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Query: UMLS:C0007222 (cardiovascular disease)
 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accelerated atherosclerosis and vascular calcifications (VC) play a central role in the pathogenesis of cardiovascular disease in chronic kidney disease (CKD) patients. Mineral metabolism disorders and increased serum calcium-phosphate product have been recently investigated as inducing factors of cardiovascular calcification. In fact, cardiovascular disease in renal failure appears greatly associated with bone metabolism alterations. Recently, the treatment of hyperphosphatemia in CKD patients changed from either calcium- or aluminium-based phosphate-binders to new free-calcium and aluminium phosphate binders, such as sevelamer hydrochloride and lanthanum carbonate. Therefore, control of serum phosphate in CKD patients becomes crucial in preventing increases in calcium-phosphate product, secondary hyperparathyroidism and ultimately VC.
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PMID:Optimising the treatment of hyperphosphatemia and vascular calcification in chronic kidney disease. 1787 66

Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD) in Japan and other Westernized countries. Over 50% of the ESRD patients die from cardiovascular events. Cardiovascular disease (CVD) in ESRD patients with diabetes mellitus (DM) are implicated in the endothelial dysfunction caused by hyperglycemia, hyperlipidemia, and hypertension, and in the vascular calcification of intimal and medial arterial blood vessels caused by hyperphosphatemia. Therefore, dietary control of hyperglycemia and hyperphosphatemia should play an important role in the management of ESRD patients with DM. Furthermore, recent findings suggest that high concentrations of serum phosphate, even if within the normal range, may be a risk factor for CVD and mortality. An in vivo study using klotho knockout mice and fibroblast growth factor 23 (FGF-23) knockout mice has revealed that correction of hyperphosphatemia and hypervitaminosis D could ameliorate the premature aging-like phenotype. A low glycemic index and low phosphate diet may provide an advantage in the prevention of aging-related diseases in healthy individuals as well as in those with chronic kidney disease.
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PMID:Advantage of a low glycemic index and low phosphate diet on diabetic nephropathy and aging-related diseases. 1787 88

Childhood and adolescence are crucial times for the development of a healthy skeletal and cardiovascular system. Disordered mineral and bone metabolism accompany chronic kidney disease (CKD) and present significant obstacles to optimal bone strength, final adult height, and cardiovascular health. Decreased activity of renal 1 alpha hydroxylase results in decreased intestinal calcium absorption, increased serum parathyroid hormone levels, and high-turnover renal osteodystrophy, with subsequent growth failure. Simultaneously, phosphorus retention exacerbates secondary hyperparathyroidism, and elevated levels contribute to cardiovascular disease. Treatment of hyperphosphatemia and secondary hyperparathyroidism improves growth and high-turnover bone disease. However, target ranges for serum calcium, phosphorus, and parathyroid hormone (PTH) levels vary according to stage of CKD. Since over-treatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardiovascular calcifications, therapy must be carefully adjusted to maintain optimal serum biochemical parameters according to stage of CKD. Newer therapeutic agents, including calcium-free phosphate binding agents and new vitamin D analogues, effectively suppress serum PTH levels while limiting intestinal calcium absorption and may provide future therapeutic alternatives for children with CKD.
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PMID:Chronic kidney disease mineral and bone disorder in children. 1804 81

Mineral metabolism disorders are well-recognized complications in patients with chronic kidney disease (CKD). Furthermore, hyperphosphatemia and secondary hyperparathyroidism are associated with both renal osteodystrophy and cardiovascular disease. During the last 5 years, new therapeutic options have become available to treat these conditions in CKD. We describe the case of a 70-year-old lady with a dialysis history of 5 years and a number of cardiovascular risk factors (hypertension, hypercholesterolemia and obesity). Unfortunately, the patient was poorly compliant with any pharmaceutical treatment. After 2 years, a pharmacological approach with a low dosage of calcium salts and sevelamer HCl, subsequently changed to lanthanum carbonate, intravenous paricalcitol, and cinacalcet HCl reached the goals suggested by the current guidelines. Every nephrologist should look at the pathogenesis and treatment of hyperphosphatemia and secondary hyperparathyroidism. New options are now available and may help the clinician to obtain satisfactory short- and long-term outcomes in the treatment of this disease.
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PMID:[Therapeutic options for mineral metabolism disorders in dialysis patients: a case report]. 1835 May 4

Abnormalities of bone mineral parameters (calcium, phosphate, vitamin D, and parathyroid hormone) are nearly omnipresent in patients with advanced chronic kidney disease (CKD). These typically consist of hypocalcemia, hyperphosphatemia, abnormalities of vitamin D metabolism, and secondary hyperparathyroidism (SHPT). Currently, several lines of evidence suggest that these abnormalities may have consequences beyond the typical consequence of renal bone disease, with a major role in determining cardiovascular disease, including arterial calcification. The 'classical' treatment of SHPT and hyperphosphatemia in HD patients consists of phosphate binders, vitamin D receptor activators (VDRAs), and/or calcimimetics. Calcium- or aluminum-based phosphate binder prescriptions and calcitriol administration are therapeutic tools not free of complications, increasing the risk of cardiovascular calcification in the HD population. New calcium- and aluminum-free phosphate binders, such as lanthanum carbonate and sevelamer hydrochloride, new VDRA (paricalcitol), and cinacalcet hydrochloride can be used to treat SHPT, slow down the atherosclerotic process, and prevent vascular calcification in HD patients.
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PMID:Preventive measures and new pharmacological approaches of calcium and phosphate disorders. 1845 82

One of the most important problems faced by nephrologists is the high degree of cardiovascular mortality in patients on dialysis. This increase in cardiovascular disease has been associated with various factors, but, among them, hyperphosphatemia stands out particularly. The serum phosphate levels considered normal in these patients have gradually decreased in recent years. Therefore, phosphate control in the chronic kidney disease patient has become a challenge that has stimulated basic research in recent years. The aim of the following review is to bring together the most novel results presented in the last year, with emphasis on the methods for control of phosphate absorption, its elimination by the kidneys and vascular calcifications, which are one of the most serious direct consequences of hyperphosphatemia.
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PMID:[Experimental advances in mineral metabolism]. 1884 20

Extensive calcification of the arterial wall and soft tissues is a frequent feature of patients with end-stage chronic kidney disease (CKD stage 5). Hyperphosphatemia and secondary hyperparathyroidism have been extensively investigated as inducing factors in cardiovascular calcification. In fact, cardiovascular disease in renal failure is associated with bone metabolism alterations. Together with passive deposition of calcium-phosphate in extraskeletal tissues, it has recently been demonstrated that inorganic phosphate induces arterial calcification directly through a real "ossification" of the tunica media in the vasculature of CKD patients. Therefore, control of serum phosphate in CKD patients becomes crucial in preventing increases in calcium x phosphate product, secondary hyperparathyroidism, and ultimately vascular calcification.
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PMID:The mechanisms of hyperphosphatemia-induced vascular calcification. 1911 91

Cardiovascular disease is the primary cause of morbidity and mortality in chronic kidney disease (CKD). Nontraditional uremia-related risk factors as well as traditional risk factors may contribute to the unique features of cardiovascular disease in patients with CKD. Vascular calcification is a prominent feature of arterial disease in CKD and may have an impact on cardiovascular mortality through modulating both arteriosclerosis (arterial stiffening) and atherosclerosis. There are two pathophysiological processes involved in the development of vascular calcification: apoptosis and phenotypic transition to chondrocytes or osteoblasts (chodro/osteogenic differentiation). In CKD, abnormal mineral metabolism, predominantly hyperphosphatemia and hypercalcemia, facilitates progression of vascular calcification in association with functional disturbances of its inhibitory molecules (inhibitors of vascular calcification) such as pyrophosphate, matrix Gla protein, fetuin-A, and osteoprotegerin.
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PMID:Vascular calcification in chronic kidney disease: pathogenesis and clinical implications. 1912 77

Vascular calcification is recognized as a major contributor to cardiovascular disease (CVD) in end stage renal disease (ESRD) patients. Susceptibility to vascular calcification is genetically determined and actively regulated by diverse inducers and inhibitors. One of these inducers, hyperphosphatemia, promotes vascular calcification and is a nontraditional risk factor for CVD mortality in ESRD patients. Vascular smooth muscle cells (SMCs) respond to elevated phosphate levels by undergoing an osteochondrogenic phenotype change and mineralizing their extracellular matrix through a mechanism requiring sodium-dependent phosphate cotransporters. Disease states and cytokines can increase expression of sodium-dependent phosphate cotransporters in SMCs, thereby increasing susceptibility to calcification even at phosphate concentrations that are in the normal range.
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PMID:The emerging role of phosphate in vascular calcification. 1914 40

Hyperphosphatemia is associated with an increased risk of cardiovascular morbidity and mortality. However, in our large cross-sectional study, high serum phosphorus levels were associated with a more favorable profile of traditional cardiovascular risk factors, suggesting that hyperphosphatemia may independently contribute to the development and progression of cardiovascular disease.
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PMID:Relationship between serum phosphate and cardiovascular risk factors in a large cohort of adult outpatients. 1918 13


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