No abstract

The prevalence of chronic kidney disease (CKD) and end-stage renal disease (ESRD) is increasing steadily. CKD does not only relate to morbidity and mortality but also has impact on quality of life, depression and malnutrition. Such patients often have significantly decreased physical activity. Recent evidence suggests that low physical activity is associated with morbidity, mortality, muscle atrophy, quality of life impairment, cardiovascular outcomes and depression. Based on this, it is now recommended to regularly improve the physical activity of these patients. Furthermore, studies have shown the beneficial effects of various exercise programs with respect to outcomes such as low physical activity muscle atrophy, quality of life, cardiovascular outcomes and depression. Despite these encouraging findings, the subject is still under debate, with various aspects still unknown. In this review, we tried to critically summarize the existing studies, to explore mechanisms and describe future perspectives regarding physical activity in CKD/ESRD patients.

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Although the studies are mostly small in size, heterogeneous and have conflicting results, we have demonstrated that serum sclerostin levels were not associated with all-cause and cardiovascular mortality.

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies ( P = .001, I = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.