Radiographic Contrast-Media-Induced Acute Kidney Injury: Pathophysiology and Prophylactic Strategies

Sadat, Umar

doi:10.5402/2013/496438

Cited by 29 publications

(28 citation statements)

References 268 publications

(258 reference statements)

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“…A good example in this aspect is contrast medium-induced AKI 189 . Pre-existence of CKD is known to significantly increase the incidence of AKI following the administration of contrast medium in patients 190 .…”

Section: Potential Mechanisms Underlying the Susceptibility Andmentioning

confidence: 99%

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

Wei

Liu

et al. 2017

Kidney International

293

222

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Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-connected. While AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in CKD patients, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of TGF-β, p53, HIF, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathological changes may contribute to the heightened sensitivity of, and non-recovery from, AKI in CKD patients.

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Section: Potential Mechanisms Underlying the Susceptibility Andmentioning

confidence: 99%

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

Wei

Liu

et al. 2017

Kidney International

293

222

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“…It causes a prolonged in-hospital stay and predicting a bad recovery (Hou et al, 1983;Briguori et al, 2011). Although a number of measures had been taken to decrease the incidence of CIN, including invention of safer CM, improvement of hydration protocols, and usage of additional protective drugs, many patients still suffered the ravages of it (Sadat, 2013;Andreucci et al, 2014). Hemodynamic changes of renal blood flow by CM (Persson et al, 2005) and direct toxic effects on renal cells (Romano et al, 2008) are thought to be the main pathogenesis of CIN.…”

Section: Introductionmentioning

confidence: 97%

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

Guan

Chen

Zuo

et al. 2017

DNA and Cell Biology

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With the rapid development of imaging diagnosis and interventional therapy, contrast media (CM) are widely used in clinics. However, contrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure accounting for 10-12% of all causes of hospital-acquired renal failure. Recent study found that inflammation may participate in the pathogenesis of CIN, but the role of it remains unclear. HK-2 cells were treated with Iohexol, Urografin, and mannitol. Two types of CM increased the release of HMGB1 in cell supernatant accompanied by increased expression of TLR2 and CXCR4. Iohexol and Urografin also caused a significant increase in NF-κB followed by the release of IL-6 and MCP-1. To clarify the role of HMGB1, TLR2, and CXCR4, glycyrrhizin, anti-TLR2-IgG, and AMD3100 were used to inhibit HMGB1, TLR2, and CXCR4, respectively. Significant decrease in the expression of TLR2, CXCR4, nuclear NF-κB, and the release of IL-6 and MCP-1 were observed. These results indicate that TLR2 and CXCR4 signaling are involved in CM-induced HK-2 cell injury model in an HMGB1-dependent pathway, which may provide a new target for the prevention and the treatment of CIN.

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“…22,23 The pathophysiology of CIN probably involves a combination of direct tubular toxicity and renal ischemic injury but remains incompletely understood. 24,25 There is also evidence suggesting renal dysfunction at admission in patients with stroke is associated with poor outcomes. 26 During emergent stroke evaluation and treatment, patients often have unknown medical histories and are unable to provide this history or history about the aforementioned CIN risk factors.…”

Section: August 2016mentioning

confidence: 99%

Safety of Computed Tomographic Angiography in the Evaluation of Patients With Acute Stroke

Ehrlich

Turner

Currie

et al. 2016

Stroke

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Background and Purpose-Noncontrasted head computed tomography (NCHCT) has long been the standard of care for acute stroke imaging. New guidelines recommending advanced vascular imaging to identify eligible patients for endovascular therapy have renewed safety concerns on the use of contrast in the emergent setting without laboratory confirmation of renal function. Methods-We compared computed tomographic angiography (CTA) versus NCHCT alone during acute stroke evaluation with focus on renal safety and timeliness of therapy delivery. We reviewed data on all emergency department patients for whom the Acute Stroke Intervention Team was activated between December 2013 and September 2014. Primary outcomes included acute kidney injury and change in serum creatinine from presentation to 24 to 48 hours (Δ serum creatinine [Cr]). We assessed therapy delay using door-to-CT and door-to-needle times. Results-Of

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Radiographic Contrast-Media-Induced Acute Kidney Injury: Pathophysiology and Prophylactic Strategies

Cited by 29 publications

References 268 publications

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

Safety of Computed Tomographic Angiography in the Evaluation of Patients With Acute Stroke

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