Diseases of the Aorta and Kidney Disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

Abstract

Chronic kidney disease (CKD) is an independent risk factor for the development of abdominal aortic aneurysm (AAA), as well as for cardiovascular and renal events and all-cause mortality following surgery for AAA or thoracic aortic dissection. In addition, the incidence of acute kidney injury (AKI) after any aortic surgery is particularly high, and this AKI per se is independently associated with future cardiovascular events and mortality. On the other hand, both development of AKI after surgery and the long-term evolution of kidney function differ significantly depending on the type of AAA intervention (open surgery vs. the various subtypes of endovascular repair). Current knowledge regarding AAA in the general population may not be always applicable to CKD patients, as they have a high prevalence of co-morbid conditions and an elevated risk for periprocedural complications. This summary of a Kidney Disease: Improving Global Outcomes Controversies Conference group discussion reviews the epidemiology, pathophysiology, diagnosis, and treatment of Diseases of the Aorta in CKD and identifies knowledge gaps, areas of controversy, and priorities for future research.

Keywords: Abdominal aortic aneurysm; Acute kidney injury; Aortic diseases; Aortic dissection; Chronic kidney disease.

Figure 1

Incidence rate of AAA hospitalizations per 1,000 for CKD measures (A: eGFR, B: ACR), adjusted for age, gender, race, and centre in the Atherosclerosis Risk in Community Study. The demographically adjusted hazard ratio (HR) for AAA development was 4.44 (95% CI 1.58–12.49) for eGFR <30 mL/min/1.73 m², 3.29 (1.89–5.72) for 30–44 mL/min/1.73 m², 2.03 (1.29–3.19) for 45–59 mL/min/1.73 m², and 1.62 (1.11–2.35) for 60–74 mL/min/1.73 m² compared with eGFR ≥90 mL/min/1.73 m². Furthermore, the demographically adjusted HR was 2.49 (1.28–4.87) for ACR ≥300 mg/g, 1.99 (1.40–2.83) for 30–299 mg/g, and 1.46 (1.08–1.97) for 10–29 mg/g compared with ACR <10 mg/g. These associations were generally similar after accounting for additional covariates or after stratifying by subgroups. Adapted with permission from Matsushita et al.

Figure 2

The effect of pre-existing CKD on survival on 47 715 patients undergoing surgery for AAA (25.7% open repairs and 74.3% EVAR). Blue line: subjects with eGFR > 60 mL/min/1.73 m² (no CKD, or CKD G1 and G2). Red line, left figure: patients with moderate CKD (G3), right figure: patients with severe CKD (G4 and G5). Adapted with permission from Aranson et al.

Figure 3

Established and potential CKD-specific risk factors and pathophysiologic mechanisms for AAA development.

Figure 4

Classification of abdominal aortic aneurysms. Infrarenal aneurysms have a proximal aortic neck that provides an adequate landing zone for the endovascular device; in juxtarenal aneurysms the aneurysm involves the infrarenal abdominal aorta adjacent to or including the lower margin of renal artery origins; suprarenal AAAs and thoraco-abdominal aneurysms extend above the orifice of renal arteries.

Figure 5

Kaplan–Meier curves indicating cumulative freedom from the combined cardiovascular end-point for patients with or without AKI after EVAR (left figure) or open repair (right figure) for AAA. From Saratzis A et al., with permission.

Figure 6

The types of endoleaks after endovascular aortic repair: Type I, leak at the proximal or distal landing of the graft; Type II, leak via branches (e.g. lumbar artery) into the aneurysm sac; Type III, modular defect or tearing of the graft material; Type IV, graft porosity.

Figure 7

Long-term kidney function after AAA repair according to treatment type. OAR, patients with open repair; EVAR (infra), patients infrarenal EVAR; EVAR (supra), patients with suprarenal EVAR; CEA patients with carotid endarterectomy, without AAA serving as the control group. From Saratzis et al., with permission.