Accuracy of Ankle-Brachial Index, Toe-Brachial Index, and Risk Classification Score in Discriminating Peripheral Artery Disease in Patients With Chronic Kidney Disease

Introduction: Chronic kidney disease (CKD) results in an increased risk of peripheral artery disease (PAD). However, the epidemiology of PAD in CKD, and particularly how the incidence differs according to sex remains incompletely defined. We sought to define how the epidemiology of peripheral arterial disease (PAD) in chronic kidney disease (CKD) differs according to sex and age. Methods: The Chronic Renal Insufficiency Cohort (CRIC) is a multi-center, prospective cohort study of CKD participants. Fine and Gray methods were used to determine the cumulative incidence of PAD, defined by an ankle brachial index (ABI) < 0.90 or a confirmed PAD event, with death as a competing event. Adjusted subdistribution hazard ratios from the Fine and Gray model determined the risk of PAD according to sex. A priori, we hypothesized that the relationship between sex and cumulative incidence of PAD differed according to age. Results: The mean age of the 3,174 participants in this study was 56.6 years and consisted of 55% males. Over a median follow-up of 5.9 years, 17.8% developed PAD and 11.1% died. Females had a 1.72-fold greater adjusted PAD risk compared to men (95% CI 1.44-2.06, p<0.001). These sex-related differences in PAD risk also differed by age (p<0.001, Figure). Women, compared to men, were at a markedly increased risk for PAD at younger ages; however, at ages greater than 70 years, the risk was similar across both sexes. Older men had a substantially greater PAD risk compared to younger men. In women, PAD risk did not vary with age. Conclusions: Females with CKD have a higher PAD risk compared to males at younger ages. There is an important need to improve our understanding of the biological and clinical basis for these differences.

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The reliability of the ankle-brachial index and toe-brachial index in the daily practice of peripheral artery disease monitoring in vascular medicine ward

Atherosclerosis ◽

10.1016/j.atherosclerosis.2018.06.778 ◽

2018 ◽

Vol 275 ◽

pp. e245

Author(s):

J. Krezel ◽

P. Klapacz ◽

M. Maga ◽

A. Wachsmann ◽

M. Plachno ◽

...

Keyword(s):

Peripheral Artery Disease ◽

Ankle Brachial Index ◽

Daily Practice ◽

Disease Monitoring ◽

Peripheral Artery ◽

Vascular Medicine ◽

Toe Brachial Index ◽

Artery Disease

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Unique aspects of peripheral artery disease in patients with chronic kidney disease

Vascular Medicine ◽

10.1177/1358863x18824654 ◽

2019 ◽

Vol 24 (3) ◽

pp. 251-260 ◽

Cited By ~ 5

Author(s):

Nkiruka V Arinze ◽

Andrew Gregory ◽

Jean M Francis ◽

Alik Farber ◽

Vipul C Chitalia

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Peripheral Artery Disease ◽

Clinical Aspects ◽

Peripheral Artery ◽

Health Care Burden ◽

High Prevalence ◽

Novel Biomarkers ◽

Artery Disease ◽

Poor Outcomes

Peripheral artery disease (PAD) represents a major health care burden. Despite the advent of screening and interventional procedures, the long-term clinical outcomes remain suboptimal, especially in patients with chronic kidney disease (CKD). While CKD and PAD share common predisposing factors, emerging studies indicate that their co-existence is not merely an association; instead, CKD represents a strong, independent risk factor for PAD. These findings implicate CKD-specific mediators of PAD that remain incompletely understood. Moreover, there is a need to understand the mechanisms underlying poor outcomes after interventions for PAD in CKD. This review discusses unique clinical aspects of PAD in patients with CKD, including high prevalence and worse outcomes after vascular interventions and the influence of renal allograft transplantation. In doing so, it also highlights underappreciated aspects of PAD in patients with CKD, such as disparities in revascularization and higher peri-procedural mortality. While previous reviews have discussed general mechanisms of PAD pathogenesis, focusing on PAD in CKD, this review underscores a need to probe for CKD-specific pathogenic pathways that may unravel novel biomarkers and therapeutic targets in PAD and ultimately improve the risk stratification and management of patients with CKD and PAD.

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Incremental effects of diabetes mellitus and chronic kidney disease in medial arterial calcification: Synergistic pathways for peripheral artery disease progression

Vascular Medicine ◽

10.1177/1358863x19842276 ◽

2019 ◽

Vol 24 (5) ◽

pp. 383-394 ◽

Cited By ~ 1

Author(s):

Prakash Krishnan ◽

Pedro R Moreno ◽

Irene C Turnbull ◽

Meerarani Purushothaman ◽

Urooj Zafar ◽

...

Keyword(s):

Diabetes Mellitus ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Peripheral Artery Disease ◽

Arterial Calcification ◽

Peripheral Artery ◽

Fetuin A ◽

Artery Disease ◽

Protein Density ◽

Medial Arterial Calcification

Diabetes mellitus (DM) and chronic kidney disease (CKD) separately are known to facilitate the progression of medial arterial calcification (MAC) in patients with symptomatic peripheral artery disease (PAD), but their combined effect on MAC and associated mediators of calcification is not well studied. The association of MAC and calcification inducer bone morphogenetic protein (BMP-2) and inhibitor fetuin-A, with PAD, is well known. Our aim was to investigate the association of MAC with alterations in BMP-2 and fetuin-A protein expression in patients with PAD with DM and/or CKD. Peripheral artery plaques (50) collected during directional atherectomy from symptomatic patients with PAD were evaluated, grouped into no-DM/no-CKD ( n = 14), DM alone ( n = 10), CKD alone ( n = 12), and DM+CKD ( n = 14). MAC density was evaluated using hematoxylin and eosin, and alizarin red stain. Analysis of inflammation, neovascularization, BMP-2 and fetuin-A protein density was performed by immunohistochemistry. MAC density, inflammation grade and neovessel content were significantly higher in DM+CKD versus no-DM/no-CKD and CKD ( p < 0.01). BMP-2 protein density was significantly higher in DM+CKD versus all other groups ( p < 0.01), whereas fetuin-A protein density was significantly lower in DM+CKD versus all other groups ( p < 0.001). The combined presence of DM+CKD may be associated with MAC severity in PAD plaques more so than DM or CKD alone, as illustrated in this study, where levels of calcification mediators BMP-2 and fetuin-A protein were related most robustly to DM+CKD. Further understanding of mechanisms involved in mediating calcification and their association with DM and CKD may be useful in improving management and developing therapeutic interventions.

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