Aortic Aneurysms in Chronic Kidney Disease Patients: A Rare Duo – Series of Six Cases : Indian Journal of Vascular and Endovascular Surgery

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Aortic Aneurysms in Chronic Kidney Disease Patients: A Rare Duo – Series of Six Cases

Jha, Manvendu; Srivastava, Atul Kumar1,; Dhillan, Rishi; Panda, Sanjay1

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Indian Journal of Vascular and Endovascular Surgery 10(1):p 72-75, Jan–Mar 2023. | DOI: 10.4103/ijves.ijves_57_22
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Abdominal aortic aneurysm (AAA) is defined by aortic dilatation associated with an abdominal aortic diameter of >50% diameter of the vessel. The prevalence of AAA in the western world is 1%–4.5% in males and 0.5% in females at 65–70 years of age.[1] The prevalence of AAA varies in different parts of the world and also as per ethnicity.[2] In India, the prevalence of AAA is not known. The traditional risk factors of AAA are age, Caucasian race, male gender, smoking, diabetes, hypertension, and cardiovascular diseases. These risk factors may overlap in patients and promote atherosclerosis. Chronic kidney disease (CKD) has been identified as a risk factor for AAA as it promotes atherosclerosis and is an independent risk factor for cardiovascular disease. Data from various cross-sectional studies have reported a 30% higher prevalence of AAA in CKD.[3] CKD can independently cause endothelial and vascular alterations in the absence of other cardiovascular risk factors.[4] Vascular stiffening and calcification are common with aging and in patients with CKD. It can cause premature death of smooth muscle cells of the vessel walls and can contribute to the development of AAA.[5] We present the clinical profiles of six patients with CKD who were detected to have AAA.


Six patients of CKD detected to have AAA in the past 2 years were included. Three each were male and female, respectively. Age ranged from 29 to 79 years. Native kidney disease was fibrillary glomerulonephritis in one patient. One patient had autosomal dominant polycystic kidney disease (ADPKD), while the remaining patients had unclassified disease who presented as advanced-stage CKD with bilateral contracted kidneys. The clinical features are summarized as per Table 1. Four patients had tuberculosis (TB) before detection of AAA (three had TB of cervical lymph nodes and one had abdominal with cervical lymph node TB). Three patients had end-stage renal disease, while two had CKD 5 and one CKD stage 4 disease, respectively. Only three patients were on dialysis, of which two patients were on hemodialysis and one patient was on peritoneal dialysis.

Table 1:
Table depicting the demographic and investigative details of all six patients

These cases were detected incidentally (5/6) when computed tomography scan of the abdomen was done for other indications, while one patient had pulsatile swelling over the abdomen.

Five patients had fusiform dilatation of the infrarenal aorta, of which two patients had associated saccular dilatation of the common iliac artery. One patient had a thoraco-AAA. The common point noted among them was the presence of calcification, even in young patients [Figure 1].

Figure 1:
3D reconstruction depicting a fusiform Thoraco-abdominal aortic aneurysm with abundant calcification

Of the six patients, three were on dialysis. One patient with good surgical risk; who was not on dialysis and had presented with Acute limb ischemia [Figure 2], underwent open surgery in the form of endo-aneurysmorrhaphy and Aorto-bifemoral bypass. Three patients underwent Endovascular aneurysm repair (EVAR) [Figure 3] while one patient with Thoracoabdominal aneurysm underwent Thoracic endovascular aneurysm repair (TEVAR) + EVAR (covering till coeliac artery) under local anesthesia. In one patient CO2 angiography was used. One patient with an aorto-iliac aneurysm died of rupture before any intervention could be done.

Figure 2:
3D reconstructed image depicting a completely thrombosed infrarenal AAA with thrombus in RT EIA
Figure 3:
3D reconstructed image depicting an infrarenal AAA with a highly angulated neckand associated Rt CIA occlusion


AAA occurs due to infiltration of inflammatory cells in the aorta associated with coexisting atherosclerosis. This leads to loss of vascular smooth muscle cells, a progressive weakening of the aorta, and renders it susceptible to rupture.[6] In the atherosclerosis risk in communities study, estimated glomerular filtration rate (eGFR) and albuminuria were significant risk factors for AAA.[7] An imbalance in the extracellular matrix was found in patients with CKD and AAA. Metalloproteinases (MMP), which are a metzincin family of proteolytic enzymes with neutrophil gelatin-associated lipocalin, were found to be raised in patients with aortic aneurysms.[8] MMPs-2-8-9 and tissue inhibitor of matrix metalloproteinase 1 were found to be overexpressed and hyperactivated in the aortic wall.[9] These MMPs also activate profibrotic and pro-inflammatory signals in the kidney leading to accelerated progression of CKD.[10] Increased arterial stiffness, alterations in calcium-phosphate metabolism, and oxidative stress can also lead to the development of AAA in patients with CKD.

In this case series, 50% of patients were female, and the mean age of onset was 52 years. AAA is more common in males, due to hormonal factors and exposure to various other risk factors.[11] Three patients in our study had age <45 years. We hypothesized that in advanced stages of CKD, both males and females are equally affected by the onset of AAA at a lesser age. This can be explained by vascular calcification and accelerated atherosclerosis in this patient group.

Hypertension is an established risk factor for AAA, particularly in females.[12] It can cause activation of MMPs and pro-inflammatory signaling cascades like nuclear factor kappa B signaling, etc.[13] All patients in this series were taking >4 antihypertensives.

All patients had an advanced stage of CKD at the time of diagnosis in this case series. Declining eGFR is a risk factor for the development of AAA.[7] ADPKD patients have a 5.4 times higher risk of the aortic aneurysm compared to non-ADPKD.[14] One patient in this study had ADPKD-related CKD.

Four patients had TB in the past and received antitubercular drugs. TB is a chronic inflammatory state. TB infection can increase the expression of MMPs through multiple intracellular signaling cascades.[15] Patients with TB were found to be at a higher risk of developing aortic aneurysm and aortic dissection.[16,17]

Most patients are detected incidentally, only a small fraction present with pulsatile swelling. Patients with AAA rupture present with acute abdomen and shock.

Surgical and endovascular repair is the mainstay of treatment; the indications of treatment for AAA remain same in patients with CKD. AAA diameter of more than 55 mm in males and 50 mm in females is considered for elective surgery. The presence of CKD is associated with high morbidity and mortality in the perioperative period.


We presented case series with the rare association between CKD and AAA. Patients with advanced stages of CKD and with a history of TB were found to have AAA. Both sexes were equally affected. In view of less number of cases, it is difficult to recommend regular screening of CKD patients for AAA. However, screening of patients with advanced stages of CKD with clinical suspicion should be conducted to identify the prevalence, risk factors, and outcome in this subset.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1. Lindholt JS, Diederichsen AC, Rasmussen LM, Frost L, Steffensen FH, Lambrechtsen J, et al. Survival, prevalence, progression and repair of abdominal aortic aneurysms:Results from three randomised controlled screening trials over three decades. Clin Epidemiol 2020; 12:95-103
2. Wang JA, Chen XF, Yu WF, Chen H, Liu XM, Lin XF, et al. Prevalence of abdominal aortic aneurysms in chinese coronary artery disease patients. Eur J Vasc Endovascular Surg 2008; 36:500
3. Chun KC, Teng KY, Chavez LA, Van Spyk EN, Samadzadeh KM, Carson JG, et al. Risk factors associated with the diagnosis of abdominal aortic aneurysm in patients screened at a regional Veterans affairs health care system. Ann Vasc Surg 2014; 28:87-92
4. Provenzano M, Coppolino G, De Nicola L, Serra R, Garofalo C, Andreucci M, et al. Unraveling cardiovascular risk in renal patients:A new take on old tale. Front Cell Dev Biol 2019; 7:314
5. Sanchis P, Ho CY, Liu Y, Beltran LE, Ahmad S, Jacob AP, et al. Arterial “inflammaging” drives vascular calcification in children on dialysis. Kidney Int 2019; 95:958-72
6. Riches K, Clark E, Helliwell RJ, Angelini TG, Hemmings KE, Bailey MA, et al. Progressive development of aberrant smooth muscle cell phenotype in abdominal aortic aneurysm disease. J Vasc Res 2018; 55:35-46
7. Matsushita K, Kwak L, Ballew SH, Grams ME, Selvin E, Folsom AR, et al. Chronic kidney disease measures and the risk of abdominal aortic aneurysm. Atherosclerosis 2018; 279:107-13
8. Serra R, Grande R, Montemurro R, Butrico L, Caliò FG, Mastrangelo D, et al. The role of matrix metalloproteinases and neutrophil gelatinase-associated lipocalin in central and peripheral arterial aneurysms. Surgery 2015; 157:155-62
9. Pasta S, Agnese V, Gallo A, Cosentino F, Di Giuseppe M, Gentile G, et al. Shear stress and aortic strain associations with biomarkers of ascending thoracic aortic aneurysm. Ann Thorac Surg 2020; 110:1595-604
10. Cheng S, Pollock AS, Mahimkar R, Olson JL, Lovett DH. Matrix metalloproteinase 2 and basement membrane integrity:A unifying mechanism for progressive renal injury. FASEB J 2006; 20:1898-900
11. Blanchard JF. Epidemiology of abdominal aortic aneurysms. Epidemiol Rev 1999; 21:207-21
12. Forsdahl SH, Singh K, Solberg S, Jacobsen BK. Risk factors for abdominal aortic aneurysms:A 7-year prospective study:The tromsøstudy 1994-2001. Circulation 2009; 119:2202-8
13. Shiraya S, Miwa K, Aoki M, Miyake T, Oishi M, Kataoka K, et al. Hypertension accelerated experimental abdominal aortic aneurysm through upregulation of nuclear factor kappa B and Ets. Hypertension 2006; 48:628-36
14. Sung PH, Yang YH, Chiang HJ, Chiang JY, Chen CJ, Liu CT, et al. Risk of aortic aneurysm and dissection in patients with autosomal-dominant polycystic kidney disease:A nationwide population-based cohort study. Oncotarget 2017; 8:57594-604
15. Sabir N, Hussain T, Mangi MH, Zhao D, Zhou X. Matrix metalloproteinases:Expression, regulation and role in the immunopathology of tuberculosis. Cell Prolif 2019; 52:e12649
16. Chen MT, Chung CH, Ke HY, Peng CK, Chien WC, Shen CH. Risk of aortic aneurysm and dissection in patients with tuberculosis:A nationwide population-based cohort study. Int J Environ Res Public Health 2021; 18:11075
17. Shi Y, Guo W, Hu W, Li X, Shangguan Y, Feng X, et al. Aortic involvement in disseminated tuberculosis –Challenges beyond the diagnosis. Infect Drug Resist 2022; 15:2633-8

Abdominal aorta; aneurysm; chronic kidney disease

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