area under curve (AUC) of 0.64. The association between elevated LVEDP and the risk of CI-AKI was stronger in patients with reduced ejection fraction (EF ≤ 40%) (OR = 4.08; 95% CI: 1.68–9.91) than those with preserved EF (OR = 1.69; 95% CI: 0.94–3.04) (p value for interaction = .0003). Patients who had LVEDP ≥ 20 mm Hg and LVEF ≤ 40% had a post-PCI incidence rate of developing CI-AKI of 36.5%. ConclusionsElevated intra-procedural LVEDP (≥20 mm Hg) is independently associated with increased risk of CI-AKI for patients undergoing cardiac catheterization and PCI, especially in the setting of reduced LVEF (≤40%).