Patients with chronic kidney disease (CKD) are at an increased risk of premature mortality, mainly from cardiovascular causes. The association between CKD on hemodialysis and accelerated atherosclerosis was described >40 years ago. However, more recently, it has been suggested that the increase in atherosclerosis risk is actually observed in early CKD stages, remaining stable thereafter. In this regard, interventions targeting the pathogenesis of atherosclerosis, such as statins, successful in the general population, have failed to benefit patients with very advanced CKD. This raises the issue of the relative contribution of atherosclerosis versus other forms of cardiovascular injury such as arteriosclerosis or myocardial injury to the increased cardiovascular risk in CKD. In this review, the pathophysiogical contributors to atherosclerosis in CKD that are shared with the general population, or specific to CKD, are discussed. The NEFRONA study (Observatorio Nacional de Atherosclerosis en NEFrologia) prospectively assessed the prevalence and progression of subclinical atherosclerosis (plaque in vascular ultrasound), confirming an increased prevalence of atherosclerosis in patients with moderate CKD. However, the adjusted odds ratio for subclinical atherosclerosis increased with CKD stage, suggesting a contribution of CKD itself to subclinical atherosclerosis. Progression of atherosclerosis was closely related to CKD progression as well as to the baseline presence of atheroma plaque, and to higher phosphate, uric acid, and ferritin and lower 25(OH) vitamin D levels. These insights may help design future clinical trials of stratified personalized medicine targeting atherosclerosis in patients with CKD. Future primary prevention trials should enroll patients with evidence of subclinical atherosclerosis and should provide a comprehensive control of all known risk factors in addition to testing any additional intervention or placebo.
The layout of this study, designed as a randomized crossover clinical trial, is to evaluate the efficacy of an intervention with mineral-medicinal water from As Burgas (Ourense) in patients suffering from fibromyalgia. Pre-intervention: randomization of group A and group B. Intervention: Phase 1: Group A: 14 baths in thermal water for a month and standard pharmacological treatment; group B, standard pharmacological treatment. Rest period, 3 months. Phase 2: Gruop A, standard treatment and Grou B, 14 baths in thermal water for a month plus standard treatment. The Fibromyalgia Impact Questionnaire (FIQ) was used; this grades from 1 (minimum) to 10 (maximum) the impact of the illness, which was measured in both phases. 25 patients were included in each group and the study was concluded with 20 patients in group A and 20 in group B. The intervention group obtained, once the baths finished, a mean score of 60,3 (±11,8) and the control group of 70,8 (±13,0) (p <0,001). Three months later, the intervention group presented a mean score of 64,4 (±10,6) and the control group of 5,0 (±11,3) (p <0,001). We can therefore conclude that the simple baths with mineral-medicinal water from As Burgas can make an improvement on the impact caused by fibromyalgia.
In our sample, AD with cerebrovascular disease had worse gait and balance than AD without cerebrovascular disease. If confirmed, these results may have clinical implications, since cerebrovascular disease can be potentially prevented.
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