scholarly journals The Effect and Underlying Mechanism of Statins in the Prevention of Post-Contrast Acute Kidney Injury: A Multicenter Retrospective Observational Study

Author(s):  
Maoning Lin ◽  
Tian Xu ◽  
Wenjuan Zhang ◽  
Duanbin Li ◽  
Ya Li ◽  
...  

Abstract Background: Post-Contrast acute kidney injury (PC-AKI) is a severe complication of coronary angiography (CAG) and percutaneous coronary intervention (PCI). At present, the mechanism and effect of statins on PC-AKI and its mechanism are still unclear. Methods: It was a multicenter retrospective obeservational study. We reviewed 4386 patients who underwent CAG or PCI, with serum creatinine recorded pre- or post-procedure within 72hrs after PCI, from December, 2006 to December, 2019 admitted to Sir Run Run Shaw Hospital and its medical consortium hospitals. Multivariate logical regression was used to explore whether preoperative use of statins was a protective factor for PC-AKI, and then path analysis model was used to explore the specific mechanism of statins. Results: In total, 4386 patients were enrolled in the study, the mean age was 67 yrs old, 17.9% with PC-AKI, 83.3% with pre-operative statin therapy. The incidence of PC-AKI was significantly lower in statin therapy group than non-statins therapy group. Multivariate regression indicated that pre-operative statin therapy was significantly negatively associated with percentage of elevated creatinine (β: -0.118, p<0.001) and PC-AKI (OR: 0.575, p<0.001). In pre-operative statin therapy group, no statistically significant deference was detected between atorvastatin and rosuvastatin group (OR: 1.052, p=0.558). Pathway model analysis indicated the direct protective effectiveness of pre-operative statin therapy on PC-AKI (p<0.001), but neither with its lipid-lowering effect (p=0.277) nor anti-inflammatory effect (p=0.596). Furthermore, It was found that “LDL-C→CRP” mediated the relationship between pre-operative statin therapy and PC-AKI (p=0.007); however, only explained less than 1% of the pre-operative statin therapy’s protective effects on PC-AKI. Conclusion: Pre-operative statin therapy is an independent protective factor of PC-AKI, which is not affected by the type of statins and not achieved by lipid-lowering effect or anti-inflammatory effect. Keywords : post-contrast acute kidney injury, statins, path analysis, mediation analysis.

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Maoning Lin ◽  
Tian Xu ◽  
Wenjuan Zhang ◽  
Duannbin Li ◽  
Ya Li ◽  
...  

Abstract Background Post-contrast acute kidney injury (PC-AKI) is a severe complication of coronary angiography (CAG) and percutaneous coronary intervention (PCI). Currently, the effect of statins on PC-AKI and its mechanism remains unclear. Methods This multicenter retrospective observational study included 4386 patients who underwent CAG or PCI from December 2006 to December 2019 in Sir Run Run Shaw Hospital and its medical consortium hospitals. Serum creatinine pre- or post-procedure within 72 h after PCI was recorded. Multivariate logical regression was used to explore whether preoperative use of statins was protective from PC-AKI. The path analysis model was then utilized to look for the mediation factors of statins. Results Four thousand three hundred eighty-six patients were enrolled totally. The median age of the study population was 68 years old, 17.9% with PC-AKI, and 83.3% on preoperative statins therapy. The incidence of PC-AKI was significantly lower in group of patients on statins therapy. Multivariate regression indicated that preoperative statins therapy was significantly associated with lower percentage of elevated creatinine (β: -0.118, P < 0.001) and less PC-AKI (OR: 0.575, P < 0.001). In the preoperative statins therapy group, no statistically significant difference was detected between the atorvastatin and rosuvastatin groups (OR: 1.052, P = 0.558). Pathway model analysis indicated a direct protective effect of preoperative statins therapy on PC-AKI (P < 0.001), but not through its lipid-lowering effect (P = 0.277) nor anti-inflammatory effect (P = 0.596). Furthermore, it was found that “low-density lipoprotein cholesterol (LDL-C)→C-reactive protein (CRP)” mediated the relationship between preoperative statins therapy and PC-AKI (P = 0.007). However, this only explained less than 1% of the preoperative protective effects of statins on PC-AKI. Conclusion Preoperative statins therapy is an independent protective factor of PC-AKI, regardless of its type. This protective effect is not achieved by lipid-lowering effect or anti-inflammatory effect. These findings underscore the potential use of statins in preventing PC-AKI among those at risk.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mona Laible ◽  
Ekkehart Jenetzky ◽  
Markus Alfred Möhlenbruch ◽  
Martin Bendszus ◽  
Peter Arthur Ringleb ◽  
...  

Background and Purpose: Clinical outcome and mortality after endovascular thrombectomy (EVT) in patients with ischemic stroke are commonly assessed after 3 months. In patients with acute kidney injury (AKI), unfavorable results for 3-month mortality have been reported. However, data on the in-hospital mortality after EVT in this population are sparse. In the present study, we assessed whether AKI impacts in-hospital and 3-month mortality in patients undergoing EVT.Materials and Methods: From a prospectively recruiting database, consecutive acute ischemic stroke patients receiving EVT between 2010 and 2018 due to acute large vessel occlusion were included. Post-contrast AKI (PC-AKI) was defined as an increase of baseline creatinine of ≥0.5 mg/dL or &gt;25% within 48 h after the first measurement at admission. Adjusting for potential confounders, associations between PC-AKI and mortality after stroke were tested in univariate and multivariate logistic regression models.Results: One thousand one hundred sixty-nine patients were included; 166 of them (14.2%) died during the acute hospital stay. Criteria for PC-AKI were met by 29 patients (2.5%). Presence of PC-AKI was associated with a significantly higher risk of in-hospital mortality in multivariate analysis [odds ratio (OR) = 2.87, 95% confidence interval (CI) = 1.16–7.13, p = 0.023]. Furthermore, factors associated with in-hospital mortality encompassed higher age (OR = 1.03, 95% CI = 1.01–1.04, p = 0.002), stroke severity (OR = 1.05, 95% CI = 1.03–1.08, p &lt; 0.001), symptomatic intracerebral hemorrhage (OR = 3.20, 95% CI = 1.69–6.04, p &lt; 0.001), posterior circulation stroke (OR = 2.85, 95% CI = 1.72–4.71, p &lt; 0.001), and failed recanalization (OR = 2.00, 95% CI = 1.35–3.00, p = 0.001).Conclusion: PC-AKI is rare after EVT but represents an important risk factor for in-hospital mortality and for mortality within 3 months after hospital discharge. Preventing PC-AKI after EVT may represent an important and potentially lifesaving effort in future daily clinical practice.


2021 ◽  
Vol 10 (18) ◽  
pp. 4140
Author(s):  
Łukasz Kuźma ◽  
Anna Tomaszuk-Kazberuk ◽  
Anna Kurasz ◽  
Małgorzata Zalewska-Adamiec ◽  
Hanna Bachórzewska-Gajewska ◽  
...  

Atrial fibrillation (AF) symptoms may mimic coronary artery disease (CAD) which reflects the difficulties in qualifying AF patients for invasive diagnostics. A substantial number of coronary angiographies may be unnecessary or even put patients at risk of post-contrast acute kidney injury (PC-AKI), especially patients with chronic kidney disease (CKD). We aimed to investigate the hypothesis indicating higher prevalence of PC-AKI in patients with AF scheduled for coronary angiography. The study population comprised of 8026 patients referred for elective coronarography including 1621 with AF. In the comparison of prevalence of PC-AKI in distinguished groups we can see that kidney impairment was twice more frequent in patients with AF in both groups with CKD (CKD (+)/AF (+) 6.24% vs. CKD (+)/AF (−) 3.04%) and without CKD (CKD (−)/AF (+) 2.32% vs. CKD (−)/AF (−) 1.22%). In our study, post-contrast acute kidney disease is twice more frequent in patients with AF, especially in subgroup with chronic kidney disease scheduled for coronary angiography. Additionally, having in mind results of previous studies stating that AF is associated with non-obstructive coronary lesions on angiography, patients with AF and CKD may be unnecessarily exposed to contrast agent and possible complications.


2019 ◽  
Vol 59 (2) ◽  
pp. 92-7
Author(s):  
Umi Rakhmawati ◽  
Indah K. Murni ◽  
Desy Rusmawatiningtyas

Background Acute kidney injury (AKI) can increase the morbidity and mortality in children admitted to the pediatric intensive care unit (PICU). Previous published studies have mostly been conducted in high-income countries. Evaluations of possible predictors of mortality in children with AKI in low- and middle-income countries have been limited, particularly in Indonesia. Objective To assess possible predictors of mortality in children with AKI in the PICU. Methods We conducted a retrospective cohort study at Dr. Sardjito Hospital, Yogyakarta, Indonesia. All children with AKI admitted to PICU for more than 24 hours from 2010 to 2016 were eligible and consecutively recruited into the study. Logistic regression analysis was used to identify independent predictors. Results Of the 152 children with AKI recruited, 119 died. In order to get a P value of <0.25, multivariate analysis is run to degree AKI, ventilator utilization, primary infection disease, MOF and age.Multivariate analysis showed that ventilator use, severe AKI, and infection were independently associated with mortality in children with AKI, with odds ratios (OR) of 19.2 (95%CI 6.2 to 59.7; P<0.001), 8.6 (95%CI 2.7 to 27.6; P<0.001), and 0.2 (95%CI 0.1 to 0.8; P=0.02), respectively. Conclusion The use of mechanical ventilation and the presence of severe AKI are associated with mortality in children with AKI admitted to the PICU. Interestingly, the presence of infection might be a protective factor from mortality in such patients. 


Author(s):  
Fernanda Moreira de Freitas ◽  
Welder Zamoner ◽  
Pamela Falbo dos Reis ◽  
André Luís Balbi ◽  
Daniela Ponce

This study aimed to evaluate the reduction in vancomycin through intermittent haemodialysis (IHD) and prolonged haemodialysis (PHD) in acute kidney injury (AKI) patients with sepsis and to identify the variables associated with subtherapeutic concentrations. A prospective study was performed in patients admitted at an intensive care unit (ICU) of a Brazilian hospital. Blood samples were collected at the start of dialytic therapy, after 2 and 4 h of treatment and at the end of therapy to determine the serum concentration of vancomycin and thus perform pharmacokinetic evaluation and PK/PD modelling. Twenty-seven patients treated with IHD, 17 treated with PHD for 6 h and 11 treated with PHD for 10 h were included. The reduction in serum concentrations of vancomycin after 2 h of therapy was 26.65 ± 12.64% and at the end of dialysis was 45.78 ± 12.79%, higher in the 10-h PHD group, 57.70% (40, 48–64, 30%) (p = 0.037). The ratio of the area under the curve to minimal inhibitory concentration (AUC/MIC) at 24 h in the PHD group was significantly smaller than at 10 h (p = 0.047). In the logistic regression, PHD was a risk factor for an AUC/MIC ratio less than 400 (OR = 11.59, p = 0.033), while a higher serum concentration of vancomycin at T0 was a protective factor (OR = 0.791, p = 0.009). In conclusion, subtherapeutic concentrations of vancomycin in acute kidney injury (AKI) patients in dialysis were elevated and may be related to a higher risk of bacterial resistance and mortality, besides pointing out the necessity of additional doses of vancomycin during dialytic therapy, mainly in PHD.


2013 ◽  
Vol 28 (4) ◽  
pp. 331 ◽  
Author(s):  
Pyoung Ahn ◽  
Hyun-Jun Min ◽  
Sang-Hyun Park ◽  
Byoung-Mu Lee ◽  
Myung-Jin Choi ◽  
...  

Author(s):  
Jing Zhao ◽  
Qiuxia Duan ◽  
Cuihong Dong ◽  
Jing Cui

Background: Acute kidney injury (AKI) is a common disease that can develop into end-stage kidney disease. Sepsis is one of the main causes of AKI. Currently, there is no satisfactory way to treat septic AKI. Therefore, we have shown the protective function of Cul4a in septic AKI and its molecular mechanism. Methods: The cellular and animal models of septic AKI were established by using lipopolysaccharide (LPS). Western blot (WB) was employed to analyze Cul4a expression. RT-qPCR was employed to test the expression of Cul4a, SOD1, SOD2, GPX1, CAT, IL-6, TNF-α, Bcl-2, IL-1β, Bax and KIM-1 mRNA. ELISA was performed to detect the contents of inflammatory factors and LDH. CCK-8 was utilized to detect the cell viability. Flow cytometry was utilized to analyze the apoptosis. DHE-ROS kit was used to detect the content of ROS. Results: Cul4a was down-regulated in cellular and animal models of septic AKI. Oxidative stress is obviously induced by LPS, as well as apoptosis and inflammation. However, these can be significantly inhibited by up-regulating Cul4a. Moreover, LPS induced the activation of the NF-κB pathway, which could also be inhibited by overexpression of Cul4a. Conclusion: Cul4a was found to be a protective factor in septic AKI, which could inhibit LPS-induced oxidative stress, apoptosis and inflammation of HK-2 cells by inhibiting NF-κB pathway.


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