Hyperuricemia and Cardiovascular Disease.
Hyperuricemia and Cardiovascular Disease. Curr Pharm Des. 2019 Apr 08;: Authors: Zhang S, Wang Y, Cheng J, Huangfu N, Zhao R, Xu Z, Zhang F, Zheng W, Zhang D Abstract Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan. PMID: 30961478 [PubMed - as supplied by publisher]
In their recent study comparing different assays to measure albumin level, van de Logt et al.1 show that the use of bromocresol green (BCG) (but not bromocresol purple [BCP]) leads to a substantial overestimation of plasma and serum albumin concentration (mean bias: 6.2 g/l), in comparison to the reference immunonephelometric assay in patients with hypoalbuminemia (including patients w ith membranous nephropathy, liver cirrhosis, or sepsis) and in chronic kidney disease patients with albumin concentrations within reference values.
Intestinal regulation of oxalate absorption is a complex mechanism, not exclusively reliant on the oxalate-degrading anaerobe Oxalobacter formigenes. Using metagenomics, Miller et al. were able to describe a network of bacterial taxa co-occurring with Oxalobacter formigenes in fecal samples from non–stone forming controls and less represented in stone formers. These findings may help to illuminate why previous intervention studies with probiotics have failed to reduce the risk of hyperoxaluria, opening new possibilities for future research.
We appreciate the letter by Dr. Sugiyama, which provides a potential mechanistic insight with regard to the relationship between chronic kidney disease and fracture risk.1 We agree with Dr. Sugiyama that lower estimated glomerular filtration rate is associated with a decline in physical activity, and as such, physical activity c ould be a confounder in the relationship between chronic kidney disease and bone mineral density. In our previous work, we found a 4-fold higher risk of low physical activity with chronic kidney disease, a greater magnitude than diabetes or nearly 2 decades of aging.
Whitlock et al.1 showed that the Fracture Risk Assessment Tool, developed to predict fracture risk in the general population, was able to be used in patients with nondialysis chronic kidney disease (CKD) and highlighted that CKD could not be an independent risk factor for fractures. To support the authors’ suggestion, I here propose the key involvement of physical activity; CKD is inversely associated with physical activity.2,3 Major causes of osteoporotic fractures are skeletal fragility and minor trauma such as falls, both of which are significantly influenced by habitual physical activity.
Vasopressin is known to contribute to disease progression in autosomal dominant polycystic disease (ADPKD) by its influence on cyclic adenosine monophosphate that directly promotes cyst growth. In addition, vasopressin probably contributes to progression by inducing glomerular hyperfiltration as shown in other forms of chronic kidney diseases. The measurement of plasma copeptin, a marker of vasopressin secretion, could help identify patients at higher risk of fast progression and those expected to benefit the most from vasopressin V2 receptor blockade.
We describe the importance of this topic and explain key assumptions necessary for the investigators to arrive at their conclusions.
Publication date: July 2019Source: Journal of Comparative Pathology, Volume 170Author(s): Y. Ohara, A. Yabuki, R. Nakamura, O. Ichii, H. Mizukawa, N. Yokoyama, O. YamatoSummaryDuring the progression of chronic kidney disease (CKD), macrophage infiltration is a crucial event leading to tubulointerstitial fibrosis. In the present study, macrophages infiltrating renal tissue in dogs and cats with CKD were analysed immunohistochemically. Iba-1 was used as a pan-macrophage marker, CD204 was used as a marker of M2 macrophages and tumour necrosis factor (TNF)-α was used as a marker of M1 macrophages. Signals for Iba1 and CD...
Publication date: June 2018Source: American Journal of Kidney Diseases, Volume 71, Issue 6Author(s): Richard J. Johnson, George L. Bakris, Claudio Borghi, Michel B. Chonchol, David Feldman, Miguel A. Lanaspa, Tony R. Merriman, Orson W. Moe, David B. Mount, Laura Gabriella Sanchez Lozada, Eli Stahl, Daniel E. Weiner, Glenn M. ChertowUrate is a cause of gout, kidney stones, and acute kidney injury from tumor lysis syndrome, but its relationship to kidney disease, cardiovascular disease, and diabetes remains controversial. A scientific workshop organized by the National Kidney Foundation was held in September 2016 to review c...
Abstract Gout is an inflammatory disease manifested by the deposition of monosodium urate (MSU) crystals in joints, cartilage, synovial bursa, tendons or soft tissues. Gout is not a new disease, which was first documented nearly 5,000 years ago. The prevalence of gout has increased globally in recent years, imposing great disease burden worldwide. Moreover, gout or hyperuricemia is clearly associated with a variety of comorbidities, including cardiovascular diseases, chronic kidney disease, urolithiasis, metabolic syndrome, diabetes mellitus, thyroid dysfunction, and psoriasis. To prevent acute arthritis attacks and compli...