Updates on the Mechanisms and the Care of Cardiovascular Calcification in Chronic Kidney Disease

International-Society-of-Nephrology (ISN) Frontiers Symposium, Tokyo, JAPAN, FEB 22-25, 2018International audienceIn chronic kidney disease (CKD), the progressive decrease in renal function leads to disturbances of mineral metabolism that generally cause secondary hyperparathyroidism. The increase in serum parathyroid hormone is associated with reduced serum calcium and calcitriol levels and/or increased serum fibroblast growth factor-23 and phosphate levels. The resulting CKD-associated disorder of mineral and bone metabolism is associated with various other metabolic dysregulations such as acidosis, malnutrition, inflammation, and accumulation of uremic toxins. It favors the occurrence of vascular calcification, which results from an imbalance between numerous inhibitors and promoters of soft-tissue mineralization. This review provides an overview of the most recent state of knowledge concerning the mechanisms that lead to the development of vascular calcification in the CKD setting. It further proposes directions for potential new therapeutic targets. Semin Nephrol 38:233-250 (C) 2018 Elsevier Inc. All rights reserved

CHRONIC RENAL FAILURE WORSENS ISCHEMIC STROKE SEVERITY AND NEUROLOGICAL CONSEQUENCES IN MICE

53rd ERA-EDTA Congress, Vienna, AUSTRIA, MAY 21-24, 2016International audienc

CHRONIC RENAL FAILURE WORSENS ISCHEMIC STROKE SIZE AND ALTERS NEUROLOGICAL FUNCTIONS IN MICE

International audienc

New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

International audienceCardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC-particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions

Association of ionized serum magnesium with progression of aortic valve calcification

Congress of the European-Society-of-Cardiology (ESC) / World Congress of Cardiology, Paris, FRANCE, AUG 31-SEP 04, 2019International audienc

Association of ionized serum magnesium with progression of aortic valve calcification

Congress of the European-Society-of-Cardiology (ESC) / World Congress of Cardiology, Paris, FRANCE, AUG 31-SEP 04, 2019International audienc

Metformin alleviates stroke severity in female mice with chronic kidney disease through AMPK activation and subsequent decrease of microglia/macrophages M1 polarization

56th Congress of the European-Renal-Association (ERA)-European-Dialysis-and-Transplant-Association (EDTA) - Burden, Access and Disparities in Kidney Disease, Budapest, HUNGARY, JUN 13-16, 2019International audienc