Association Between Physical Activity and Mortality in End-Stage Kidney Disease: a Systematic Review of Observational Studies

Background: End-stage Kidney Disease patients have a high mortality and hospitalization risk. The association of these outcomes with physical activity is described in the general population and in other chronic diseases. However, few studies examining this association have been completed in end-stage Kidney Disease patients, raising the need to systematically review the evidence on the association of physical activity with mortality and hospitalization in this population. Methods: Electronic databases (EBSCO, Scopus and Web of Science) and hand search were performed until March 2020 for observational studies reporting the association of physical activity with mortality or hospitalization in adult end-stage Kidney Disease patients on renal replacement therapy (hemodialysis, peritoneal dialysis and kidney transplant). Methodological quality of the included studies was assessed using the Quality in Prognosis Studies tool. The review protocol was registered in PROSPERO (CRD42020155591). Results: Eleven studies were included: six in hemodialysis, three in kidney transplant, and two in hemodialysis and peritoneal dialysis patients. Physical activity was self-reported, except in one study that used accelerometers. All-cause mortality was addressed in all studies and cardiovascular mortality in three studies. Nine studies reported a significant reduction in all-cause mortality with increased levels of physical activity. Evidence of a dose-response relationship was found. For cardiovascular mortality, a significant reduction was observed in two of the three studies. Only one study investigated the association of physical activity with hospitalization. Conclusions: Higher physical activity was associated with reduced mortality in end-stage Kidney Disease patients. Future studies using objective physical activity measures could strengthen these findings. The association of physical activity with hospitalization should be explored in future investigations.info:eu-repo/semantics/publishedVersio

Global Policy Barriers and Enablers to Exercise and Physical Activity in Kidney Care

Objective: Impairment in physical function and physical performance leads to decreased independence and health-related quality of life in people living with chronic kidney disease and end-stage kidney disease. Physical activity and exercise in kidney care are not priorities in policy development. We aimed to identify global policy-related enablers, barriers, and strategies to increase exercise participation and physical activity behavior for people living with kidney disease. Design and Methods: Guided by the Behavior Change Wheel theoretical framework, 50 global renal exercise experts developed policy barriers and enablers to exercise program implementation and physical activity promotion in kidney care. The consensus process consisted of developing themes from renal experts from North America, South America, Continental Europe, United Kingdom, Asia, and Oceania. Strategies to address enablers and barriers were identified by the group, and consensus was achieved. Results: We found that policies addressing funding, service provision, legislation, regulations, guidelines, the environment, communication, and marketing are required to support people with kidney disease to be physically active, participate in exercise, and improve health-related quality of life. We provide a global perspective and highlight Japanese, Canadian, and other regional examples where policies have been developed to increase renal physical activity and rehabilitation. We present recommendations targeting multiple stakeholders including nephrologists, nurses, allied health clinicians, organizations providing renal care and education, and renal program funders. Conclusions: We strongly recommend the nephrology community and people living with kidney disease take action to change policy now, rather than idly waiting for indisputable clinical trial evidence that increasing physical activity, strength, fitness, and function improves the lives of people living with kidney disease

Race Affects Elastance Responses Following Endurance Exercise Training

The ventricular-vascular coupling ratio is comprised of the ratio of arterial elastance to ventricular elastance. Briefly, arterial elastance (Ea) may be described as total arterial load, and ventricular elastance (Elv) also considers both geometric and physiological variables to quantify left ventricular stiffness. Together, these measures may be indexed to body size (EaI and ElvI) to compile a load-independent portrayal of net cardiac and vascular interaction. Optimal EaI/ElvI results in ideal coronary perfusion and blood distribution to the periphery. Blood pressure (BP) and arterial stiffness are important determinants of EaI/ElvI. African Americans (AA) have consistently been reported to have higher large artery stiffness and BP compared to Caucasian Americans (CA). However, exercise training reduces both BP and large artery stiffness. Our purpose was to determine the effects of race on coupling after an 8 week exercise training intervention. We hypothesized a reduction in the ratio due to a reduction in EaI that would be more pronounced in CA compared to AA adults. We used applanation tonometry to measure central blood pressures and carotid-femoral pulse wave velocity to quantify central arterial stiffness and cardiac ultrasonography to quantify LV volumes before and after our training intervention. We used the formulas: Ea=ESP/SV and Elv=ESP/ESV and divided these numbers by BSA as calculated using Mostellar’s formula. Both AA and CA maintained their pre-training coupling ratios (p>0.05 for time effect and race*time interaction), however, CA did so by uniformly augmenting both EaI and ElvI (Ea was 0.76±0.1 to 0.77±0.09 mmHg/ml/m2 in AA and 0.68±0.09 to 0.75±0.1 mmHg/ml/m2, p=0.02 for CA; ElvI was 1.20±0.11 to 1.22±0.1 mmHg/ml/m2 in AA and 0.99±0.1 to 1.16±0.1 mmHg/ml/m2 in CA p0.05). This occurred despite similar reductions in central arterial stiffness, BP, and ESP in both races. We conclude that, although the coupling ratio was similarly maintained in CA and AA, the responses to training were quite different.published or submitted for publicationis peer reviewe

Advances in exercise therapy in pre-dialysis CKD, hemodialysis, peritoneal dialysis and kidney transplantation

Purpose of review Chronic kidney disease (CKD) is characterized by poor levels of physical activity which contribute to increased morbidity across the disease trajectory. The short nature, small samples, and poor methodology across most studies have failed to translate the role of exercise in CKD into its adoption as a frontline adjunct therapeutic option. This review focuses on recent advances surrounding the benefits of exercise interventions across the CKD spectrum. Recent findings Key recent advances in exercise studies have focused on the efficacy of novel intervention strategies across the CKD spectrum. These include high-intensity interval training, virtual reality gaming, intradialytic yoga, electrical stimulation of muscles, blood flow restriction training, and protocols combining exercise with nutritional supplementation. Research is also beginning to explore the role of prehabilitation for patients prior to dialysis and kidney transplantation. Summary Studies continue to demonstrate wide-ranging benefits of exercise across CKD; however, implementation of exercise remains scarce. Future research needs include evaluating the efficacy of larger and/or more comprehensive interventions on clinically important outcomes. It is hoped with increasing global evidence, high-quality clinical studies, and sustained clinician and patient engagement, exercise programs will become better prioritized in the nephrology field

Physical activity, hormone replacement therapy and plasma lipoprotein-lipid levels in postmenopausal women

Analgesics are commonly used to manage pain in cancer patients. It has been suggested that there might be a relation between analgesics and the outgrowth of metastases. Opioids might increase and non-steroidal anti-inflammatory drugs decrease the risk of metastasis. Robust analysis of all preclinical evidence, however, has so far been lacking. Therefore, we conducted a systematic review and meta-analysis on the effect of treatment with analgesics on metastasis in experimental animal models. One hundred forty-seven studies met the inclusion criteria. Study characteristics, outcome data on the number, and incidence of metastases were extracted, and methodological quality was assessed. In the meta-analysis, we included 215 (+/-4000 animals) and 137 (+/-3000 animals) comparisons between analgesic vs control treatment, respectively, on the number and incidence of metastases. Overall, treatment with analgesics significantly decreases the number and risk of metastasis. This effect appears mainly to be the consequence of the efficacy of NSAIDs. Other factors that modify the efficacy are species, type of NSAIDs administered, timing, and duration of treatment. There is no evidence indicating that treatment with any analgesics increases the occurrence of metastases. Our findings appear robust for the various animal models and designs included in this review, which increases our confidence in the result and translatability to the clinical situation

Molecular mechanisms of autosomal recessive hypercholesterolemia

Mutations in the phosphotyrosine-binding domain protein ARH cause autosomal recessive hypercholesterolemia (ARH), an inherited form of hypercholesterolemia due to a tissue-specific defect in the removal of low density lipoproteins (LDL) from the circulation. LDL uptake by the LDL receptor (LDLR) is markedly reduced in the liver but is normal or only moderately impaired in cultured fibroblasts of ARH patients. To define the molecular mechanism underlying ARH we examined ARH mRNA and protein in fibroblasts and lymphocytes from six probands with different ARH mutations. None of the probands had detectable full-length ARH protein in fibroblasts or lymphoblasts. Five probands were homozygous for mutations that introduced premature termination codons. No relationship was apparent between the site of the mutation in ARH and the amount of mRNA. The only mutation identified in the remaining proband was a SINE VNTR Alu (SVA) retroposon insertion in intron 1, which was associated with no detectable ARH mRNA. I-125-LDL degradation was normal in ARH fibroblasts, as previously reported. In contrast, LDLR function was markedly reduced in ARH lymphoblasts, despite a 2-fold increase in LDL cell surface binding in these cells. These data indicate that all ARH mutations characterized to date preclude the synthesis of full-length ARH and that ARH is required for normal LDLR function in lymphocytes and hepatocytes, but not in fibroblasts. Residual LDLR function in cells that do not require ARH may explain why ARH patients have lower plasma LDL levels than do patients with homozygous familial hypercholesterolemia who have no functional LDLRs