Pharmacologic Prophylaxis of Contrast-Induced Nephropathy

Toso, Anna; Leoncini, Mario; Maioli, Mauro; Bellandi, Francesco

doi:10.1016/j.iccl.2020.02.006

Cited by 4 publications

(2 citation statements)

References 90 publications

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“…N-acetylcysteine, nicorandil, and statins have been proven to protect kidneys in patients with kidney injuries, but their mechanisms remain to be further clarified [ 21 – 23 ]. Accordingly to the results of a small randomized trial and meta-analysis, specific drugs, such as N-acetylcysteine, ascorbic acid, aminophylline, trimetazidine, fenoldopam, etc., were effective in the treatment of CI-AKI, but they failed to prevent or treat CI-AKI in a large randomized trial.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway

Yue

et al. 2023

BMC Nephrol

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Background Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure. However, there is no effective treatment of CI-AKI, and its mechanism is unknown. Interestingly, atorvastatin has been reported to be effective in renal injury. Therefore, the aim of this study was to explore the effect and possible molecular mechanism of atorvastatin in CI-AKI. Methods On the CI-AKI in vitro model, rat tubular epithelial cells (NRK-52E) were treated with 18 mg I/ml meglumine diatrizoate (MEG) and then pretreated with atorvastatin. pcDNA3.1-TLR4 treatment was performed to overexpress toll-like receptor 4 (TLR4) in NRK-52E cells. Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) kits were used to detect NRK-52E cell viability as well as LDH release in each group, respectively; qRT-PCR to determine mRNA expression of TLR4 in cells; western blot to detect protein expression levels of pyroptosis-related proteins (NLRP3, caspase-1, ASC, and GSDMD) and TLR4/MyD88/NF-κB signaling pathway-related proteins (TLR4, MyD88, NF-κBp65, and p-NF-κB p65) in cells. Results MEG treatment significantly inhibited the viability of NRK-52E cells, increased pro-inflammatory factor levels and promoted pyroptosis, representing successful establishment of a rat tubular epithelial cell (NRK-52E) CI-AKI in vitro model. Notably, atorvastatin increased the activity of MEG-treated NRK-52E cells and alleviated cell injury in a concentration-dependent manner. In addition, atorvastatin significantly down-regulated the expression of TLR4 in MEG-treated NRK-52E cells. However, overexpression of TLR4 inhibited the effects of atorvastatin on increasing cell viability, alleviating cell injury, reducing pro-inflammatory factors (IL-1β, IL-6, and TNF-α) levels, and inhibiting apoptosis (by down-regulating the expression of NLRP3, caspase-1, ASC, and GSDMD). Furthermore, atorvastatin also inhibited the expression of TLR4/MyD88/NF-κB pathway-related proteins (TLR4, MyD88, and p-NF-κB p65). Conclusion Atorvastatin can attenuate CI-AKI through increasing the activity of MEG-treated renal tubular epithelial cells, relieving cell injury, as well as inhibiting pyroptosis and inflammation. More importantly, the mechanism was achieved by inhibiting the TLR4//MyD88/NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway

Yue

et al. 2023

BMC Nephrol

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“…Isto porque, estudos e meta-análises vem demonstrando resultados favoráveis ao uso das estatinas, mais especificamente rosuvastatina e atorvastatina, em diversas populações (51)(52)(53). Esse desfecho favorável parece estar relacionado à efeitos pleiotrópicos, não mediados por lipídios, devido a inibição da síntese de mevalonato e da redução de seus metabólitos (60).…”

Section: Consequências Da Nefropatia Induzida Por Contrasteunclassified

Eficácia do protocolo de hidratação oral como alternativa à hidratação endovenosa em indivíduos suscetíveis a desenvolver nefropatia induzida por contraste após coronariografia e intervenção coronária percutânea

Rodrigues Pioli

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Impact of atorvastatin reload on the prevention of contrast-induced nephropathy in patients on chronic statin therapy: A prospective randomized trial

Hammami,

Masmoudi,

Jdidi

et al. 2023

PLoS ONE

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Background This trial aimed to assess the efficacy of Atorvastatin reloading on the prevention of Contrast-induced nephropathy (CIN) in patients pre-treated with this statin and undergoing coronary catheterization. Methods This was a prospective randomized controlled study including patients on chronic atorvastatin therapy. We randomly assigned the population to the Atorvastatin Reloading group (AR group), by reloading patients with 80 mg of atorvastatin one day before and three days after the coronary procedure, and the Non-Reloading group (NR group), including patients who received their usual dose without a reloading dose. The primary endpoints were the incidence of cystatin (Cys)-based CIN and Creatinine (Scr)-based CIN. The secondary endpoints consisted of the changes in renal biomarkers (Δ biomarkers) defined as the difference between the follow-up level and the baseline level. Results Our population was assigned to the AR group (n = 56 patients) and NR group (n = 54 patients). The baseline characteristics of the 2 groups were similar. Serum creatinine (SCr)-based CIN occurred in 11.1% in the NR group, and in 8.9% in the AR group without any significant difference. Cys-based CIN occurred in 37% in the NR group and 26.8% in the AR group without any significant difference. The subgroup analysis showed that high dose reloading had significantly reduced the CYC-based CIN risk in patients with type 2 diabetes (43.5% vs 18.8%, RR = 0.43. CI 95% [0.18–0.99])). The comparison of “Δ Cystatin” and Δ eGFR between the AR and NR groups didn’t show any significant difference. However, cystatin C had significantly increased between baseline and at 24 hours in the NR group (0.96 vs 1.05, p = 0.001), but not in the AR group (0.94 vs 1.03, p = 0.206). Conclusions Our study did not find a benefit of systematic atorvastatin reloading in patients on chronic atorvastatin therapy in preventing CIN. However, it suggested that this strategy could reduce the risk of CyC-based CIN in diabetic type 2 patients.

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Pharmacologic Prophylaxis of Contrast-Induced Nephropathy

Cited by 4 publications

References 90 publications

Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway

Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway

Eficácia do protocolo de hidratação oral como alternativa à hidratação endovenosa em indivíduos suscetíveis a desenvolver nefropatia induzida por contraste após coronariografia e intervenção coronária percutânea

Impact of atorvastatin reload on the prevention of contrast-induced nephropathy in patients on chronic statin therapy: A prospective randomized trial

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