1.
[Subclinical micronutrients deficiencies related to metabolic syndrome].
Jiménez Ortega, AI, Martínez García, RM, Velasco Rodríguez-Belvis, M, Ruiz Herrero, J, Salas González, MªD, Ortega, RM
Nutricion hospitalaria. 2018;(Spec No6):60-63
Abstract
Metabolic syndrome is the name given to a set of risk factors that increases the risk of cardiovascular disease and other health problems, such as diabetes and stroke. There are different cut-off points to establish the definition of metabolic syndrome according to various international organizations, although in all definitions are considered four main data related to: 1) obesity; 2) alteration of glucose metabolism; 3) alteration of lipid metabolism; and 4) hypertension. Strategies for the treatment of the metabolic syndrome include changes in lifestyle (diet and physical activity), along with pharmacological treatment in certain cases. There is little evidence of the effect of different micronutrients in this syndrome, although there are many investigations in this line.
2.
Mineral metabolism and cardiovascular disease in CKD.
Fujii, H, Joki, N
Clinical and experimental nephrology. 2017;(Suppl 1):53-63
Abstract
The mineral bone disorder of CKD, called Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), has a major role in the etiology and progression of cardiovascular disease in CKD patients. Since the main emphasis in CKD-MBD is on three categories (bone abnormalities, laboratory abnormalities, and vascular calcifications), we have routinely accepted ectopic cardiovascular calcifications as a central risk factor in the pathophysiology of CKD-MBD for cardiac events. However, recent compelling evidence suggests that some CKD-MBD-specific factors other than vascular calcification might contribute to the onset of cardiovascular disease. Most notable is fibroblast growth factor-23 (FGF23), which is thought to be independently associated with cardiac remodeling. Slow progression of cardiac disorders, such as vascular calcification and cardiac remodeling, characterizes cardiac disease due to CKD-MBD. In contrast, fatal arrhythmia may be induced when QT prolongation occurs with CKD-MBD treatment, such as with lower Ca dialysate or the use of calcimimetics. Sudden onset of fatal cardiac events, such as heart failure and sudden cardiac death, due to fatal arrhythmia would be another distinctive phenomenon of CKD-MBD. This may be defined as CKD-MBD-specific cardiac complex syndrome.
3.
Mineral metabolism abnormalities and vitamin D receptor activation in cardiorenal syndromes.
Ronco, C, Cozzolino, M
Heart failure reviews. 2012;(2):211-20
Abstract
Over the last decade, it has become increasingly clear that the cardiovascular and renal systems are interdependent. Primary disorders of either system have been shown to disturb the other system. As a result, a class of cardiorenal syndromes (CRS) has been identified wherein a vicious cycle is established as an acute/chronic dysfunction of either the kidney or the heart exacerbates the loss of function in the other organ. Progressive loss of kidney function observed in patients with CRS (mostly types 2 and 4) leads to reduced production of calcitriol (active vitamin D) and an imbalance in calcium and phosphorus levels, which are correlated with increased rates of cardiovascular events and mortality. In addition, hypocalcemia can lead to prolonged and excessive secretion of parathyroid hormone (PTH), eventually leading to development of secondary hyperparathyroidism. Therefore, based on this important mechanism of organ damage, one of the major goals of therapy for patients with CRS is to restore regulatory control of PTH. Although administration of calcitriol increases serum calcium levels and reduces PTH levels, it is also associated with elevated serum levels of calcium-phosphorus product. Therefore, compounds that selectively activate vitamin D receptors, potentially reducing calcium × phosphate toxicity, are likely to enhance cardiorenal protection and provide significant clinical benefit.