In our study, the effects of perioperative GDFT and traditional fluid therapy on the development of postoperative acute kidney injury were compared in patients undergoing open heart surgery. There was no difference in the frequency of AKI development in patients undergoing cardiac surgery, between GDFT and the traditional fluid theraphy method. A shorter hospital stay was found in the patient group receiving GDFT. Although there was no statistical difference in the group receiving GDFT, it was determined that less amount of fluid was required. Less postoperative fluid requirement was observed in the group receiving GDFT. Intraoperative and post-operative fluid balance in the group that received GDFT was more negative than the group that received fluid therapy with traditional methods. Intraoperative and postoperative ES requirement was lower in the group that received GDFT. Among the biomarkers used in the diagnosis of acute renal failure, Cystatin-C was observed to be higher in the fluid therapy group performed with traditional methods; KIM-1, GFR and creatinine biomarkers did not differ significantly between the two groups.
When the literature is reviewed, studies comparing hemodynamic management in the development of AKI after cardiac surgery are limited. When these limited studies were examined, arterial hypotension and arterial pressure fluctuations after cardiac surgery, systemic venous congestion, low cardiac output and high CVP were reported as independent risk factors for the development of postoperative AKI [5, 16]. When current studies are examined, the most important step in the development of AKI is fluid therapy. The two most common causes of AKI in critically ill patients are sepsis and hypovolemia [17]. Therefore, fluid therapy is important in preventing the development of AKI. However, in cases where AKI is caused by nephrotoxics or renal inflammation, the response to fluid therapy is reduced [18]. In these situations, fluid overload may contribute to the development or worsening of AKI [19]. Therefore, the importance of GDFT in preventing the development of AKI is increasing. GDFT aims to keep systemic blood flow and oxygen delivery to tissues at optimal levels by avoiding fluid overload and hypovolemia. It has been shown that renal functions are preserved with GDFT in cardiac (AVR, CABG) and non-cardiac high-risk surgery (major abdominal surgery, orthopedics, plastic surgery, radical cystectomy, genitourinary surgery) cases [11, 13, 20, 21].
Esophageal Doppler is one of the methods used in the GDFT protocol [22, 23]. Volume status, contractility and afterload measurements are performed to understand hemodynamic status and optimize blood circulation [24, 25]. In our study, GDFT was applied with esophageal Doppler and transthoracic echocardiography measurements. The CI's of the patients were monitored and balanced crystalloid fluid therapy was administered to increase SV by 10%. There was no statistically significant difference in esophageal Doppler measurements over time in patients, and optimal fluid therapy was observed.
There are publications reporting that GDFT reduces postoperative complications in patients undergoing cardiac surgery and lung surgery [22, 23]. AKI is an important postoperative complication and it has been reported that the incidence of postoperative AKI is lower in patients followed with a GDFT protocol targeting SV-max for the first 8 hours after cardiac surgery, compared to those treated with standard treatment [26]. Meersch M. et al. applied GDFT to prevent cardiac surgery-associated AKI in high-risk cases, and followed the severity of AKI according to KDIGO criteria, from the first 72 hours to the 90th day postoperatively. They reported that the development of AKI was significantly lower in the group receiving GDFT. They attributed this positive result to the reduction of volume overload and organ edema with GDFT; showed that tissue edema leads to the development of postoperative AKI and worsening of pre-existing AKI [27]. There are also studies showing that GDFT does not improve the development of AKI in patients undergoing major abdominal and gastrointestinal surgery compared to standard treatment [28, 29]. They considered progress over time in standard fluid therapy protocols as the reason for this. In our study, we did not find a significant difference in the development of AKI between the patient groups receiving standard treatment with GDFT. The reason for this can be considered as achieving optimal treatment targets in the patient group receiving standard treatment. CVP and lactate values were obtained, which did not create a statistically significant difference between the patient group receiving standard treatment and the group undergoing GDFT.
The differences in the results of the studies may be due to the use of different methods in the evaluation of AKI. Many different methods have been used to define AKI. Such as changes in creatinine level [26, 28], AKI Network criteria [23], KDIGO classification [29, 30]. In our study, the development of AKI was evaluated with the KDIGO classification. Creatinine, GFR, cystatin-C and KIM-1 were used as biomarkers. No significant difference was observed between the groups in the development of AKI over time according to the KDIGO classification. While there was a significant difference in cystatin-C levels between the groups among biomarkers, no significant difference was found between creatinine, GFR and KIM-1. Cystatin-C level was shown to be significantly higher than creatinine level in the postoperative 2nd hour in patients who developed AKI after CABG surgery. It has been suggested that cystatin-C measurements in the early period can be used in the diagnosis of AKI associated with cardiac surgery [31]. In the Logistic Regression analysis performed by taking all cases in our study, Cystatin-C level at the postoperative 4th hour was found to be an independent risk factor for the development of AKI. Cystatin-C levels were found to be lower in the GDFT group than in the standard treatment group. According to our study plan, patients were followed up for AKI that developed within 48 hours (intensive care follow-up period). The presence of AKI that developed after this period was not evaluated. This significant difference in cystatin-C levels may be due to the late appearance of AKI clinical findings. Serum KIM-1 levels, another biomarker, were found to be high within 2 days post-operatively in patients who developed AKI after cardiac surgery [32]. Although it has been reported in the literature that serum KIM-1 can be a blood biomarker that specifically reflects acute and chronic kidney damage, the development of kidney damage has mostly been evaluated with urinary KIM-1 [32]. In our study, KIM-1 was studied in serum to obtain a new biomarker, and urine KIM-1 values were not included in the study. No statistically significant difference was found between the groups in terms of the change of KIM-1 values according to time. However, even though it was not statistically significant, KIM-1 values were found to be lower in the patients who underwent GDFT at the postoperative 48th hour. This late KIM-1 elevation observed in patients who received standard treatment may be related to the late clinical findings of AKI.
When the secondary data of the group receiving GDFT were evaluated, the hospital stay of the cases was found to be significantly shorter. In our study, the fluid requirement and ES requirement were significantly less in the group that received GDFT, and the postoperative balance was more negative. This may be due to the fact that CVP was increased enough to increase MAP to keep MAP above 75 mmHg in the standard treatment group. Because more fluid was given in the group receiving intraoperative and postoperative standard treatment, and CVP was numerically higher in the group receiving standard treatment, although no statistically significant difference was found in the control group.
Limitation
The first limitation of our study is the low number of patients in both groups. In addition, the patients were followed up to the postoperative 48th hour. AKI cases that developed at the end of this period could not be evaluated. Third, the KIM-1 biomarker was evaluated in serum but not in urine. A possible urinary KIM-1 difference between the groups could not be evaluated.