Association of Monocyte Chemoattractant Protein-1 with Death and Atherosclerotic Events in Chronic Kidney Disease.
Association of Monocyte Chemoattractant Protein-1 with Death and Atherosclerotic Events in Chronic Kidney Disease. Am J Nephrol. 2018 Jun 06;47(6):395-405 Authors: Gregg LP, Tio MC, Li X, Adams-Huet B, de Lemos JA, Hedayati SS Abstract BACKGROUND: Monocyte chemoattractant protein-1 -(MCP-1), a marker of inflammation and monocyte recruitment to atherosclerotic plaques, is associated with cardiovascular (CV) outcomes in patients with acute coronary syndrome. Although plasma levels are elevated in chronic kidney disease (CKD), associations with reduced kidney function or outcomes in CKD have not been explored. METHODS: In this population-based, probability-sampled, longitudinal cohort of 3,257 participants, including 286 (8.8%) patients with CKD, we studied the association of plasma MCP-1 with estimated glomerular filtration rate (eGFR), albuminuria, death, and intermediate and hard CV outcomes in CKD and non-CKD individuals. Cox proportional hazards regression assessed associations of baseline MCP-1 with all-cause death and atherosclerotic events. RESULTS: MCP-1 was higher in CKD than non-CKD participants (p
Background: Beta cells are central in the pathophysiology of diabetes, since their functional adaptation maintains euglycemia in insulin-resistant individuals and beta cell dysfunction is required for the clinical picture of frank diabetes. The pathophysiological mechanisms driving compensation and decompensation are incompletely understood and little is known about the influence of chronic kidney disease (CKD) on beta cell function.Summary: In compensated insulin resistance, beta cells enhance their function at all stages in the stimulus-secretion coupling cascade, from the most proximal membrane depolarization to the int...
Condition: Chronic Kidney Diseases Intervention: Sponsor: Islamia University of Bahawalpur Recruiting
Authors: Messa P, Alfieri CM Abstract Secondary hyperparathyroidism (SHP) is a frequent complication of kidney diseases. At variance with all the other forms of SHP, which are compensatory conditions, renal SHP has many pathogenetic peculiarities, which have been only in part defined. Furthermore, in the long course of chronic kidney diseases (CKD), SHP sometimes transforms into a hypercalcemic condition resembling the autonomous form of hyperparathyroidism (tertiary hyperparathyroidism; THP). The clinical consequences of SHP in CKD patients are manifold, encompassing not only bone and mineral disorders, but also o...
What is the relationship between gout and chronic kidney disease, and what role could urate-lowering therapy play in the development of CKD in these patients?Arthritis Research &Therapy
Authors: Lascasas JMSS, Fonseca I, Malheiro J, Santos S, Campos A, Castro A, Moreira C, Correia S, Beirão I, Lobato L, Cabrita A Abstract INTRODUCTION: Chronic kidney disease (CKD) is an independent risk factor for several unfavorable outcomes including cardiovascular disease (CVD), particularly in the elderly, who represent the most rapidly growing segment of the end-stage kidney disease (ESKD) population. Portugal has the highest European unadjusted incidence and prevalence rates of ESKD. In 2012, we started to follow a cohort of elderly CKD patients, we describe their baseline characteristics, risk profil...
ConclusionsAlthough we showed no independent association between neighborhood context and eGFR decline, it is associated with many CKD risk factors and further work is needed to clarify whether it has an independent role in CKD.
ConclusionWith increasing pressure for cost containment in an era of bundled payment models, the very low rate of laboratory associated interventions suggest that routine postoperative laboratory tests is not justified. Obtaining laboratory after primary, unilateral TKA should be driven by patients’ risk factors.
This study aimed to examine the relationship between 25-hyfromxyvitamin D (25OHD) and chronic kidney disease (CKD) incidence.
ConclusionsEvidence from our series of causal inference approaches using genetics does not support a causal effect of SU level on eGFR level or CKD risk. Reducing SU levels is unlikely to reduce the risk of CKD development.
Conflicting results have been reported from studies evaluating serum uric acid (SUA) levels as an independent risk factor for cardiovascular mortality in patients with chronic kidney disease (CKD).