Exertional fatigue, defined as the overwhelming and debilitating sense of sustained exhaustion that impacts the ability to perform activities of daily living, is highly prevalent in chronic kidney disease (CKD) and end-stage renal disease (ESRD). Subjective reports of exertional fatigue are paralleled by objective measurements of exercise intolerance throughout the spectrum of the disease. The prevalence of exercise intolerance is clinically noteworthy, as it leads to increased frailty, worsened quality of life, and an increased risk of mortality. The physiological underpinnings of exercise intolerance are multifaceted and still not fully understood. This review aims to provide a comprehensive outline of the potential physiological contributors, both central and peripheral, to kidney disease-related exercise intolerance and highlight current and prospective interventions to target this symptom. In this review, the CKD-related metabolic derangements, cardiac and pulmonary dysfunction, altered physiological responses to oxygen consumption, vascular derangements, and sarcopenia are discussed in the context of exercise intolerance. Lifestyle interventions to improve exertional fatigue, such as aerobic and resistance exercise training, are discussed, and the lack of dietary interventions to improve exercise tolerance is highlighted. Current and prospective pharmaceutical and nutraceutical strategies to improve exertional fatigue are also broached. An extensive understanding of the pathophysiological mechanisms of exercise intolerance will allow for the development of more targeted therapeutic approached to improve exertional fatigue and health-related quality of life in CKD and ESRD.
Although there have been many improvements in prognosis for patients with cancer, anticancer therapies are burdened by the risk of cardiovascular toxicity. Heart failure is one of the most dramatic clinical expressions of cardiotoxicity, and it may occur acutely or appear years after treatment. This article reviews the main mechanisms and clinical presentations of left ventricular dysfunction induced by some old and new cardiotoxic drugs in cancer patients, referring to the most recent advances in the field. The authors describe the mechanisms of cardiotoxicity induced by anthracyclines, which can lead to cardiovascular problems in up to 48% of patients who take them. The authors also describe mechanisms of cardiotoxicity induced by biological drugs that produce left ventricular dysfunction through secondary mechanisms. They outline the recent advances in immunotherapies, which have revolutionised anticancer therapies.
This study evaluated preliminary physical fitness, physical activity, and blood lipid profile data obtained from overweight adolescents upon enrolling in a healthy weight management program and following 6 months of program participation. One hundred and sixty-eight participants (13.4+/-1.8 years, 37.9+/-8.3 kg/m(2), 59.5% female and 76.2% African-American) enrolled in the program. The intervention addressed factors related to nutrition, physical activity, and other behaviors related to weight management. Sixty-four participants (38.1%) completed 6 months of program participation. While there was no significant reduction in body mass or body mass index (BMI), BMI z-score was reduced by 1.2% (p < 0.05), cardiorespiratory fitness was increased by 10.8% (p = 0.001), body fat percentage was reduced by 2.6% (p = 0.001), total cholesterol was reduced by 7.2% (p < 0.001), and low density lipoprotein (LDL-C) was reduced by 8.4% (p < 0.001) at 6 months. Continued development and evaluation of programs designed to prevent and treat child and adolescent overweight is warranted to address this major public health issue.
A dedicated neurosonographer could diagnose the iCACC with the same accuracy as MRI and in up to 90% of cases the newborn will have a regular development.
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