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

Vascular calcification and cardiovascular disease mortality are highly correlated with increased serum phosphate levels in end-stage renal disease patients. Mechanistic studies in cultured human smooth muscle cells (SMCs) indicate that increased phosphate levels induces both calcification and phenotypic transition through a pathway requiring a sodium-dependent phosphate cotransporter. Thus, in addition to contributing to increased calcium x phosphate product (Ca x P), hyperphosphatemia may have direct effects on SMCs that predispose these cells to calcium deposition in end-stage renal disease patients.
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PMID:Mechanisms of vascular calcification in uremia. 1549 Mar 98

Cardiovascular disease is the largest cause of mortality in hemodialysis patients. Cardiovascular mortality is fivefold to twentyfold higher in hemodialysis patients than in the general population. Atherosclerosis and vascular calcification are the characteristic complications in hemodialysis patients. Hemodialysis patients have traditional risk factors such as abnormal lipid metabolism and uremia-related risk factors such as oxidative stress and hyperphosphatemia. Oxidative stress takes place by increased production of oxidants by leukocytes and antioxidant loss of vitamin C and E. Oxidatively modified LDL exist in the circulation by excess of oxidative stress in hemodialysis patients. Oxidative stress is a major contributor to accelerated development atherosclerosis. Oxidative stress and hyperphosphatemia also influence vascular calcification. The pattern of vascular calcification in hemodialysis patient is characterized by mineral deposition in the tunica media. It is reported that the obvious calcification in aorta and artery of the MGP knockout mouse is recognized. It is indicated that MGP has the inhibitory effect of the calcification of vessel wall. Vitamin E protects atherosclerosis and vascular calcification in hemodialysis patients. It is also important to control hyperphosphatemia for vascular calcification.
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PMID:[Atherosclerosis and vascular calcification in hemodialysis patients]. 1557 60

Hyperphosphatemia and an increased serum calcium-phosphate (CaxP) product are associated with cardiovascular mortality in adult dialysis patients. Target levels for the treatment of elevations in serum phosphorus (P) and the CaxP product have recently been redefined, but are difficult to achieve in clinical practice. This problem may be especially prevalent in children and adolescents who have a higher recommended P intake than adults and also a higher calcium (Ca) load with the intake of comparatively higher doses of Ca-containing phosphate binders. Current treatment practice with Ca-containing P binders carries the risk of hypercalcemic episodes and ectopic calcifications, including vascular calcifications, which are associated with an increased risk of cardiovascular disease. Novel P binders in the development phase include several iron-containing preparations. Clinical experience with lanthanum carbonate is limited to date and further studies are needed to establish its safety. The only available Ca-free P binder with widespread use and large-scale clinical safety data in adults is sevelamer. Preliminary data suggest that this drug can also be safely given to children.
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PMID:The therapeutic potential of novel phosphate binders. 1565 Aug 84

Dialysis, in its routine 3 x week manifestation, undoubtedly is life saving. The therapy is limited by a number of factors that persist despite the development of safe machines and highly efficient dialyzers. The turnover of known, and very likely, many unknown uremic toxins, is rapid so that 3 x week dialysis is accompanied by relatively high levels of these substances. Only the lower part of the range of molecular weights of those putative uremic toxins, which are small proteins, are removed by current therapies. For substances such as phosphorus, long dialysis is successful in removing the excess retained dietary phosphorus, perhaps the only proven uremic toxin. The difficulty of achieving a normal extracellular volume is probably a major factor in the progression and poor outcomes of cardiovascular disease despite the potential improvement with management of hyperlipidemia, inflammation, potential arrhythmias, and cardiac failure due to other pathogenetic mechanisms. New developments in understanding of Vitamin D metabolism, Ca receptor inhibitor drugs, and control of hyperphosphatemia may reduce the problems of kidney bone disease and the adverse cardiovascular effect of calcium phosphorus disposition. Dialysis more frequent than 3 x week is already routinely, if only infrequently, used to deal with the very large volume or overhydrated patient. However, daily dialysis--whether short or long-is now beginning as a therapy with a large randomized NIH trial in the offing. Currently, the net growth of dialysis is approximately 4% a year, but it would not be surprising if there were a gradual increase in growth rates as CKD patients live longer due to control of cardiac disease. Eventually, the treatment of early kidney disease should reduce the dialysis population, particularly if diabetes can be better controlled or even prevented. The dialysis aspect of nephrology as a profession for physicians, nurses, and technicians appears to be on a long course with increasing demand and the need for applying what is already known, while awaiting new technical developments. Wearable artificial kidneys, involving the application of technology and use of new materials, are currently being investigated. The presence of nephrologists during the actual dialysis treatment is certainly not as evident as it was in the past. Reimbursement methodology has ensured at least a minimum of documented visits by nephrologists or nurse practitioners to the dialysis patient during treatment. It is controversial as to the value of this, but evidence has been presented that certain outcomes, such as use of appropriate dialysis dose and blood chemistries, are improved by more frequent visits. The present is over.
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PMID:Technology: kidneys--the present of dialysis. 1567 76

Cardiovascular disease is the first cause of morbidity and mortality in dialysis patients. Hyperphosphatemia and elevated serum calcium-phosphate levels have recently been investigated as inducing factors on extraskeletal calcification in this population. In vitro studies demonstrated that human aortic smooth muscle cells calcify when incubated in a high phosphate medium, where calcium and calcitriol are not changed. Furthermore, the lack of inhibitory proteins, such as fetuin and matrix Gla protein, is a possible main determinant of calcium-phosphate deposition in soft tissues. The classical treatment of hyperphosphatemia and secondary hyperparathyroidism in dialysis patients consists of calcium-based phosphate binders and calcitriol administration. Unfortunately, this "first-generation" therapy is not free of dramatic side effects. New free-calcium and -aluminum phosphate binders, new vitamin D metabolites, and calcimimetics are examples of "second-generation" therapies that may prevent vascular calcification and possibly prevent some of the burden of cardiovascular disease in uremia.
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PMID:[Cardiovascular calcification and accelerated atherosclerosis in chronic kidney disease]. 1577 28

Vascular calcifications are more frequent in dialysis patients than in the general population or in patients with cardiovascular disease (CVD) and normal renal function. The reasons for this high incidence are multiple; they include traditional factors such as hypertension, diabetes, dyslipidemia, and specific factors such as sodium overload, hyperomocysteinemia, chronic inflammation and oxidative stress, as well as mineral metabolism disturbances. Specifically, hyperphosphatemia and the elevated calcium (Ca) x phosphate product have been associated with an increased risk for the development of vascular calcification and death. Treatment with Ca salts can induce hypercalcemia, increased Ca x phosphate product and Ca overload. Sevelamer substitution for Ca salts has been documented to attenuate the progression of coronary artery and aortic calcification. A possible mechanism explaining this observation could be ongoing Ca loading related to oral Ca ingestion. Treatment with Ca salts could induce Ca overload, particularly in patients dialyzed against a high dialysate Ca (>1.5 mmol/L) solution, which is known to determine a positive dialysis balance. Conversely, an overall negative Ca balance can result from low Ca dialysate use (1.25 mmol/L) when the patients do not receive Ca supplements or vitamin D metabolites. Maintaining normal Ca and phosphate balances remains a primary goal in the management of dialysis patients. Control of hyperphopshataemia should be achieved either using Ca and aluminum-free phosphate binders, such as sevelamer, or Ca salts, alone or in combination, provided that a daily oral elemental Ca intake of 1.5 g is not exceeded.
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PMID:[Control of calcium and phosphate metabolism and prevention of vascular calcifications in uremic patients]. 1578 2

Vascular calcification is prevalent in aging as well as a number of pathological conditions, and it is now recognized as a strong predictor of cardiovascular events in the general population as well as diabetic and end-stage renal disease patients. Vascular calcification is a highly regulated process involving inductive and inhibitory mechanisms. This article focuses on two molecules, phosphate and osteopontin, that have been implicated in the induction or inhibition of vascular calcification, respectively. Elevated phosphate is of interest because hyperphosphatemia is recognized as a major nonconventional risk factor for cardiovascular disease mortality in end-stage renal disease patients. Studies to date suggest that elevated phosphate stimulates smooth muscle cell phenotypic transition and mineralization via the activity of a sodium-dependent phosphate cotransporter. Osteopontin, however, appears to block vascular calcification most likely by preventing calcium phosphate crystal growth and inducing cellular mineral resorption.
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PMID:Regulation of vascular calcification: roles of phosphate and osteopontin. 1583 23

The role of vitamin D in left ventricular hypertrophy and cardiac function. Cardiovascular disease is the leading cause of death among patients with end-stage renal disease (ESRD). Traditional cardiac risk factors, as well as other factors specific to the ESRD population such as hyperphosphatemia, elevated calcium and phosphate product, abnormal lipid metabolism, hyperhomocysteinemia, and chronic inflammation play a role in the excessive risk of cardiovascular death in this population. Left ventricular disorders are proven risk factors for cardiac mortality in hemodialysis patients. These disorders are present in incident ESRD patients at rates far above the general population. There is an accumulating body of evidence that suggests that vitamin D plays a role in cardiovascular disease. Abnormal vitamin metabolism, through deficiency of the active form of 1,25-dihydroxyvitamin D(3), and acquired vitamin D resistance through the uremic state, have been shown to be important in ESRD. Vitamin D deficiency has long been known to affect cardiac contractility, vascular tone, cardiac collagen content, and cardiac tissue maturation. Recent studies using vitamin D receptor deficient mice as a model demonstrate a crucial role of vitamin D in regulation of the renin-angiotensin system. Additionally, there is emerging evidence linking treatment with vitamin D to improved survival on hemodialysis and improvement in cardiac function. The emergence of this data is focusing attention on the previously underappreciated nonmineral homeostatic effects of vitamin D that very likely play an important role in the pathogenesis of cardiac disease in ESRD.
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PMID:The role of vitamin D in left ventricular hypertrophy and cardiac function. 1588 12

As renal function declines in patients with end-stage renal disease (ESRD), excess dietary phosphorus accumulates in the bloodstream. Routine dialysis removes up to 70% of absorbed phosphorus; therefore, hyperphosphatemia is found in the majority of patients with ESRD. The consequences of this imbalance include secondary hyperparathyroidism and osteodystrophy. Recent studies have also documented that hyperphosphatemia can lead to soft-tissue and vascular calcification; the latter is strongly associated with cardiovascular disease and, thus, increased mortality and morbidity. The reduction of phosphorus levels is, therefore, an important therapeutic target in this patient group. Management of hyperphosphatemia using conventional phosphate binders is not always successful. However, emerging therapies aim to reduce the incidence of hyperparathyroidism, bone disease, and calcification in this patient population. In this article, the consequences of hyperphosphatemia are reviewed, and recent developments in the treatment of the condition are discussed.
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PMID:The clinical management of hyperphosphatemia. 1601 7

Pathogenesis of vascular calcification in chronic kidney disease. Background. Hyperphosphatemia and hypercalcemia are independent risk factors for higher incidence of cardiovascular events in patients with chronic kidney disease. In addition to increased calcium-phosphate product, hyperphosphatemia accelerates the progression of secondary hyperparathyroidism with the concomitant bone loss, possibly linked to vascular calcium-phosphate precipitation. Results. The control of serum phosphate levels reduces vascular calcification not only by decreasing the degree of secondary hyperparathyroidism and calcium-phosphate product, but also by reducing the expression of proteins responsible for active bone mineral deposition in cells of the vasculature. The calcium and aluminum-free phosphate-binders provide a new and effective therapeutic tool in preventing vascular calcifications in chronic kidney disease in animal models and in hemodialysis patients. Conclusion. Additional investigations are necessary to examine the benefits of different phosphate-binders in reducing mortality from cardiovascular disease.
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PMID:Pathogenesis of vascular calcification in chronic kidney disease. 1637 46


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