RESUMEN
Vascular calcification (VC) is common in dialysis and non-dialysis chronic kidney disease (CKD) patients, even in the early stage of the disease. For this reason, it can be considered a CKD hallmark. VC contributes to cardiovascular disease (CVD) and increased mortality among CKD patients, although it has not been proven. There are more than one type of VC and every form represents a marker of systemic vascular disease and is associated with a higher prevalence of CVD in CKD patients, as shown by several clinical studies. Major risk factors for VC in CKD include: Increasing age, dialysis vintage, hyperphosphatemia (particularly in the setting of intermittent or persistent hypercalcemia), and a positive net calcium and phosphate balance. Excessive oral calcium intake, including calcium-containing phosphate binders, increases the risk for VC. Moreover, it has been demonstrated that there is less VC progression with non-calcium-containing phosphate binders. Unfortunately, until now, a specific therapy to prevent progression or to facilitate regression of VC has been found, beyond careful attention to calcium and phosphate balance.
Asunto(s)
Fosfatos/metabolismo , Calcificación Vascular/metabolismo , Animales , Apoptosis , Autofagia , Humanos , Hierro/metabolismo , Miocitos del Músculo Liso/metabolismo , Fósforo/metabolismo , Insuficiencia Renal Crónica/metabolismoRESUMEN
Vitamin K is a composite term referring to a group of fat-soluble vitamins that function as a cofactor for the enzyme γ-glutamyl carboxylase (GGCX), which activates a number of vitamin K-dependent proteins (VKDPs) involved in haemostasis and vascular and bone health. Accumulating evidence demonstrates that chronic kidney disease (CKD) patients suffer from subclinical vitamin K deficiency, suggesting that this represents a population at risk for the biological consequences of poor vitamin K status. This deficiency might be caused by exhaustion of vitamin K due to its high requirements by vitamin K-dependent proteins to inhibit calcification.
Asunto(s)
Insuficiencia Renal Crónica/tratamiento farmacológico , Deficiencia de Vitamina K/tratamiento farmacológico , Vitamina K/sangre , Vitamina K/farmacología , Huesos/metabolismo , Ligasas de Carbono-Carbono/metabolismo , Suplementos Dietéticos , Humanos , Estado Nutricional , Ensayos Clínicos Controlados Aleatorios como Asunto , Insuficiencia Renal Crónica/sangre , Deficiencia de Vitamina K/sangre , Warfarina/administración & dosificación , Warfarina/efectos adversosRESUMEN
Chronic low-grade inflammation is emerging as the pathophysiological mechanism underlying of the several chronic degenerative diseases. Atherosclerosis, inflammation and oxidative stress are some of the issues that arise from the general context of chronic inflammation. In this manuscript we analyzed the role of the immune system, metabolism and inflammation's molecular mediators in order to show an overview about only apparently different problems. Finally, we proposed some possible solutions to improve the survival and quality of life of patient with chronic kidney disease.