
==== Front
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Renal Failure
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10.1080/0886022X.2024.2397051
2397051
Version of Record
Research Article
Acute Kidney Injury
Differences in mortality and risk factors, two years after endovascular repair of ruptured abdominal aortic aneurysms – Reassessment analysis
B. Antoń et al.
Renal Failure
Antoń Bartłomiej a
Małyszko Jolanta b
Stabiszewski Piotr c
Kaszczewski Piotr a
Antoń Piotr d
Kuźma Łukasz e
Nazarewski Sławomir a
Gałązka Zbigniew a
a Department of General, Vascular, Endocrine and Transplant Surgery, Medical University of Warsaw, Warsaw, Poland
b Department of Nephrology, Dialysis and Internal Medicine, Medical University of Warsaw, Warsaw, Poland
c Department of Vascular Surgery, St. Padre Pio Provincial Hospital in Przemyśl, Przemyśl, Poland
d Department of Vascular Surgery, University of Warmia and Mazury, Olsztyn, Poland
e Department of Invasive Cardiology, Medical University of Bialystok, Bialystok, Poland
CONTACT Jolanta Małyszko jolmal@poczta.onet.pl Department of Nephrology, Dialysis and Internal Medicine, Medical University of Warsaw, Banacha 1A, 02–097, Warsaw, Poland
9 9 2024
2024
9 9 2024
46 2 239705130 6 2024
20 8 2024
21 8 2024
KnowledgeWorks Global Ltd.6 9 2024
published online in a building issue6 9 2024
© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group
2024
The Author(s)
https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

Abstract

Objective

The prevalence of abdominal aortic aneurysms (AAA) increases with age. Elective intervention for AAA is critical to prevent rupture associated with very high mortality among older males.

Methods

The aim of this study was to address the impact of post-contrast acute kidney-PC-AKI injury among patients treated with endovascular repair of ruptured AAA-EVAR on outcomes such as new onset chronic kidney disease-CKD and mortality among patients within a two-year trial.

Results

The same study group (of n = 192 patients) underwent reassessment, two years after EVAR treatment. The overall mortality rate was 16.67%, and it was higher in the AKI group − 38.89%. CKD patients had a mortality rate of 23.88% (n = 16). Among patients with an aneurysm diameter >67 mm mortality rate reached 20% (n = 6), while in the previously reported diabetes mellitus group 37.93% (n = 11). New onset of CKD was diagnosed in 23% of cases. Preexisting CKD patients with PC- AKI contributed to a 33.33% mortality rate (n = 8).

Conclusion

This study concludes that PC-AKI impacts outcomes and survival in endovascularly treated AAAs. Type 2 diabetes and preexisting chronic kidney disease are associated with higher mortality within a 2-year follow-up, however gender factor was not significant. A larger aneurysm diameter is related with a higher prevalence of PC-AKI. These factors should be taken into account during screening, qualifying patients for the treatment and treating patients with AAA. It may help to identify high–risk individuals and tailor preventive measurements and treatment options accordingly, improving treatment results and reducing mortality.

Keywords

Abdominal aortic aneurysm
mid–term mortality
acute kidney injury
EVAR
The author(s) reported there is no funding associated with the work featured in this article.
==== Body
pmcIntroduction

Abdominal aortic aneurysms (AAAs) are the most frequent true aneurysms, affecting up to 8% of males and 2% of females over 60 years old. Moreover, the prevalence rises several percent every ten years of patients lifespan [1–3]. About 75% of AAAs remain asymptomatic and are detected serendipitously during abdominal imaging conducted for unrelated indications [4–6]. Therefore, the elective AAA intervention is undertaken proactively to forestall aneurysmal rupture, which is eventuality characterized by an 80% fatality rate and ranks aneurysm rupture as the tenth most prevalent cause of mortality among males aged 65 to 74 in the United States [7–9].

Since its inception in 1991, endovascular aneurysm repair (EVAR) has steadily enhanced therapeutic options for patients with favorable aneurysmal anatomy [10]. The prevalence of EVAR increased from 52% (in 2003) up to recent 91% of elective management [10]. There was some (on average 140 mL) iodinated radiocontrast injected in the aorta or arterial system, to capture the images of the aorta to determine the location of the patient’s renal arteries. Then vascular sheaths are introduced into the patient’s femoral arteries, through which guidewires, catheters, and the endograft are passed. EVAR involves the placement of an expandable stent graft within the aorta to treat aortic disease without operating directly on the aorta. Given the practicality of EVAR (as the method involves the necessity for an appropriate infrarenal aortic neck, sufficient access vessel dimensions, and the absence of marked aortoiliac tortuosity and arterial wall calcification [11–15]) coupled with positive initial clinical outcomes, in patients with chronic conditions and advanced age [16], the demand of this procedure constantly increase, successively replacing classical open surgery interventions [17].

The renal repercussions of EVAR could be considerable and complex, including contrast–induced nephropathy, ischemia–reperfusion damage, renal microembolization, and the necessity for further contrast imaging for follow–up and re–intervention [18]. However, this is still less invasive compared to the renal harm caused by open surgical repair [19,20].

Acute kidney injury (AKI), defined as a prompt loss in renal function following surgery, has serious consequences, including increased midterm mortality [21] of slightly less than 20% in individuals undergoing elective EVAR [22,23]. This is observed especially in patients with inadequate cardiovascular reserve [24,25].

Study shows that, after EVAR for ruptured AAA, more than 25% of patients experience severe AKI [26]. Post-contrast acute kidney injury (PC-AKI) is the third most common cause of hospital acquired AKI [27]. This is well described consequence associated with the administration of iodinated contrast medium intravascularly [28].

The other condition related to increased morbidity and mortality in EVAR patients is the presence of chronic kidney disease (CKD). It has been found that coexisting CKD (CKD 3a HR 1.25; 95% CI) and dialysis (HR, 4.48; 95% CI) were independent risk factors for a worse 1-year survival following EVAR [10].

The postoperative incidence of PC-AKI amongst the population with CKD stage 4 exceeded 50% in the research by Krasznai et al. [29] and 64% in the study of Antoń et al. [30]. However, the optimal hydration strategy for EVAR patients, particularly those with CKD, remains an area of active research [31].

The authors’ previous study identified that an aneurysm diameter greater than 67 mm (p < .01), male gender, and preexisting chronic kidney disease are independent factors in the development of PC-AKI [30]. The significant association with larger aneurysm diameters underscores the increased risk posed by greater hemodynamic stress and potential vascular complications. Male gender as an independent risk factor may reflect underlying physiological and genetic predispositions that increase susceptibility to renal impairment post-contrast exposure. Additionally, the compromised renal function in patients with preexisting chronic kidney disease confirms their vulnerability to contrast-induced renal injury.

In this study we present a continuation of the mid-term-assessment analysis of the same study group and evaluating previous assumptions highlighting the influence of the formerly acknowledged conditions on the mortality and comorbidities as well as new (onset of CKD) developed during the follow-up period.

Materials and methods

A retrospective and observational data of 192 patients (24% female and median age of 73), who underwent endovascular abdominal aortic aneurysm repair between 2015 and 2021 at St. Padre Pio Provincial Hospital in Przemyśl, were reviewed. New clinical data from the 2 years follow-up period, which are presented in Table 1, were examined in addition to previously analyzed [30] comorbidities such as: hypertension, diabetes mellitus, atrial fibrillation, chronic coronary syndrome, chronic obstructive pulmonary disease (COPD), and chronic renal disease. The new data include laboratory tests results from the whole 2-year follow-up (both hospitalizations and outpatients clinic visits) as well as data on mortality. Due to the nature of reassessment, collected data are focused on the new onset CKD and mortality, serum creatinine concentration (IQR), CKD-EPI eGFR- Chronic Kidney Disease Epidemiology Collaboration Estimated Glomerular Filtration Rate (eGFR). Ethical approval was waived by the local Ethics Committee.

Table 1. Collected data analysis within 2 year reassessment, initial study group N = 192.

Variables	N	Dead	Alive	p	
Age (years); mean (SD)	192	73.5 (7.4)	73.2 (8.1)	.74	
Male; N (%)	192	22 (68.75)	124 (77.5)	.29	
Obesity; N (%)	192	4 (12.5)	11 (6.88)	.28	
Hypertension; N (%)	192	17 (53.13)	94 (58.75)	.56	
Diabetes mellitus; N (%)	192	11 (34.38)	18 (11.25)	<.001	
Atrial fibrillation; N (%)	192	6 (18.75)	28 (17.5)	.87	
Chronic coronary syndrome; N (%)	192	11 (34.38)	51 (31.88)	.78	
COPD; N (%)	192	3 (9.38)	11 (6.88)	.62	
History of acute coronary syndrome; N (%)	192	4 (12.5)	22 (13.75)	.85	
History of stroke; N (%)	192	3 (9.38)	15 (9.38)	.99	
History of neoplasm; N (%)	192	3 (9.38)	17 (10.63)	.83	
Chronic kidney disease; N (%)	192	16 (50)	51 (31.88)	.049	
Serum creatinine concentration (mg/dl); mean (SD)	192	1.23 (0.95–1.7)	0.98 (0.79–1.19)	.003	
eGFR ml/min/1.73 m²; mean (SD)	192	59 (34–75.25)	72.5 (56.75–97.5)	.41	
eGFR <45 mL/min/1.73 m²; N (%)	192	10 (31.25)	16 (10)	.002	
eGFR <30 mL/min/1.73 m²; N (%)	192	8 (25)	4 (2.5)	
eGFR <15 mL/min/1.73 m²; N (%)	192	3 (9.38)	2 (1.25)	
Blood urea nitrogen concentration (mg/dl); mean (SD)	189	42.5 (35–62.25)	39 (31–48)	.04	
Blood glucose level (mg/dL); mean (SD)	190	127 (103.5–203.5)	107 (95–124)	.01	
Serum sodium concentration (mEq/L); mean (SD)	192	140 (137–142)	140 (138–142)	.43	
Serum potassium concentration (mEq/L); mean (SD)	192	4.2 (3.88–4.5)	4.4 (4.2–4.8)	.48	
Serum chloride concentration (mEq/L); mean (SD)	192	100.5 (97–104)	102 (100–104)	.16	
Aortic diameter; mean (SD)	129	53 (51–67.5)	52 (46.25–63.5)	.28	
Aortic aneurysms ≥67 mm; N (%)	129	6 (31.58)	24 (21.82)	.35	
Iodine contrast volume (ml.); mean (SD)	149	150 (111.3–195)	130 (92–185)	.35	
PC–AKI; N (%)	192	14 (43.75)	22 (13.75)	<.001	
New onset of CKD (eGFR <60 ml/min/1.73 m²); % (N)	95	7 (53.85)	15 (17.44)	.002	
N: patients count of available data; COPD: chronic obstructive pulmonary disease; eGFR: estimated glomerular filtration rate; PC–AKI: post–contrast acute kidney injury; SD: standard deviation.

The characteristics of the studied population are presented in the form of standard deviations (SD). All predictors with a P value of less than 0.2 and no significant multicollinearity impact were considered. The threshold of statistical significance for all tests was set at p < .05.

Results

In this study data of 192 patients were reexamined after two years after intervention. The median age, among patients, remains at 73 years. There were 24% of all female patients in the trial. Mean contrast volume was 149.6 mL in the whole population, 179.3 mL in the PC-AKI population, and 142.1 mL in the non-PC-AKI population.

In Tables 2 and 3 clinical characteristics, comparisons between patients with and without PC-AKI, CKD, diabetes, presence of CKD and post–contrast acute kidney injury, presence of diabetes and post–contrast acute kidney injury, dead and alive, as well as predictors for PC-AKI and mortality were presented. Two-year follow up showed mortality at the level of 16.7% (n = 32). Diabetes mellitus significantly influenced the mortality rate, resulting in nearly 34% of total dead patients (n = 11). In the group of patients with preexisting CKD mortality was assessed at the level of 23.88% (n = 16) and it was 50% of all deceased, [p < .049]. Mortality among patients with PC–AKI, within a 2–a year follow-up reached approximately 44% (n = 14) versus mortality among patients without developed PC–AKI − 56.2% (n = 18) [p < .001]. New onset of CKD was developed in 22 subjects, while after two years reassessment 68% (n = 15) of them survived. Examined aortic aneurysms (≥67 mm) were found in approximately 30% (n = 6) of deceased patients.

Table 2. Characteristics of the mortality rate and laboratory kidney function parameters compared with preexisting CKD and post-contrast acute kidney injury PC-AKI in patients after a 2-year follow-up.

Variables	N	CKD	non–CKD	p	
Serum creatinine concentration (mg/dl); median (IQR)	148	1.47 (1.11–2.07)	0.85 (0.73–0.97)	<.001	
eGFR ml/min/1.73 m²; median (IQR)	142	45 (26.25–56.75)	89 (77–109)	<.001	
Death; N (%)	192	16 (23.88)	16 (12.8)	.049	
 	 	CKD(+)/PC–AKI(+)	CKD (+)/PC–AKI(–)	 	
Serum creatinine concentration (mg/dl); median (IQR)	49	2.72 (1.93–4.1)	1.19 (1.02–1.44)	.01	
eGFR ml/min/1.73 m²; median (IQR)	47	24.5 (14–34.5)	54 (45–63.75)	.03	
Death; N (%)	67	8 (33.33)	8 (18.6)	.18	
 	 	Patients with PC–AKI	Patients without
PC–AKI	 	
New onset of CKD (eGFR <60 ml/min/1.73 m²); N (%)	22	6 (66.67)	16 (18.6)	<.001	
Serum creatinine concentration (mg/dl); median (IQR)	148	2.19 (1.73–3.46)	0.9 (0.74–1.04)	<.001	
eGFR ml/min/1.73 m²; median (IQR)	142	29.5 (17.5–37.3)	87 (68–104)	<.001	
Death; N	32	14	18	<.001	
N: patients count of available data; IQR: Interquartile range; eGFR: estimated glomerular filtration rate; PC–AKI: post–contrast acute kidney injury; SD: standard deviation.

Initial study group N = 192.

Table 3. Characteristics of the studied population with comparison of patients with and without post–contrast acute kidney injury – laboratory data after a 2-year follow-up.

 	Diabetes (n = 29, 6.6%)	Male (n = 146, 76%)	Aortic aneurysms ≥67 mm; n = 30,15.6 %)	
CKD (+) N(%)	12 (17.91)	p = .43	43 (64.2)	p = .005	8 (18.6)	p = .38	
24-72h post treatment	
PC-AKI (−)	24 (15.38)	p = .82	115 (73.72)	p < .001	21 (18.75)	p = .002	
PC-AKI (+)	5 (13.89)	p = .82	31 (86.11)	p < .001	9 (52.94)	p = .002	
CKD (+)/PC-AKI (−)	9 (20.93)	p < .001	23 (53.49)	p = .015	1 (3.23)	p < .001	
CKD (+)/PC-AKI (+)	3 (12.5)	p < .001	20 (83.33)	p = .015	7 (58.33)	p < .001	
2 years follow up	
Death (N%)	11 (34.38)	p < .001	22 (68.75)	p = .29	6 (31.58)	.35	
New -CKD (+)	4	.028	20	p = (.007)	1	.0067	
N: patients count of available data; IQR: Interquartile range; eGFR: estimated glomerular filtration rate; PC–AKI: post–contrast acute kidney injury; SD: standard deviation.

Initial study group N = 192.

Serum creatinine and corresponding eGFR in the whole group did not differ significantly before and after the procedure. However, serum creatinine 2 years after the EVAR was significantly higher relative to baseline values (p = .049).

The two-year follow-up has shown that serum creatinine concentration was elevated in the group of PC-AKI [from 1.38 (1.07–2.09) mg/dl–2.19 (1.73–3.46) mg/dl) and decreased in the group on non-PC-AKI patients [from 0.96 (0.79–1.15) mg/dl to 0.9 (0.74–1.04) md/dl] (p < .001). We also found the new onset of chronic kidney disease in 23.16% of all population, 66.67% of the population with PC–AKI, and 18.6% of the non-PC-AKI population (p < .001). We also compared a group of patients that were affected with PC-AKI and CKD (CKD + PC-AKI+) and a group of patients with CKD and without PC-AKI (CKD + PCAKI-). In 24 months follow-up we found that within the CKD + PCAKI + group mean serum creatinine concentration was 2.72 mg/dl (1.93–4.1) versus 1.19 mg/dl (1.02–1.44) in the group of patients with CKD + PC-AKI− (p < .01).

The follow-up study presents 11 (34.38%) of deceased patients who had type 2 diabetes mellitus while only 18 (11.25%) of alive patients suffered from type 2 diabetes mellitus (p < .001). 14 (43.75%) patients who did not survive 2 years were PC–AKI + and 22 (13.75%) of alive patients were PC–AKI+ (p < .001). Sixteen (50%) of patients who did not survive 2 years had CKD, while 51 (31.88%) of alive patients had CKD (p < .049). 100% (n = 5) of patients with diabetes and PC–AKI + were males, 60% (n = 3) of them have not survived 2 years after EVAR.

The average research participant’s aorta diameter was 53 (47–65) mm. The population with PC–AKI had a mean aortic diameter of 68 (53–76) mm, whereas in the population without PC–AKI it was 52 (47.75–61.25) mm. 67 (34.9%) of the study’s participants had preexisting chronic kidney disease, including 24 (66.67%) patients with PC–AKI and 43 (27.56%) patients without PC-AKI [p < .001]. In the follow-up of 2 years mortality rate amongst patients with aneurysm diameter ≥67 mm was 20% (n = 6) while in a group with a diameter <67 mm it was 13.13% (n = 13) although it is not statistically significant (p = .35).

Discussion

In our study we found that patients with preexisting chronic kidney disease, as well as those with post contrast acute kidney injury and diabetes mellitus have a higher risk of death during long–term follow–up after EVAR compared to individuals without these conditions.

The findings highlighted the significance of considering CKD, PC-AKI, and diabetes mellitus as important risk factors for adverse outcomes and increased mortality rates in patients undergoing EVAR. Although in the study of Antoń et al. [30] male gender and aneurysm diameter were independent factors for PC-AKI development, they do not seem to play a crucial role in a mid-term follow-up survival (p = .29, p = .35). This information can help healthcare professionals in risk assessment, patient selection, and perioperative management to improve outcomes and patient care. It showed the importance of monitoring and managing renal function in patients during the follow–up period after EVAR. In our study we observed a statistically significant difference in mortality between patients with postoperative contrast–induced acute kidney injury (PC–AKI) and those without PC–AKI (38.89% vs 11.54%). In the study by Takahashi et al. [32] the mortality rate in both groups (with PC–AKI and without PC–AKI) was around 15%, and the difference in mortality between the groups was not statistically significant (p < .17). Regarding the incidence of PC–AKI after EVAR, Rastogi et al. [33] reported an incidence of 8.5% after infrarenal EVAR and higher rates of 18% after fenestrated EVAR and 38% after branched EVAR. In our study, the incidence of PC–AKI was in line with the mortality rate of 18% reported by Saratzis et al. [34] in a recent study group. It is important to acknowledge that even though this study shows the 2-years mortality amongst patients who developed PC–AKI (38.89%) vs 11.54% amongst patients without PC–AKI is 3.37 times higher, the size of the population in this study may be a limitation, and further studies with a larger population would provide more robust evidence. Our findings contributed to the understanding of the association between PC–AKI and mortality in patients undergoing EVAR.

Prior studies demonstrated a strong and substantial correlation between postoperative PC–AKI and medium– to long–term outcomes in vascular patients, PC–AKI and increased morbidity and mortality as well as a strong and substantial correlation between PC–AKI following large endovascular treatment. Specifically, PC–AKI after such interventions has been independently associated with a threefold increase in morbidity and a twofold increase in death rate at five years [35].

A metaanalysis involving almost 42,000 patients who underwent endovascular interventions found that postoperative AKI, including PC–AKI, was linked to an increased incidence of cardiovascular events over a five–year follow–up period. This suggested that PC–AKI was associated with a higher risk of adverse cardiovascular outcomes in the long term. PC–AKI was also found to be independently associated with a faster decline in renal function over the long term [21]. This indicated that PC–AKI could contribute to the deterioration of renal function beyond the immediate postoperative period [36]. The question of whether PC–AKI was the cause or merely a marker of a higher death rate was investigated in several studies. However, it is important to note that decreasing renal function has consistently been identified as an independent risk factor for all–cause death [37]. Taken together, these findings emphasized the importance of monitoring and managing renal function in vascular patients, particularly in the context of large endovascular treatments. PC–AKI should be considered a significant clinical concern due to its association with increased morbidity, mortality, cardiovascular events, and accelerated renal function deterioration. Future research may provide further insights into the precise mechanisms underlying these associations and guide strategies for the prevention and management of PC–AKI in clinical practice.

Consequently, in the group of patients with baseline kidney dysfunction, it was possible that the additional renal damage caused by contrast exposure might have a more pronounced effect on mortality. It suggested that PC–AKI could be a contributing factor to the higher death rate observed in this population [38]. Furthermore, PC–AKI may serve as a more accurate predictor of mortality, especially in high–risk groups such as those with chronic kidney disease (CKD). In our previous study [30] it was found that PC–AKI occurred in 35.82% of patients with preexisting CKD and in 25.58% non–CKD patients (p < .001). The 2–year mortality amongst CKD patients was 23.88% and 12.8% in non–CKD patients (p = .049). The correlation between PC–AKI and mortality warranted further investigation in prospective studies to better understand its role as a prognostic factor. The meta-analysis of Marques–Rios et al. [39] provided additional evidence on the predictors of long–term mortality after endovascular aneurysm repair (EVAR) and identifies several factors that overlap with our study. Advanced age was identified as a predictor of long–term mortality after EVAR. Female sex was associated with an increase in long–term cause of death, although the specific associations may vary. Larger aneurysm diameter was generally associated with an increased risk of mortality following EVAR. Various comorbidities, such as heart failure, ischemic heart disease, peripheral vascular disease, cerebrovascular disease, diabetes mellitus, chronic obstructive pulmonary disease (COPD), and chronic kidney disease (CKD), were identified as independent predictors of long–term mortality after EVAR. CKD was also an important predictive factor for long term follow-up and mortality within other cardiovascular diseases, such as acute coronary syndrome, mitral stenosis or mitral insufficiency [40].

The studies by Hjellestad et al. [41] and Khashram et al. [42] examined the association between diabetes mellitus and long–term mortality after endovascular aneurysm repair (EVAR). It appears that these studies provided differing findings on the relationship between diabetes mellitus and mortality. Hjellestad et al. [41] found that preexisting diabetes mellitus was a prognostic factor for higher long–term mortality after EVAR. This suggests that patients with diabetes mellitus may have an increased risk of mortality compared to those without diabetes mellitus. On the other hand, Khashram et al. [42] found no significant association between diabetes mellitus and higher mortality after EVAR. Their results suggested that diabetes mellitus may not independently contribute to increased long–term mortality in patients undergoing EVAR. The discrepancies between these studies may be due to differences in study design, patient populations, follow–up duration, or other factors. It is important to consider that individual studies can have limitations and that the cumulative evidence from multiple studies provides a more comprehensive understanding of the topic. The conflicting findings regarding the association between diabetes mellitus and long–term mortality after EVAR highlighted the complexity of this relationship. It may be influenced by various factors such as patient characteristics, comorbidities, treatment protocols, and other confounding variables. Our results were in line with data published by Hjellestad et al. [41].

Khashram et al. [43] reported that end stage chronic kidney disease and the necessity for dialysis in patients treated endovascularly for AAA increased long-term mortality which supported our results. On the other hand, de Bruin et al. [44] found no connection between kidney impairment and long-term mortality with respectively (HR:3.15, CI 95% [2.45–4.04]) and (HR: 1.54, CI 95% [1.43–1.67]). The mismatch in findings between these studies highlighted the complexity of the relationship between renal impairment and long–term mortality after endovascular treatment for AAA. In a recent retrospective analysis of the prospectively collected data by Ntalouka et al. [45], among 322 patients after EVAR, AKI was diagnosed in 1.6% within 30 days after the procedure, whereas in our population AKI developed in 18.8%. The prevalence of CKD in their study was low-8.6%, while in ours 34.9%. It also should be stressed, that maximal aneurysm diameter and past smoking were predictors of postoperative complications in the multivariate model. A similar AKI prevalence reaching 13.5% were reported by Novak et al. [46]. They also reported that postoperative AKI occurs more often in patients with worse preoperative renal function and were associated with higher long-term mortality. In addition, in the study of Caradu et al. [47], PC-AKI occurred in 13.7% (14 out of 102 patients), and similarly to our study over a median follow-up of 24 months (3-39), overall mortality was also significantly higher in patients with PC-AKI (78.6 vs 33.0%, p = 0.002). Moreover, Finnesgard et al. [48] described the results of the US Aortic Research Consortium of 10, prospective, nonrandomized, physician-sponsored investigational device exemption studies evaluating fenestrated/branched-EVAR in 2413 consecutive patients, between 2005 and 2023, followed for a median of 2.2 years. They found that AKI, as defined by the KDIGO criteria, occurred in 18% of patients after EVAR and its severity was associated with increased 30-days postoperative mortality. Similar data on AKI occurrence after fenestrated EVAR and 30-days mortality were published by Taher et al. [49]. Moreover, in the recent paper by DeJong et al. [50], who reviewed EVAR cases in the Vascular Quality Initiative between 2003 and 2021, many risk factors contributed to postoperative worsening of kidney function i.e., age, female gender, hypertension, chronic obstructive pulmonary disease, anemia, reoperation at index admission; baseline renal insufficiency, larger aneurysm diameter; increased blood loss; and higher volumes of intra-operative crystalloid. It may be due to a much larger sample size, while in our study only serum creatinine and diameter of aortic aneurysm reached significance in multivariable analysis. In addition, LaFontaine et al. [51] evaluated 38,775 EVAR patients, including 1978 with ruptured aneurysm before EVAR. They concluded that the most important factor for AKI was the rupture of the aneurysm, and more importantly that survival of patients developing AKI was decreased regardless of surgery indication (elective, urgent or emergent).

In our study, mainly diabetes and chronic kidney disease were related to mortality in patients treated for AAA. Further research is needed to clarify the role of kidney impairment, including various stages of CKD, as a prognostic factor for long–term mortality after endovascular repair for AAA. This will help guide clinical decision–making and optimizing patient care for those with renal impairment.

Last, but not least, we also would like to stress, that other etiologies than the contrast material alone, may contribute to the AKI and subsequent CKD. It is not at all certain that the contrast is the culprit. It could be that the procedure itself: athero-embolization, temporary occlusion of the renal artery orifice within the aorta etc. There is no absolute evidence that the cause of worsening of the kidney function is a contrast medium. In our previous study by Chomicka et al. [52] we found that AKI was more common in the non-enhanced computed tomography population (25.4% vs. 17.9%). We concluded that PC-AKI was not a great risk for patients, even those with chronic kidney disease, underlying that the fear of using contrast agents was not justified. Therefore, the worsening of kidney function after contrast administration would rather actually be called post-procedure-CKD rather than post-contrast CKD.

Limitations of the study

The most important limitations of this study may be the size of its population. It may limit the generalizability of the findings. Additionally, the lack of clinical data for 21% of patients for further analysis, single center study with only infrarenal EVARs, retrospective analysis are further constraints. Thus, the results may not be applicable to other settings. Lastly, the two-year follow-up period may not capture long-term outcomes. Future research with larger, multicenter cohorts and longer follow-up is needed to confirm these findings.

Conclusions

Post-contrast acute kidney injury (PC–AKI), type 2 diabetes mellitus, and pre-existing chronic kidney disease are important clinical conditions associated with worse midterm outcomes and survival rates (higher mortality) in patients after endovascular aneurysm repair (EVAR). A larger aneurysm diameter is related with a higher prevalence of PC-AKI.

These factors should be taken into account during screening, qualifying patients for the treatment, and treating patients with AAA. It may help to identify high–risk individuals and tailor preventive measurements and treatment options accordingly, improving treatment results and reducing mortality.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Upon request from the corresponding author.
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