Traditional and non-traditional risk factors for incident peripheral arterial disease among patients with chronic kidney disease

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Abstract

<div class="section"> <a class="named-anchor" id="d1062510e484">  </a> <h5 class="section-title" id="d1062510e485">Background</h5> <p id="d1062510e487">The risk of peripheral arterial disease (PAD) is higher in patients with chronic kidney disease (CKD) compared with those without. However, reasons for this increased risk are not fully understood. </p> </div><div class="section"> <a class="named-anchor" id="d1062510e489">  </a> <h5 class="section-title" id="d1062510e490">Methods</h5> <p id="d1062510e492">We studied risk factors for incident PAD among 3169 participants in the Chronic Renal Insufficiency Cohort (CRIC) Study. Patients with CKD aged 21–74 years were recruited between 2003 and 2008 and followed for a median of 6.3 years. Incident PAD was defined as a new onset ankle-brachial index (ABI) of <0.9 or confirmed clinical PAD. </p> </div><div class="section"> <a class="named-anchor" id="d1062510e494">  </a> <h5 class="section-title" id="d1062510e495">Results</h5> <p id="d1062510e497">In a multivariate-adjusted model, older age, female sex, non-Hispanic Black, current smoking, diabetes, higher pulse pressure, lower high-density lipoprotein cholesterol, higher low-density lipoprotein cholesterol, and lower estimated glomerular filtration rate were significantly associated with the increased risk of incident PAD. After adjustment for these traditional risk factors as well as use of medications and CRIC Study clinic sites, the following baseline novel risk factors were significantly associated with risk of incident PAD [hazard ratio and 95% confidence interval (CI) for a one standard deviation (SD) higher level]: log[C-reactive protein (CRP)] (1.16, 1.06–1.25, P < 0.001), white blood cell count (1.09, 1.01–1.18, P = 0.03), fibrinogen (1.15, 1.06–1.26, P = 0.002), log(myeloperoxidase) (1.12, 1.03–1.23, P = 0.01), uric acid (0.88, 0.80–0.97, P = 0.01), glycated hemoglobin (1.16, 1.05–1.27, P = 0.003), log(homeostatic model assessment-insulin resistance) (1.21, 1.10–1.32, P < 0.001) and alkaline phosphatase (1.15, 1.07–1.24, P < 0.001). </p> </div><div class="section"> <a class="named-anchor" id="d1062510e499">  </a> <h5 class="section-title" id="d1062510e500">Conclusions</h5> <p id="d1062510e502">Among patients with CKD, inflammation, prothrombotic state, oxidative stress, glycated hemoglobin, insulin resistance and alkaline phosphatase are associated with an increased risk of PAD, independent of traditional risk factors. </p> </div>

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The Chronic Renal Insufficiency Cohort (CRIC) Study: Design and Methods.

Harold I. Feldman, Kenneth Jamerson, L. Lee Hamm … (2003)

Insights into end-stage renal disease have emerged from many investigations but less is known about the epidemiology of chronic renal insufficiency (CRI) and its relationship to cardiovascular disease (CVD). The Chronic Renal Insufficiency Cohort (CRIC) Study was established to examine risk factors for progression of CRI and CVD among CRI patients and develop models to identify high-risk subgroups, informing future treatment trials, and increasing application of preventive therapies. CRIC will enroll approximately 3000 individuals at seven sites and follow participants for up to 5 yr. CRIC will include a racially and ethnically diverse group of adults aged 21 to 74 yr with a broad spectrum of renal disease severity, half of whom have diagnosed diabetes mellitus. CRIC will exclude subjects with polycystic kidney disease and those on active immunosuppression for glomerulonephritis. Subjects will undergo extensive clinical evaluation at baseline and at annual clinic visits and via telephone at 6 mo intervals. Data on quality of life, dietary assessment, physical activity, health behaviors, depression, cognitive function, health care resource utilization, as well as blood and urine specimens will be collected annually. (125)I-iothalamate clearances and CVD evaluations including a 12-lead surface electrocardiogram, an echocardiogram, and coronary electron beam or spiral CT will be performed serially. Analyses planned in CRIC will provide important information on potential risk factors for progressive CRI and CVD. Insights from CRIC should lead to the formulation of hypotheses regarding therapy that will serve as the basis for targeted interventional trials focused on reducing the burden of CRI and CVD.

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Myeloperoxidase, a leukocyte-derived vascular NO oxidase.

Stephan Baldus, Aldons J Lusis, Wenxin Ma … (2002)

Myeloperoxidase (MPO) is an abundant mammalian phagocyte hemoprotein thought to primarily mediate host defense reactions. Although its microbicidal functions are well established in vitro, humans deficient in MPO are not at unusual risk of infection. MPO was observed herein to modulate the vascular signaling and vasodilatory functions of nitric oxide (NO) during acute inflammation. After leukocyte degranulation, MPO localized in and around vascular endothelial cells in a rodent model of acute endotoxemia and impaired endothelium-dependent relaxant responses, to which MPO-deficient mice were resistant. Altered vascular responsiveness was due to catalytic consumption of NO by substrate radicals generated by MPO. Thus MPO can directly modulate vascular inflammatory responses by regulating NO bioavailability.

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Estimating GFR among participants in the Chronic Renal Insufficiency Cohort (CRIC) Study.

Dawei Xie, John W. Kusek, Fang-Chi Hsu … (2012)

Glomerular filtration rate (GFR) is considered the best measure of kidney function, but repeated assessment is not feasible in most research studies. Cross-sectional study of 1,433 participants in the Chronic Renal Insufficiency Cohort (CRIC) Study (ie, the GFR subcohort) to derive an internal GFR estimating equation using a split-sample approach. Adults from 7 US metropolitan areas with mild to moderate chronic kidney disease; 48% had diabetes and 37% were black. CRIC GFR estimating equation. Urinary (125)I-iothalamate clearance testing (measured GFR [mGFR]). Laboratory measures, including serum creatinine and cystatin C, and anthropometrics. In the validation data set, the model that included serum creatinine level, serum cystatin C level, age, sex, and race was the most parsimonious and similarly predictive of mGFR compared with a model additionally including bioelectrical impedance analysis phase angle, CRIC clinical center, and 24-hour urinary creatinine excretion. Specifically, root mean square errors for the separate models were 0.207 versus 0.202, respectively. Performance of the CRIC GFR estimating equation was most accurate for the subgroups of younger participants, men, nonblacks, non-Hispanics, those without diabetes, those with body mass index <30 kg/m(2), those with higher 24-hour urine creatinine excretion, those with lower high-sensitivity C-reactive protein levels, and those with higher mGFRs. Urinary clearance of (125)I-iothalamate is an imperfect measure of true GFR; cystatin C level is not standardized to certified reference material; lack of external validation; small sample sizes limit analyses of subgroup-specific predictors. The CRIC GFR estimating equation predicts mGFR accurately in the CRIC cohort using serum creatinine and cystatin C levels, age, sex, and race. Its performance was best in younger and healthier participants. Copyright © 2012 National Kidney Foundation, Inc. All rights reserved.