Advances in the pathogenesis and prevention of contrast-induced nephropathy

Zhang, Fangfei; Lu, Zeyuan; Wang, Rui

doi:10.1016/j.lfs.2020.118379

Cited by 82 publications

(76 citation statements)

References 127 publications

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“…It remains a complex mechanism for the pathophysiology of AKI following cardiac surgery and PCI, several major injury mechanisms have been proposed as the etiology in the development of AKI, including the direct nephrotoxic effects, hypoperfusion, ischaemia-reperfusion injury, increased viscosity of fluid in vascular and tubular cells, neurohumoral activation, oxidative stress, apoptosis, immune-inflammation injury, and epigenetic regulation (18,19).…”

Section: Discussionmentioning

confidence: 99%

Risk factor analysis of acute kidney injury after one-stop hybrid coronary revascularization

Li¹,

Gao²,

Guo³

et al. 2021

Ann Palliat Med

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Background: One-stop hybrid coronary revascularization (HCR) combines coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) procedures simultaneously. Acute kidney injury (AKI) is a common complication after CABG or PCI. This study explored the risk factors for developing AKI after one-stop HCR.Methods: A total of 123 consecutive patients who underwent one-stop HCR between April 2018 and November 2020 were included in this single-center retrospective study. Postoperative AKI was observed in 11 patients (the AKI group), and 112 patients did not develop postoperative AKI (the non-AKI group).Baseline characteristics and perioperative variables were extracted from the electronic medical records and statistically analyzed.Results: Postoperative AKI occurred in 11 (8.9%) patients. Compared to patients who did not develop AKI, patients in the AKI group were older (71.0±9.5 vs. 64.1±9.2 years, P=0.019), had higher preoperative creatinine levels (92.6±16.8 vs. 69.8±14.4 mmol/L, P<0.001), experienced a greater volume of postoperative drainage on the first day [850 mL (410, 1,500) vs. 500 mL (321, 700), P=0.045], had a higher proportion of chronic renal insufficiency (eGFR <60 mL/min/1.73 m 2 ) (36.4% vs. 7.1%, P=0.012), and had more perioperative transfusions (63.6% vs. 22.3%, P=0.007). Multivariate logistics analyses revealed that advanced age [odds ratio (OR) 5.44, P=0.014] and perioperative transfusions (OR 4.62, P=0.028) were independent risk factors for developing AKI after one-stop HCR.Conclusions: One-stop HCR did not increase the incidence of postoperative AKI in our center. Advanced age (≥75 years) and perioperative transfusions were independent risk factors for developing AKI after onestop HCR. Further studies need to be conducted to confirm the risk factors of AKI after HCR procedures.

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Section: Discussionmentioning

confidence: 99%

Risk factor analysis of acute kidney injury after one-stop hybrid coronary revascularization

Li¹,

Gao²,

Guo³

et al. 2021

Ann Palliat Med

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“…Hence, contrast-induced acute kidney injury (CI-AKI) has become a more common problem in clinical practice and is an important cause of hospital-acquired acute renal insufficiency [1][2][3] despite numerous attempts to reduce the incidence of CI-AKI, such as the improvement of hydration protocols and pretreatment with antioxidants, which are sup-posed to be less nephrotoxic. Although the exact pathophysiological mechanisms of CI-AKI are not fully understood, renal vasoconstriction with resultant renal medullary hypoxia and direct toxic effects of radiocontrast on renal tubules are two major mechanisms that have been found to be involved in the pathogenesis of CI-AKI [1,2,4]. In addition, the apoptosis and cell death of both renal epithelial and endothelial cells can result from CM due to the cytotoxicity caused by iodine [5].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Alleviates Contrast-Induced Acute Kidney Injury by Activation of Sirt3

Zhang¹,

Suo²,

Liu³

et al. 2021

Oxidative Medicine and Cellular Longevity

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Oxidative stress and apoptosis play a vital role in the pathogenesis of contrast-induced acute kidney injury (CI-AKI). The purpose of our study was to investigate the protective effects and mechanisms of melatonin against CI-AKI in a CI-AKI mouse model and NRK-52E cells. We established the CI-AKI model in mice, and the animals were pretreated with melatonin (20 mg/kg). Our results demonstrated that melatonin treatment exerted a renoprotective effect by decreasing the level of serum creatinine (SCr) and blood urea nitrogen (BUN), lessening the histological changes of renal tubular injuries, and reducing the expression of neutrophil gelatinase-associated lipid (NGAL), a marker of kidney injury. We also found that pretreatment with melatonin remarkably increased the expression of Sirt3 and decreased the ac-SOD2 K68 level. Consequently, melatonin treatment significantly decreased the oxidative stress by reducing the Nox4, ROS, and malondialdehyde (MDA) content and by increasing the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity levels. The antiapoptotic effect of melatonin on CI-AKI was revealed by decreasing the ratio of Bax/Bcl2 and the cleaved caspase3 level and by reducing the number of apoptosis-positive tubular cells. In addition, melatonin treatment remarkably reduced the inflammatory cytokines of interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), and transforming growth factor β (TGFβ) in vivo and in vitro. Sirt3 deletion and specific Sirt3 siRNA abolished the above renoprotective effects of melatonin in mice with iohexol-induced acute kidney injury and in NRK-52E cells. Thus, our results demonstrated that melatonin exhibited the renoprotective effects of antioxidative stress, antiapoptosis, and anti-inflammation by the activation of Sirt3 in the CI-AKI model in vivo and in vitro. Melatonin may be a potential drug to ameliorate CI-AKI in clinical practice.

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“…The underlying mechanisms of CIN are complicated and not yet completely expounded. Current studies suggest that the occurrence of CIN is mainly associated with the following mechanisms: hypoxia damage to the renal parenchyma, direct toxicity of contrast media, oxidative stress, immunizing inflammatory response, cell pyroptosis, and apoptosis (5,6).…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin Attenuates Experimental Contrast-Induced Nephrology: A Role for the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling Pathway

et al. 2021

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The aim of the present study was to investigate the effect of erythropoietin (EPO) on contrast-induced nephrology (CIN) in vivo and in vitro. Male C57BL/6J mice were divided into four groups: control, CIN (iohexol 6.0 g/kg), EPO (3,000 IU/kg), and CIN+EPO. Hematoxylin and eosin (H&E) staining and biochemical index analyses were performed to evaluate renal injury. The cellular proliferation rate was detected using the Cell Counting Kit-8 (CCK-8) assay. In addition, a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and flow cytometric assay were used to assess the apoptosis of tissue and cells, respectively. Renal protein expression associated with apoptosis, pyroptosis, and signaling pathways was determined by Western blot (WB) assays for tissues and cells. The results showed that EPO significantly decreased serum creatinine, blood urea nitrogen, and cystatin C levels and alleviated renal histological changes in vivo. The protein levels of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway components were overexpressed in the EPO treatment group. Furthermore, EPO suppressed the cell apoptosis and pyroptosis; decreased the protein levels of cleaved caspase-3, Bax, gasdermin D (GSDMD), and caspase-1; and enhanced the expression of Bcl-2. In summary, EPO could exert renoprotective effect by activating the JAK2/STAT3 signaling pathway, which may be a novel potential therapy for the treatment of CIN in the clinic.

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Advances in the pathogenesis and prevention of contrast-induced nephropathy

Cited by 82 publications

References 127 publications

Risk factor analysis of acute kidney injury after one-stop hybrid coronary revascularization

Risk factor analysis of acute kidney injury after one-stop hybrid coronary revascularization

Melatonin Alleviates Contrast-Induced Acute Kidney Injury by Activation of Sirt3

Erythropoietin Attenuates Experimental Contrast-Induced Nephrology: A Role for the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling Pathway

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