Preventive effect of trimetazidine on contrast-induced nephropathy undergoing percutaneous coronary intervention in elderly moderate and high risk diabetics stratified by mehran score

Abstract

Background: The aim of this research was to use the Mehran risk score to classify elderly diabetics with coronary heart disease to assess the preventive effect of trimetazidine on contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI) in different risk population. Methods: An uncompromised of 760 elderly diabetics that went through PCI were included in this research. The patients were first divided into three groups in the light of MRS: low-risk, moderate-risk, and high-risk group, then randomized into trimetazidine group and the control group respectively. The first endpoint was the amount of CIN, which is described as a rise in serum creatinine levels by ⩾44.2 μmol/L or ⩾25% ratio within 48 or 72 hours after medication. Second endpoint included differences in creatinine clearance rate (CrCl), blood urea nitrogen (BUN), serum creatinine (Scr), cystatin-C (Cys-C), and the incidence of major adverse events after administration. Results: In the three groups, the incidence of CIN in trimetazidine and control group was 5.0% versus 4.9%(χ2 = 0.005, p > 0.05), 8.0% versus 18.0% (χ2 = 7.685, p < 0.05), 10.4% versus 27.1% (χ2 = 4.376, p < 0.05), respectively. The multivariable logistic regression result demonstrated that trimetazidine intervention was a profitable element of CIN in moderate and high-risk groups (OR = 0.294, 95% CI 0.094-0.920, p = 0.035). Conclusion: Our study confirmed that trimetazidine can be considered for preventive treatment of CIN occurrence in elderly diabetics with moderate and high-risk population, while there is no obvious advantage compared with hydration therapy in low-risk patients.

Preventing contrast-induced acute kidney injury with probucol and hydration in patients with coronary heart disease: A systematic review and meta-analysis of randomized controlled trials

“…Five trials [18,19,21,22,25] reported the eGFR 72 hours after contrast medium exposure. The eGFR was higher in the probucol with hydration group than the hydration-only group (MD: 5.94, 95% CI: 3.70–8.17, P < .001; I 2 = 2%, P = .39, fixed effect model; Table 2 and Fig.…”

“…The same results were observed for the Scr level after 48 hours (MD: -13.78, 95% CI: -22.08 to -5.49, P = .001; I 2 = 91%, P < .001; random effect model, 6 trials [12,13,16,17,21,24] ; Table 2 and Fig. 6B) and 72 hours (MD: -8.76, 95% CI: -12.25 to -5.26, P < .001; I 2 = 82%, P < .001, random effect model, 12 trials [12,13,[16][17][18][19][20][21][22][23][24][25] ; Table 2 and Fig. 6C).…”

“…Mean differences (MD) with 95% CIs were used as the effective index for continuous outcomes. The heterogeneity of the trials was assessed using Cochran Q Incidence of CI-AKI in total 14 [12][13][14][15][16][17][18][19][20][21][22][23][24][25] 3306 .26 17% Fixed 0.33 (0.25, 0.44) <.001 Incidence of CI-AKI in subgroups: volume of CM <200 mL 12 [12][13][14][15][18][19][20][21][22][23][24][25] 3040 .19 26% Fixed 0.35 (0.26, 0.46) <.001 volume of CM ≥ 200 mL 2 [16,17] 266 .99 0% Fixed 0.22 (0.08, 0.60) .003 IOCM 7 [18][19][20][22][23][24][25] 1532 .07 49% Fixed 0.52 (0.34, 0.81) .003 LOCM 7 [12][13][14][15][16][17]21] 1774 .71 0% Fixed 0.37 (0.27, 0.51) <.001 SCr at 24 h 4 [12,13,16,17] 649 .81 0% Fixed −6.09 (−9.67, −2.51) .001 SCr at 48 h 6…”

Trimetazidine Protects from Mercury-Induced Kidney Injury

“…It has the potential to be used to treat the metabolic remodeling of heart failure (HF). TMZ can inhibit the excessive release of oxygen-free radicals, increase glucose metabolism, limit intracellular acidosis, and prevent the accumulation of protons, sodium, and calcium in muscle cells during cardiac ischemic [9, 39, 40]. Besides beneficial effects on the heart, several studies have shown the protective effects of TMZ on kidney injury [8-12, 14, 15, 40].…”

“…Different studies showed that 3-KAT in the mitochondrial matrix inhibit pyruvate dehydrogenase. Thus, by inhibiting 3-KAT, TMZ could increase pyruvate dehydrogenase activity, which in turns substantially increase myocardial glucose oxidation and increase the oxygen use during myocardial hypoxia [40, 43]. In addition, Li et al [43] proposed that a potential mechanism for the cardioprotective effect of TMZ linked with the regulation of adenosine monophosphate-activated protein kinase expression, where activation of adenosine monophosphate-activated protein kinase in turns increase glucose uptake via glucose transporter 4, and increase fatty acid uptake and oxidation by increasing the activity of carnitine palmitoyltransferase 1.…”