CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 4, September/October 2023 AFRICA 203 Zoccali et al. reported on patients with initially normal CIMT levels that elevated CRP was related to changes in the CIMT. The interaction between these two resulted in a single independent predictor of intimal lesion progression.33 Likewise, in our study, pre- and postoperative CRP elevation was a direct indicator of systemic inflammation in patients with postoperative AKI. The relationship between elevated CIMT and postoperative AKI suggested that inflammatory processes were operative on AKI. Since atherosclerosis is a chronic inflammatory disease, the lack of studies in the literature regarding the relationship between CIMT and postoperative AKI was the main reason to perform this study. ESR is a simple and inexpensive laboratory test that measures aggregation tendency of red blood cells that were shown to be elevated in tissue injury and necrosis, and a risk factor for atherothrombotic cardiovascular disease.35 Singh et al. reported that ESR was correllated with atherosclerosis markers and might carry important prognostic information about later catastrophic events, such as stroke, myocardial infarction and AKI, which verified the strength of the inflammatory response related to carotid artery atherosclerosis.36 Early diagnosis of AKI, which means awareness of a surreptitious onset of postoperative acute renal failure, may be facilitated by determining ESR and CRP levels.22 Likewise, high pre-operative and early postoperative levels of ESR were related to AKI in our study. Also, the CIMT of patients with a high ESR was found to be significantly increased. The unpredictability of AKI and progression to chronic kidney disease due to ineffective treatment make AKI a global problem to be solved.27 Determining renal function disorder in the postoperative period may enable the detection of patients with increased long-term risk in order to take preventative measures during follow up.9 Very little evidence has been obtained from randomised studies regarding protection or supporting specific interventions to prevent AKI.25 Novel biomarkers of kidney injury may identify subclinical diagnosis, severity and prognosis of AKI following cardiac surgery and enable interventions for the reduction of incidence of and protection from AKI.11 The primary aim of our study was to determine the predictive value of pre-operative CIMT as a marker of possible AKI in the early postoperative period. An independent correlation was found. Experimental evidence shows that initiation and continuation of AKI arise from inflammation-mediated injury.15 AKI diagnosis is delayed until at least the extension phase, when alterations in endothelial leukocyte interactions may be a prominent activity.37 Recent studies have shown the relationship between estimated glomerular filtration rate (eGFR) and subclinical atherosclerosis.4 Ito et al. reported that not the level of diabetic nephropathy graded by urinary albumin discharge, but eGFR was correlated with CIMT in type 2 diabetes.38 These alterations may relate to peritubular capillary loss in the long term, which can be preserved by experimental treatment during the early phases of injury and repair.10 CPB induces systemic inflammatory response syndrome, negatively affecting renal perfusion. In a study where CABG with CPB was compared with CABG on a beating heart with CPB support, no difference was found in terms of postoperative AKI.39 Our study population included only patients operated on for isolated CABG on standard CPB. Although there were no statistically significant differences between the AKI and non-AKI groups regarding the duration of CPB, the relationship found between AKI and CIMT, PLR, NLR, ESR and CRP, regardless of other risk factors, suggested that systemic inflammation may be operative both on CIMT increase and the occurrence of AKI. Therefore, if AKI occurred in patients, it might be foreseen that they were exposed to systemic inflammatory processes. CIMT levels found in this study might be a marker for subclinical systemic inflammation already in the pre-operative period, as well as for postoperative AKI. Inflammation playing a role in the aetiopathogenesis of AKI revives the use of CIMT as a predictor to prevent this injury.27 Lorenz et al. showed in their study that elevated CIMT was an independent marker of vascular events, and this relationship was stronger, particularly among younger individuals. This study was well standardised in terms of risk stratification, ultrasonographic examination and CIMT measurements.5 In another study in a Chinese population, systemic arterial changes were shown to begin in the early phase of chronic kidney disease. It was reported that traditional factors might be operative on elevation of CIMT, however, the relationship between elevated CIMT and patient prognosis should be examined in depth.17 A correlation between LDL-C and CIMT was also mentioned to exist when adjusted to traditional risk factors such as advanced age, male gender, smoking and family history of cardiovascular disease.6 Likewise, among the population operated on for isolated CABG and standardised with strict exclusion criteria in our study, statistically significantly higher pre-operative CIMT in the AKI group suggested a common cause for both AKI and CIMT, such as systemic inflammation. Our study groups were statistically similar in terms of age, gender, smoking and pre-operative LDL-C levels. One of the few studies on a relationship between CIMT and postoperative AKI in patients operated on for CABG was from Onk et al., which was different from our study in terms of exclusion of patients who died and selection method of the groups.18 In our study, the real-life data of a stable, homogeneous and well-selected group was sought completely in terms of inflammatory response over a six-year period. CIMT was found as an independent predictor of postoperative AKI, together with pre-operative CRP, ESR, PLR and NLR. Additionally, a greater increase in the markers of postoperative inflammation in the AKI group supports the relationship between AKI and inflammation. With these results, risk for AKI may be defined by gaining information about the pre-operative inflammatory status of the patient, using CIMT. Unlike other suggested markers, the potential advantage of CIMT is that it is radiologically measured and is not a blood test; therefore, it will remain unaffected by temporary disturbances of blood analysis and inflammatory markers due to pre-operative acute events. From the relationship found between pre-operative CIMT and postoperative AKI, sufficient time may be obtained for both surgical and pharmacological planning and modification in the pre-operative period to prevent postoperative AKI. Limitations of the study First, this was a retrospective, observational study so causal inference cannot be assumed, and it was subject to bias from several factors. Although we attempted to control selection
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