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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2021  |  Volume : 32  |  Issue : 2  |  Page : 318-327
Acute kidney injury in patients with ST-segment elevation acute myocardial infarction: Predictors and outcomes


1 GBUZ TO “Regional Clinical Hospital No. 1”; Department of Cardiology and Cardiac Surgery, Federal State Budgetary Educational Institution of Higher Education Tyumen State Medical University of the Ministry of Healthcare of the Russian Federation, Tyumen, Russia
2 Department of Hospital Therapy, Federal State Budgetary Educational Institution of Higher Education Tyumen State Medical University of the Ministry of Healthcare of the Russian Federation, Tyumen, Russia

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Date of Web Publication11-Jan-2022
 

   Abstract 


The development of acute kidney injury (AKI) in patients during hospitalization worsens the prognosis. The study aimed to estimate the prognostic value of AKI in patients with ST-segment elevation myocardial infarction (MI) in prospective follow-up study. A prospective follow-up of 12 months included 268 patients with ST-segment elevation MI who underwent percutaneous coronary intervention. The incidence of AKI was assessed and its effect on the outcome of ST-segment elevation MI during the observed period was traced. AKI was diagnosed according to Kidney Disease: Improving Global Outcomes recommendations. AKI was recorded in 20.5%. The incidence of AKI increased with decrease in the level of glomerular filtration rate on admission (P = 0.047) and an increase in the stage of acute heart failure according to Killip on admission (P = 0.006). The development of AKI was associated with an increase in-hospital mortality, increasing with a worsening stage of AKI (P<0.001), the same pattern was characteristic for death from cardiovascular causes during follow-up. AKI increases the risk of death from cardiovascular causes by four times [odds ratio 95% 4.400 (1.928–10.040), P <0.001]. The multivariate analysis revealed risk factors for the development of AKI: age >75 years (P = 0.006), female (P = 0.008), Killip >I (P = 0.045). AKI is common in patients with ST-segment elevation MI and is associated with a poor prognosis. The development of AKI is associated with an increase mortality, increasing with a worsening stage of AKI.

How to cite this article:
Mezhonov EM, Vialkina IA, Vakulchik KA, Shalaev SV. Acute kidney injury in patients with ST-segment elevation acute myocardial infarction: Predictors and outcomes. Saudi J Kidney Dis Transpl 2021;32:318-27

How to cite this URL:
Mezhonov EM, Vialkina IA, Vakulchik KA, Shalaev SV. Acute kidney injury in patients with ST-segment elevation acute myocardial infarction: Predictors and outcomes. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Aug 15];32:318-27. Available from: https://www.sjkdt.org/text.asp?2021/32/2/318/335442



   Introduction Top


Chronic kidney disease (CKD) is an extremely common comorbid disease among patients with various types of acute coronary syndrome (ACS), according to the ACTION-GTWG register CKD occurred in 30.5% of patients with segment elevation myocardial infarction (STEMI).[1] Despite the success of modern methods of revascularization, the presence of CKD is a risk factor for death in patients with MI.[2] The development of acute kidney injury (AKI) in patients during hospitalization due to STEMI worsens the prognosis, so according to the ACTION- GTWG register the incidence of AKI in patients with STEMI was 16.1%, including 4% with severe AKI (creatinine >88.4 μmol/ L), and hospital mortality among patients with moderate (increased creatinine from 44.2to 8.4 μmol/L) and severe AKI was 14.2% and 31.8%, respectively, while in patients without AKI - 2.1%.[3] AKI is associated with an unfavorable short-term and long-term prognosis and directly correlates with the severity of renal dysfunction.[4],[5],[6] A major problem is the contrast-induced AKI (CI-AKI), which develops after percutaneous coronary intervention (PCI) in patients with ACS. A progressive decline in renal function is observed in 16%–28% of patients with ACS after PCI defined as an increase in creatinine levels by more than 25% within 48 h after PCI.[7],[8] In patients with STEMI, the development of AKI is possible due to various mechanisms: reduction of ejection fraction, conducting PCI, nephrotoxic effect of drugs. The main risk factor for AKI is considered to be preceding CKD, in addition are not excluded the effects of diabetes, dehydration, heart failure and left ventricular dysfunction, age over 80 years, and severe hypotension.[9],[10] The development of AKI is an important predictor of death and cardiovascular complications in patients with ACS. The purpose of this study was to study the frequency of development and prognostic value of AKI as a risk factor for cardiovascular death among patients with STEMI.


   Materials and Methods Top


The prospective 12 months follow-up study included 268 patients with STEMI after PCI who were admitted to hospital during the one year period, aged 32–95 years (mean age - 62.3 ± 10.78 years), of which 193 (72%) are men. All patients underwent a complete clinical examination. Laboratory and instrumental examination included clinical blood tests, electrocardiogram, echocardiography, biochemical blood analysis with mandatory determination of the creatinine level on admission and in the 2ndand 7th days of admission, as well as more often if necessary. For the diagnosis of MI, we used the criteria of Russian recommendations for the diagnosis and treatment of patients with STEMI.[11] PCI was performed using radial or femoral access (at the discretion of the operator). Patients received acetylsalicylic acid 250 mg and clopidogrel 600 mg or ticagrelor 180 mg and an intravenous bolus of unfractionated heparin (4000–6000 IU, adapted by weight) before PCI. All patients received non-ionic, triiodinated, low-osmolar, water soluble X-ray contrast medium 300 or 370 mg iodine/mL (Ultravist, Bayer AG, Germany or Iopamiro, Patheon Italia S.p.A., Italy). After clarifying the nature of the lesion of the coronary arteries, direct stenting of the coronary arteries or balloon predilation was performed followed by stenting at the discretion of the operator. To assess the functional state of the kidneys was calculated glomerular filtration rate (GFR) using the CKD-EPI formula. CKD was diagnosed based on the criteria of the Russian recommendations.[12],[13] AKI was diagnosed according to the recommendations of Kidney Disease: Improving Global Outcomes (KDIGO).[14] AKI stage 1 was recorded in the event of an increase in creatinine level 1.5–1.9 times higher than the baseline, which, as is known or assumed, occurred within sevendays or increased by ≥26.5 μmol/L for 48 h, AKI stage 2 - creatinine level rises 2.0–2.9 times higher than baseline, which, as is known or assumed, occurred within seven days, AKI stage 3 - creatinine level rises three times higher than baseline, which is known or assumed, occurred within seven days or increased to ≥353.6 μmol/L within 48 h. AKI was considered transient when creatinine level was reduced to baseline values (±10%) by the time of discharge, otherwise it was defined as persistent. In most cases the creatinine level was unknown before admission to the hospital so it was difficult to judge the presence of CKD.

The exclusion criteria were: a sharp deviation of the patient’s muscle mass from the average values, pronounced exhaustion and obesity (body mass index<15 and >40 kg/m2), pregnancy, diseases of the skeletal muscles (muscular dystrophy), paralysis/paresis of the extremities, condition after kidney transplantation, suspected difficulties follow-up of patients. All patients received standard pharmacological therapy according to the recommendations for managing patients with STEMI. Outcomes were assessed on 3rd, 6th and 12 months after discharge of the patient from the hospital during a telephone survey. The end point was defined as death from cardiovascular causes. Death was considered cardiovascular unless another reason was apparent. The study of creatinine was performed by the kinetic colorimetric method on the analyzer Cobas Integra Instrument (Roche Diagnostic, Germany).


   Statistical Analysis Top


Statistical processing of the obtained results was performed using the IBM SPSS Statistics for Windows, version 23.0 (IBM SPSS, IBM Corp., Armonk, N.Y., USA). To determine the statistical significance of differences in continuous values depending on the distribution parameters unpaired Student’s t-test or Mann–Whitney U-test was used. When comparing three independent groups and more than one characteristic, depending on the distribution parameters, the Kruskal–Wallis criterion or univariate analysis of variance were used. To identify predictors of unfavorable outcomes, a direct step-by-step binary logistic regression algorithm with relative risk and 95% confidence interval was selected. Variables with a value of P<0.05 in the univariate analysis were included in the multivariate analysis. To conduct a survival analysis Kaplan–Meier estimates and survival function plots were used. The differences were considered reliable at a bilateral significance level of P <0.05 for all analyzes. In the case of a normal distribution, the data are presented as M±SD, where M is the arithmetic mean, SD is the standard deviation, otherwise the data are presented as the median and interquartile range - Me (25th percentile; 75th percentile). The study was conducted in accordance with the principles of the 1964 Declaration of Helsinki.


   Results Top


Depending on the initial GFR values at admission to the hospital the patients were divided into groups CKD stages as per KDIGO classification of CKD. Renal dysfunction (GFR <60 mL/min) occurred in 21.3% of patients. Data on the severity of renal dysfunction in patients is reflected in [Figure 1].
Figure 1: The distribution of patients depending on the level of glomerular filtration rate.

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AKI developed in 20.5% of patients with STEMI, including AKI stage 1 (17.2%), AKI stage 2 (3%), AKI stage 3 (0.4%). Clinical and demographic characteristics of patients depending on the presence of AKI are presented in [Table 1] and [Table 2].
Table 1: Demographic characteristics of patients and therapy depending on the presence of acute kidney injury.

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Table 2: Clinical characteristics of patients depending on the presence of acute kidney injury.

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The incidence of AKI in patients with GFR<60 mL/min at admission to hospital was 33.3%, while at a level of GFR>60 mL/min - 17.1% (P=0.007). The incidence of AKI increased with a decrease in the level of GFR when admitted to hospital, so when the level of GFR over 90 mL/min the frequency of AKI of different stages reached 13.6%, with the level of GFR from 60 to 89 mL/min - 19.5%, GFR from 45 to 59 mL/min - 28.6%, with the level of GFR from 30 to 44 mL/min - 40.0%, with the level of GFR from 15 to 29 mL/min - 42.9% (P=0.047). GFR<60 mL/min upon admission to the hospital increased the odds ratio (OR)of the development of AKI by twice times (OR 95% 2.431 [1.260–4.690], P = 0.008). Patients with AKI were less likely to have an angiotensin converting enzyme inhibitor (ACEI)/angiotensin receptor antagonist (ARB) and statins than patients without AKI (P=0.005 and P=0.027, respectively).

The incidence of development AKI was also associated with the Killip stage of acute heart failure (AHF) at admission, AKI was more frequent with higher degrees of AHF, so with Killip I AKI was found in 18.6%, Killip II - 20.0%, Killip III - 33.3%, and with Killip IV - 71.4% (P = 0.006). Killip ≥I increases the OR of AKI by three times [OR 95% 2.736 (1.165–6.426), P = 0.021], Killip ≥III increases the OR of AKI by four times [OR 95% 4.362 (1.557–12.217), P = 0.005].

The average dose of the contrast medium used during PCI did not differ in patients with GFR >60 mL/min and GFR <60 mL/min and was 143 ± 52.5 mL and 157 ± 53.8 mL (P = 0.079), while the contrast media volume/GFR index in patients with GFR >60 mL/min and GFR <60 mL/min was significantly different and amounted to 1.49 (1.11; 2.22) and 3.7 (1.95; 4.72), respectively (P <0.001). The contrast media volume/GFR index in patients with AKI was higher than in patients without AKI and was 2.15 (1.35; 3.57) and 1.72 (1.14; 2.35) (P = 0.005), thus not the actual volume of the contrast medium, but the contrast media volume/GFR index more accurately reflects the effect of the contrast medium on the development of AKI, and the index volume of contrast/GFR more than 2.67 increased OR development AKI 3.5 times [OR 95% 3.547 (1.430–8.794), P = 0.006]. Among other traditional risk factors for AKI in patients with ACS age can also be distinguished in our study. Patients with AKI were older compared with patients without AKI - 61.2 ± 9.86 and 66.4 ± 13.08 years (P = 0.001). While the frequency of diabetes mellitus (P = 0.692), anemia (P = 0.786), hypertension (P = 0.087) and the anterior localization of STEMI (P = 0.804) did not differ in patients with AKI and without the development of this complication. Anamnestic indications of kidney disease before admission to the hospital due to the development of an index event were present in nine patients (3.4%) and were equally common among patients with development and without AKI (P = 0.898). There were no cases of renal replacement therapy for AKI in our study. The development of AKI was not associated with an increase in the frequency of all cases of bleeding according to the criteria of the TIMI group (P = 0.206). The frequency of various variants of coronary artery lesions according to coronary angiography in patients with developed AKI and without it was comparable (P =0.512).

During the follow-up period from 2day to 14 months (median 12 months), in 27 patients (10.1%) was recorded an endpoint: 21 cases of in-hospital mortality during the index event, six deaths from cardiovascular causes during a time interval of 12 months, three of which died from acute decompensation of heart failure, three from repeated MI.

The development of AKI was associated with an increase in-hospital mortality in patients with STEMI, increasing with a worsening stage of AKI, so with AKI stage 1 in-hospital mortality was 17.4%, AKI stage 2 - 25.0%, AKI stage 3- 100% (P <0.001). The same pattern was characteristic for death from cardiovascular causes during the 12 months period. An OR analysis of the onset of death from cardiovascular causes within 12 months, depending on the presence or absence of AKI, showed that AKI increases the risk of this end point by four times [OR 95% 4.400 (1.928–10.040), P <0.001], while AKI stage 1 increases the risk of in-hospital mortality by four times [OR 95% 4.274 (1.585–11.526), P = 0.004], and AKI ≥stages 2 - 10 times [OR 95% 10.150 (2.210–46.613), P = 0.003].

In four out of 55 (7.3%) cases of AKI was transient, while 92.7% of AKI cases were persistent and were not resolved at the time of discharge. The transient nature of AKI did not improve the prognosis of patients compared with persistent AKI, so the incidence of deaths from cardiovascular causes in patients with transient AKI was 25% and persistent AKI - 23.5% (P = 1.0).

Two patients did not received antiplatelet drugs due to the development of large or moderate bleeding according to the TIMI group criteria after prehospital thrombolysis was performed, one patient had drug intolerance to acetylsalicylic acid, two patients could not take P2Y12 inhibitors (ticagrelor and clopidogrel) due to known drug intolerance. These cases ultimately affected the frequency of administration of these drugs in the general group of patients. 97.7% and 96.4% of patients with AKI and without AKI, respectively, received double antiplatelet therapy (P = 0.593).

Univariate analysis revealed several risk factors for the development of AKI [Table 3]: age >75 years (P <0.001), GFR less than 60 mL/min (P = 0.008), female gender (P <0.001), Killip >I (P = 0.021), the index contrast media volume/GFR >2.67 (P = 0.006), intra-aortic balloon pump (P =0.016). In order to reduce the risk of reassessing statistical data, variables with a value of P <0.05 in a univariate analysis were included in the multivariate analysis. In the multivariate analysis the following risk factors for the development of AKI were confirmed: age >75 years (P=0.006), female gender (P=0.008), Killip>I (P =0.045).
Table 3: Risk factors for the development of AKI.

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Kaplan-Meier survival curves depending on the degree of AKI diverged early which gave a statistically significant difference in cardiovascular mortality (Log-Rank P <0.001) and overall mortality (Log-Rank P <0.001), the separation of the curves continued throughout the observation period, with an increase in the probability of death from cardiovascular causes [Figure 2] and overall mortality [Figure 3] during the follow-up of 12 months with an increase in the stage of AKI.
Figure 2: Kaplan–Meier curves for death from cardiovascular causes depending on the degree of acute kidney injury.
AKI: Acute kidney injury.


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Figure 3: Kaplan–Meier curves for overall mortality depending on the degree of acute kidney injury.
AKI: Acutekidneyinjury.


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   Discussion Top


According to our data the incidence of AKI in patients with STEMI was 20.5%, which is slightly higher than the incidence of AKI in patients with ACS according to a meta- analysis Vandenberghe et al, in which AKI developed on average in 12.7% of patients,[15] and in the Marenzi et al study, where the incidence of AKI in patients with STEMI was 15%.[16] In the study of Abellás-Sequeiros et al in patients with ACS and the development of CI-AKI, the dose of the contrast medium was higher compared to patients without CI-AKI 194.2 ± 100.6 mL and 162.6 ± 130.1 mL (P = 0.01) respectively.[17] In our study, the dose of contrast medium did not differ between two groups, while the contrast media volume/GFR index in patients with AKI was higher than in patients without AKI (P = 0.005), and the contrast media volume/GFR more than 2.67 increased OR of AKI development by 3.5 times [OR 95% 3.547 (1.430–8.794), P = 0.006]. In the Ibaraki Cardiovascular Assessment Study[18] in patients with STEMI the risk of developing CI-AKI did not increase with an increase in contrast media volume/GFR, while in patients with stable angina contrast media volume/GFR ≥3.0 was a predictor of development CI-AKI after PCI. The average dose of the contrast medium used during PCI, did not differ in patients with GFR >60 mL/min and GFR<60 mL/min (P = 0.079). Thus, it is not the actual volume of the contrast medium, but the index contrast media volume/GFR more accurately reflects the influence of the contrast medium on the development of AKI. Probably due to increased risk of renal impairment in patients with initially low GFR values after PCI, despite the use of medium dosages of the contrast medium. At the same time patients with STEMI who underwent PCI are a population with an increased risk of developing AKI, for which interventions aimed at preventing the development of AKI, especially hydration, are difficult to implement due to the need for urgent PCI. An accurate assessment of the contribution of the contrast medium to the development of AKI in patients with STEMI is associated with a number of difficulties, among which the absence of a control group of patients is crucial, since PCI is the method of choice for treating patients with STEMI. According to the data of M.V. Menzorov the incidence of AKI in patients with STEMI in whom the strategy of throm-bolytic therapy was chosen as the method of myocardial revascularization was 25%,[19] which is comparable to the incidence of AKI in our study, where all patients underwent PCI. In the work of Caspi et al the incidence of AKI in patients with STEMI after PCI and in the control group (thrombolytic therapy or absence of reperfusion therapy) was also comparable (10.3% vs. 12.1%, respectively, P = 0.38).[20]

According to Buargub and Elmokhtar inhospital mortality in patients with ACS and AKI reached 25.7%, while in patients without AKI it was 6.12% (P = 0.014).[21] These data are consistent with our results so in-hospital mortality in patients with AKI and without AKI was 20% and 4.7%, respectively (P <0.001). In the work of Liao et al, Killip ≥III in multivariate analysis increased OR of development of AKI by four times (OR 95% 3.79 (1.68–8.55), P <0.001).[22] According to the results of our study Killip >I increase the risk of development AKI by three times [OR 95% 2.549 (1.019–6.374), P =0.045], and Killip ≥III increase the risk of development AKI by four times [OR 95% 4.362 (1.557–12.217), P=0.005].


   Conclusion Top


AKI is quite common in patients with STEMI and is associated with a poor prognosis. Given the high prevalence and adverse effect on the prognosis of AKI in patients with STEMI it seems appropriate to study the serum creatinine level immediately upon admission of the patient to the hospital and over the course of his stay in the hospital, which will allow to identify patients at risk of AKI and take such preventive measures as, adequate patient hydration, the use of the minimum necessary volume of contrast medium, the use of an low-osmolar contrast medium and the restriction or rejection of the use of potentially nephrotoxic drugs. The onset of AKI in patients with STEMI can be predicted using predictors: age >75 years (P = 0.006), female gender (P = 0.008), Killip >I (P = 0.045).

Conflict of interest: None declared.



 
   References Top

1.
Fox CS, Muntner P, Chen AY, et al. Use of evidence-based therapies in short-term outcomes of ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction in patients with chronic kidney disease: A report from the National Cardiovascular Data Acute Coronary Treatment and Intervention Outcomes Network registry. Circulation 2010;121:357-65.  Back to cited text no. 1
    
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Nauta ST, van Domburg RT, Nuis RJ, Akkerhuis M, Deckers JW. Decline in 20-year mortality after myocardial infarction in patients with chronic kidney disease: Evolution from the prethrombolysis to the percutaneous coronary intervention era. Kidney Int 2013;84:353-8.  Back to cited text no. 2
    
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Fox CS, Muntner P, Chen AY, Alexander KP, Roe MT, Wiviott SD. Short-term outcomes of acute myocardial infarction in patients with acute kidney injury: A report from the National Cardiovascular Data Registry. Circulation 2012;125:497-504.  Back to cited text no. 3
    
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Goldberg A, Kogan E, Hammerman H, Markiewicz W, Aronson D. The impact of transient and persistent acute kidney injury on long-term outcomes after acute myocardial infarction. Kidney Int 2009;76:900-6.  Back to cited text no. 4
    
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Choi JS, Kim YA, Kim MJ, et al. Relation between transient or persistent acute kidney injury and long-term mortality in patients with myocardial infarction. Am J Cardiol 2013; 112:41-5.  Back to cited text no. 5
    
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Marenzi G, Cabiati A, Bertoli SV, et al. Incidence and relevance of acute kidney injury in patients hospitalized with acute coronary syndromes. Am J Cardiol 2013;111:816-22.  Back to cited text no. 6
    
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Senoo T, Motohiro M, Kamihata H, et al. Contrast-induced nephropathy in patients undergoing emergency percutaneous coronary intervention for acute coronary syndrome. Am J Cardiol 2010;105:624-8.  Back to cited text no. 7
    
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Nemoto N, Iwasaki M, Nakanishi M, et al. Impact of continuous deterioration of kidney function 6 to 8 months after percutaneous coronary intervention for acute coronary syndrome. Am J Cardiol 2014;113:1647-51.  Back to cited text no. 8
    
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Wichmann JL, Katzberg RW, Litwin SE, et al. Contrast-induced nephropathy. Circulation 2015;132:1931-6.  Back to cited text no. 9
    
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Shacham Y, Leshem-Rubinow E, Gal-Oz A, et al. Association of left ventricular function and acute kidney injury among ST-elevation myocardial infarction patients treated by primary percutaneous intervention. Am J Cardiol 2015;115:293-7.  Back to cited text no. 10
    
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Ruda MY, Averkov OV, Golitsyn SP, et al. Clinical guidelines. Diagnosis and management of ST-segment elevation myocardial infarction. KardiologicheskiiVestnik 2014;4: 2-59.  Back to cited text no. 11
    
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Smirnov AV, Shilov EM, Dobronravov VA, et al. National guidelines. Chronic kidney disease: Basic principles of screening, diagnosis, prevention and treatment approaches. Nephrology (Saint-Petersburg) 2012;16:89-115.  Back to cited text no. 12
    
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Moiseev VC, Mukhin NA, Smirnov AV, et al. Cardiovascular risk and chronic kidney disease: Cardio-nephroprotection strategies. Russ J Cardiol 2014;8:7-37.  Back to cited text no. 13
    
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Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney IntSuppl 2012;2:1-126.  Back to cited text no. 14
    
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Vandenberghe W, Gevaert S, Kellum JA, et al. Acute kidney injury in cardiorenal syndrome type 1 patients: A systematic review and meta- analysis. Cardiorenal Med 2016;6:116-28.  Back to cited text no. 15
    
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Marenzi G, Cosentino N, Moltrasio M, et al. Acute kidney injury definition and in-hospital mortality in patients undergoing primary percutaneous coronary intervention for ST- segment elevation myocardial infarction. J Am Heart Assoc 2016;5:e003522.  Back to cited text no. 16
    
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Abellás-Sequeiros RA, Raposeiras-Roubín S, Abu-Assi E, et al. Mehran contrast nephropathy risk score: Is it still useful 10 years later? J Cardiol 2016;67:262-7.  Back to cited text no. 17
    
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Abe D, Sato A, Hoshi T, et al. Clinical predictors of contrast-induced acute kidney injury in patients undergoing emergency versus elective percutaneous coronary intervention. Circ J 2014;78:85-91.  Back to cited text no. 18
    
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Menzorov MV, Shutov AM, Serov VA, Saenko YV, Grishenkin IY. Type of thrombolytic agent and rate of acute kidney injury in patients with myocardial infarction. Kardiologiia 2015;55:16-20.  Back to cited text no. 19
    
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Caspi O, Habib M, Cohen Y, et al. Acute kidney injury after primary angioplasty: Is contrast-induced nephropathy the culprit? J Am Heart Assoc 2017;6:e005715.  Back to cited text no. 20
    
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Buargub M, Elmokhtar ZO. Incidence and mortality of acute kidney injury in patients with acute coronary syndrome: A retrospective study from a single coronary care unit. Saudi J Kidney Dis Transpl 2016;27:752-7.  Back to cited text no. 21
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Liao Y, Dong X, Chen K, Fang Y, Li W, Huang G. Renal function, acute kidney injury and hospital mortality in patients with acute myocardial infarction. J Int Med Res 2014; 42:1168-77.  Back to cited text no. 22
    

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Correspondence Address:
Evgeny Mikhailovich Mezhonov
GBUZ TO “Regional Clinical Hospital No. 1”, Tyumen
Russia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-2442.335442

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