n randomized, controlled, blinded, imitation-controlled study the nephroprotective effect of RIPC in CHD patients with low-moderate CIN risk was investigated. As a result, 26 patients were randomizedfor RIPC and 25 for sRIPC. It is considered, that CIN develops in 9% of cases when iodinated contrast agent is injected [18], and in 20–30% among those with a baseline creatinine >2 mg/dl [2]. In our study, CIN developed in 28% of cases in sRIPC group, and in RIPC – only in 3.8%. The resultsUncorrected Author Proof approximately correspond to the data by Er et al. [9] who indicated 28% CIN reduction after RIPC,given the fact that in the above-referred study the GFR baseline threshold for inclusion in the studywas higher –≤60 mL/min/1,73 m2 in contrast to the present one (≤80 mL/min/1,73m2 173 ). Menting etal. [25] not noted the effect of RIPC on CIN occurrence in patients with moderate CIN risk, but in the high risk ones (≥11 points according to the Mehran score). Our data corresponds also with study of Igarashi et al. [17], who used more RIPC cycles (4 versus 3 in our study) and estimated another kidney-sensitive marker – liver-type fatty acid-binding protein (L-FABR) in patients with moderate CKD. As a result, CIN incidence decreased from 26.9% to 7.7% in compare to sham and L-FABRdeclined (p = 0,003), due to, as proposed by the authors, oxidative stress modification.As it is known, NGAL and cystatin-C have higher sensitivity and specificity of the predictive power in identification of AKI compared to creatinine and urea [7, 19]. For instance, creatinine increases in case of 50% of kidney tissue damage [15]. NGAL has proved as an early, sensitive, specific and predictive biomarker of AKI after contrast agent administration [32]. When the concentration of cystatin-C increases by 10%, it also shows itself to be a CIN marker which is 100% sensitive and 30% specificity[27, 32]. If in RIPC group there was a downward trend for all the four biomarkers after CAG, in the sRIPC group – they tended to increase, for creatinine and urea was significant. The comparison of changes between the sRIPC/RIPC groups before/after CAG was also significant.Thus in the study RIPC showed nephroprotective effect and considerably prevented CIN in patients with CHD and low-moderate GFR decline.This study has certain limitations. In particular, the sampling size is rather small; patients widely varied in kidney failure and GFR degree. However, the comparison of the obtained data with the findings of other studies allows us to suggest that the achieved results are reliable.
n randomized, controlled, blinded, imitation-controlled study the nephroprotective effect of RIPC in<br> CHD patients with low-moderate CIN risk was investigated. As a result, 26 patients were randomized<br>for RIPC and 25 for sRIPC. It is considered, that CIN develops in 9% of cases when iodinated contrast agent is injected [18], and in 20–30% among those with a baseline creatinine >2 mg/dl [2]. In our study, CIN developed in 28% of cases in sRIPC group, and in RIPC – only in 3.8%. The results<br>Uncorrected Author Proof approximately correspond to the data by Er et al. [9] who indicated 28% CIN reduction after RIPC,given the fact that in the above-referred study the GFR baseline threshold for inclusion in the study<br>was higher –≤60 mL/min/1,73 m2 in contrast to the present one (≤80 mL/min/1,73m2 173 ). Menting etal. [25] not noted the effect of RIPC on CIN occurrence in patients with moderate CIN risk, but in<br> the high risk ones (≥11 points according to the Mehran score). Our data corresponds also with study of Igarashi et al. [17], who used more RIPC cycles (4 versus 3 in our study) and estimated another kidney-sensitive marker – liver-type fatty acid-binding protein (L-FABR) in patients with moderate CKD. As a result, CIN incidence decreased from 26.9% to 7.7% in compare to sham and L-FABR<br>declined (p = 0,003), due to, as proposed by the authors, oxidative stress modification.<br>As it is known, NGAL and cystatin-C have higher sensitivity and specificity of the predictive power in identification of AKI compared to creatinine and urea [7, 19]. For instance, creatinine increases in case of 50% of kidney tissue damage [15]. NGAL has proved as an early, sensitive, specific and predictive biomarker of AKI after contrast agent administration [32]. When the concentration of cystatin-C increases by 10%, it also shows itself to be a CIN marker which is 100% sensitive and 30% specificity[27, 32]. If in RIPC group there was a downward trend for all the four biomarkers after CAG, in the sRIPC group – they tended to increase, for creatinine and urea was significant. The comparison of changes between the sRIPC/RIPC groups before/after CAG was also significant.Thus in the study RIPC showed nephroprotective effect and considerably prevented CIN in patients with CHD and low-moderate GFR decline.<br>This study has certain limitations. In particular, the sampling size is rather small; patients widely varied in kidney failure and GFR degree. However, the comparison of the obtained data with the findings of other studies allows us to suggest that the achieved results are reliable.
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