Contrast-Induced Nephropathy: Pathophysiology and Preventive Strategies

Jorgensen, Ann L.

doi:10.4037/ccn2013680

Cited by 79 publications

(70 citation statements)

References 24 publications

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“…CIAKI is also associated with replacement therapy, prolonged hospitalization, increased medical cost and increased mortality [4, 5]. The factors contributed to the pathophysiology of CIAKI are still under controversy, but primarily involve the tubular toxicity, microvascular alteration, oxidative stress, inflammation and tubular obstruction [4, 6-8]. Among these factors, inflammatory damage may be regarded as one of the most crucial factors in the development of CIAKI.…”

Section: Introductionmentioning

confidence: 99%

“…CIAKI is the third most common cause of acute renal failure in hospitalized patients [1], accounting for up to 12% of all cases of acute renal failure [2, 3]. CIAKI is also associated with replacement therapy, prolonged hospitalization, increased medical cost and increased mortality [4, 5]. The factors contributed to the pathophysiology of CIAKI are still under controversy, but primarily involve the tubular toxicity, microvascular alteration, oxidative stress, inflammation and tubular obstruction [4, 6-8].…”

Section: Introductionmentioning

confidence: 99%

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Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Tan

Zheng

Huang

et al. 2017

Cell Physiol Biochem

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Background: Contrast-induced acute kidney injury (CIAKI) is a common cause of hospital-acquired acute kidney injury (AKI). S100A8/A9-TLR4-NLRP3 inflammasome pathway triggers inflammation, apoptosis and tissue injury in several AKI models. Nevertheless, the underlying mechanism of S100A8/A9-TLR4-NLRP3 inflammasome pathway in CIKAI is not clear. We aimed to investigate the possible role of S100A8/A9-TLR4-NLRP3 inflammasome in the pathophysiology of CIAKI. Methods: We treated male rats and NRK-52E cells by iopromide to establish in vivo and in vitro models of CIAKI. We collected serum and urine samples to detect renal function. We obtained kidney tissue for histological analysis and detection of protein concentration. We used inhibitor of TLR4 and NLRP3-siRNA to further testify their role in CIAKI in NRK-52E cells. Results: Iopromide caused elevation of SCr, BUN and NGAL level, decrease of endogenous creatinine clearance, morphological injury and tubular apoptosis, enhanced IL-1β and IL-18 expression, and increased expression of S100A8/A9, TLR4 and NLRP3 inflammsome. In NRK-52E cells, iopromide caused enhanced apoptotic rates and ROS generation, which could be ameliorated by inhibitor of TLR4 and NLRP3-siRNA. Moreover, inhibition of TLR4 dampened NLRP3 expression. Conclusion: S100A8/A9-TLR4-NLRP3 inflammasome pathway represented a key mechanism of CI-AKI, which provided a potential therapeutic target.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Tan

Zheng

Huang

et al. 2017

Cell Physiol Biochem

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“…Contrast-induced acute kidney injury (CI-AKI) is now the third most common cause of hospital-acquired renal failure. CI-AKI is associated with increased costs of medical care and long admissions and is a strong predictor of poor early and late outcomes [1, 3], especially in patients who are in need of dialysis [4]. Therefore there is a clear need to establish an appropriate and reproducible experimental animal model that can be used to help understand and prevent this disease.…”

Section: Introductionmentioning

confidence: 99%

A Novel Contrast-Induced Acute Kidney Injury Model Based on the 5/6-Nephrectomy Rat and Nephrotoxicological Evaluation of Iohexol and IodixanolIn Vivo

Liu

Luo

Tan

et al. 2014

Oxidative Medicine and Cellular Longevity

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Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. We found that six weeks after ablative surgery was the preferred time to induce CI-AKI. We compared multiple pretreatment plans and found that dehydration for 48 hours before iodixanol (320, 10 mL/kg) administration was optimal to induce CI-AKI in the 5/6 NE rats. Compared with iodixanol, iohexol induced a significantly greater reduction in renal function, severe renal tissue damage, intrarenal hypoxia, and apoptotic tubular cells. Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model.

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“…Iodinated CM-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury, which is associated with a lengthened hospital stay, increased health care costs and higher risk of mortality (1)(2)(3). Therefore, it is of great importance to explore effective strategies to prevent CIN.…”

Section: Introductionmentioning

confidence: 99%

Atorvastatin alleviates iodinated contrast media-induced cytotoxicity in human proximal renal tubular epithelial cells

Liu

Lei

Duan

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Contrast media (CM)-induced nephropathy (CIN) is a serious complication of intravascularly applied radiocontrast media. At present, no drugs have been approved for the prevention of CIN. The present study aimed to explore the effects and potential mechanisms of atorvastatin on iodinated CM-induced cytotoxicity in the human proximal renal tubular epithelial cells. The cytotoxic effect of iohexol (50, 100 and 200 mg I/ ml) and the protective effect of atorvastatin pretreatment (1, 20 and 40 µM) were assessed. The cytotoxicity of iohexol was evaluated via the MTT cell viability and lactate dehydrogenase assays. The amount of apoptotic cells was determined by flow cytometry. Morphological changes in HK-2 cells were observed via transmission electron microscopy. The mRNA expression of NOX4 and p22phox was measured through reverse transcription-quantitative polymerase chain reaction analysis. The cytotoxicity was induced by iohexol in HK-2 cells. Atorvastatin was identified to significantly alleviate the suppression of cell viability induced by iohexol. Notably, 40 µM atorvastatin also significantly reduced the mRNA expression of intracellular NOX4 and p22phox, and the percentage of apoptotic cells. Furthermore, morphological changes characteristic of injured cells were alleviated by atorvastatin pretreatment. These results suggest that atorvastatin exhibits a protective effect on HK-2 cells against iohexol-induced cytotoxicity through the downregulation of NOX4 and p22phox. Thus, atorvastatin is a potential therapeutic agent for the prevention of CIN and required further study.

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Contrast-Induced Nephropathy: Pathophysiology and Preventive Strategies

Cited by 79 publications

References 24 publications

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

A Novel Contrast-Induced Acute Kidney Injury Model Based on the 5/6-Nephrectomy Rat and Nephrotoxicological Evaluation of Iohexol and IodixanolIn Vivo

Atorvastatin alleviates iodinated contrast media-induced cytotoxicity in human proximal renal tubular epithelial cells

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