Pharmacological Strategies to Prevent Contrast-Induced Acute Kidney Injury

Pattharanitima, Pattharawin; Tasanarong, Adis

doi:10.1155/2014/236930

Cited by 44 publications

(45 citation statements)

References 131 publications

(117 reference statements)

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“…This is also important in reducing the concentration and viscosity of contrast. [23] There is also a theoretical concern for prolonged tubular exposure to iondinated contrast mediaum due to low tubular flow rates. [24] According to the Canadian Association of Radiologist consensus guidelines for prevention of contrast induced nephropathy update which were published in 2014, [6] 1.…”

Section: Fluid Hydrationmentioning

confidence: 99%

Contrast-Induced Nephropathy: Identifying the Risks, Choosing the Right Agent, and Reviewing Effective Prevention and Management Methods

Nicola

Shaqdan

Aran

et al. 2015

Current Problems in Diagnostic Radiology

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Section: Fluid Hydrationmentioning

confidence: 99%

Contrast-Induced Nephropathy: Identifying the Risks, Choosing the Right Agent, and Reviewing Effective Prevention and Management Methods

Nicola

Shaqdan

Aran

et al. 2015

Current Problems in Diagnostic Radiology

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“…However, although strategies for preventing CI-AKI have been extensively studied, pharmacological renal protection strategies still need to be explored [13]. …”

Section: Introductionmentioning

confidence: 99%

Relaxin Attenuates Contrast-Induced Human Proximal Tubular Epithelial Cell Apoptosis by Activation of the PI3K/Akt Signaling Pathway In Vitro

Xie

Cao

Yang

et al. 2017

BioMed Research International

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Background. Contrast-induced acute kidney injury (CI-AKI) is one of the main causes of iatrogenic acute kidney injury (AKI); however, therapeutic strategies for AKI remain limited. This study aims to explore the effect of relaxin (RLX) on contrast-induced HK-2 apoptosis and its underlying mechanisms. Methods. Renal tubular epithelial cells (HK-2) were incubated either with or without ioversol, human H2 relaxin, and LY294002 (the inhibitor of the PI3K/Akt signal pathway). Cell viability was evaluated with a CCK-8 assay. Apoptotic morphologic alterations were observed using the Hoechst 33342 staining method. Apoptosis was detected with Annexin V staining. Western blot analysis was employed to measure the expression of pAkt (S473), Akt, cleaved caspase-3, Bcl-2, Bax, and actin proteins. Results. Ioversol reduced the viability of HK-2 cells. Western blotting results revealed decreased expression of phosphorylated Akt in cells treated with ioversol. The activities of caspase-3 and Bax protein increased, while the expression of Bcl-2 protein decreased. As a result, the Bax/Bcl-2 ratio increased after treatment with ioversol. These effects were reversed when HK-2 cells were cotreated with RLX. However, with preadministration of PI3K/Akt pathway inhibitor LY294002, the effect of RLX was blocked. Conclusion. Our study demonstrates that relaxin attenuates ioversol induced cell apoptosis via activation of the PI3K/Akt signaling pathway, suggesting that RLX might play a protective role in the treatment of CI-AKI.

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“…Although hypoxia of the renal medulla [20–22] due to reduction of renal blood flow (RBF) especially in peritubular capillaries [23] and consequent oxidative stress are thought to be the major effectors of CI-AKI [13, 24–26], the exact pathomechanism is unknown [15, 20]. Thus CI-AKI is a subject of intense research.…”

Section: Introductionmentioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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Contrast-induced acute kidney injury (CI-AKI) can occur in 3–25% of patients receiving radiocontrast material (RCM) despite appropriate preventive measures. Often patients with an atherosclerotic vasculature have to receive large doses of RCM. Thus, animal studies to uncover the exact pathomechanism of CI-AKI are needed. Sensitive and specific histologic end-points are lacking; thus in the present review we summarize the histologic appearance of different rodent models of CI-AKI. Single injection of RCM causes overt renal damage only in rabbits. Rats and mice need an additional insult to the kidney to establish a clinically manifest CI-AKI. In this review we demonstrate that the concentrating ability of the kidney may be responsible for species differences in sensitivity to CI-AKI. The most commonly held theory about the pathomechanism of CI-AKI is tubular cell injury due to medullary hypoxia. Thus, the most common additional insult in rats and mice is some kind of ischemia. The histologic appearance is tubular epithelial cell (TEC) damage; however severe TEC damage is only seen if RCM is combined by additional ischemia. TEC vacuolization is the first sign of CI-AKI, as it is a consequence of RCM pinocytosis and lysosomal fusion; however it is not sensitive as it does not correlate with renal function and is not specific as other forms of TEC damage also cause vacuolization. In conclusion, histopathology alone is insufficient and functional parameters and molecular biomarkers are needed to closely monitor CI-AKI in rodent experiments.

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Pharmacological Strategies to Prevent Contrast-Induced Acute Kidney Injury

Cited by 44 publications

References 131 publications

Contrast-Induced Nephropathy: Identifying the Risks, Choosing the Right Agent, and Reviewing Effective Prevention and Management Methods

Contrast-Induced Nephropathy: Identifying the Risks, Choosing the Right Agent, and Reviewing Effective Prevention and Management Methods

Relaxin Attenuates Contrast-Induced Human Proximal Tubular Epithelial Cell Apoptosis by Activation of the PI3K/Akt Signaling Pathway In Vitro

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

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