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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

End-stage renal disease (ESRD) patients have a high cardiovascular mortality rate. Precise estimates of the prevalence, risk factors and prognosis of different manifestations of cardiac disease are unavailable. In this study a prospective cohort of 433 ESRD patients was followed from the start of ESRD therapy for a mean of 41 months. Baseline clinical assessment and echocardiography were performed on all patients. The major outcome measure was death while on dialysis therapy. Clinical manifestations of cardiovascular disease were highly prevalent at the start of ESRD therapy: 14% had coronary artery disease, 19% angina pectoris, 31% cardiac failure, 7% dysrhythmia and 8% peripheral vascular disease. On echocardiography 15% had systolic dysfunction, 32% left ventricular dilatation and 74% left ventricular hypertrophy. The overall median survival time was 50 months. Age, diabetes mellitus, cardiac failure, peripheral vascular disease and systolic dysfunction independently predicted death in all time frames. Coronary artery disease was associated with a worse prognosis in patients with cardiac failure at baseline. High left ventricular cavity volume and mass index were independently associated with death after two years. The independent associations of the different echocardiographic abnormalities were: systolic dysfunction-older age and coronary artery disease; left ventricular dilatation-male gender, anemia, hypocalcemia and hyperphosphatemia; left ventricular hypertrophy-older age, female gender, wide arterial pulse pressure, low blood urea and hypoalbuminemia. We conclude that clinical and echocardiographic cardiovascular disease are already present in a very high proportion of patients starting ESRD therapy and are independent mortality factors.
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PMID:Clinical and echocardiographic disease in patients starting end-stage renal disease therapy. 773 Nov 45

Hyperparathyroidism (HPT) is common in patients on dialysis, and parathyroidectomy (PTx) is often required. We present a retrospective, descriptive analysis of data corresponding to 148 patients on dialysis undergoing PTx due to severe refractory HPT (PTH 1401 +/- 497 pg/mL, Ca 10.6 +/- 0.8 mg/dL, P 6.9 +/- 1.7 mg/dL). Demographic data were compared with those recorded in 309 patients on dialysis not subjected to PTx who were managed at the same hospital. In the PTx group, the factors age (49.3 +/- 14 years), male gender (48.6%), and diabetes (0.7%) were significantly lower than in the non-PTx group (61.5 +/- 14.9 years, male gender 59%, diabetes 19.4%), while time on dialysis was longer (8.6 +/- 5.8 vs. 5.5 +/- 5.4 years). In 129 of the study patients (87.4%), four or more glands were identified, and total PTx plus autotransplantation (AT) in the forearm was performed. In the remaining 19 patients, two to three glands were identified, and AT was not undertaken. Four of the 19 patients were successfully operated on again for persistent HPT, seven showed PTH levels <250 pg/mL, and eight maintained severe HPT. Perioperative complications included one death due to cardiac insufficiency, two repeat operations due to bleeding, and one patient with chronic hoarseness. Hospital stay was prolonged in 20% of patients due to a hungry bone syndrome. Among those patients with PTx and AT, HPT recurred in 21 patients (16.2%) at 3.1 +/- 2.3 years. In 13 of these patients, autograft was removed at 7.5 +/- 2.9 years. Serum calcium and phosphate levels improved after PTx, and these results were maintained for 5 years (9.6 +/- 0.8 and 4.2 +/- 1.2 mg/dL, respectively). In conclusion, PTx with AT is a safe option for the treatment of severe HPT that is accompanied by low morbidity and mortality and a good outcome. Medical treatment should not be prolonged at the expense of long repeated bouts of hypercalcemia and/or hyperphosphatemia with their irreversible consequences.
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PMID:Parathyroidectomy: whom and when? 1275 76

Severity of heart disease of almost all types, as well as mortality risk associated with heart disease, increases in step with severity of kidney disease, although not necessarily in a linear fashion. Heart failure is more common and just as lethal as ischemic heart disease in patients with severe chronic kidney disease (CKD). The incidence of nonfatal heart disease in dialysis and transplant populations has now been described in detail. Although standard risk factors for heart disease that are more common among patients with CKD than in the general population do not adequately explain the greatly increased risk of heart disease in patients with severe CKD, neither do as yet identified "nontraditional" risk factors. However, in addition to the factors not common in the general population, such as anemia, hyperphosphatemia, and markers of systemic inflammation, patients with CKD in the modern era may also exhibit excessive thrombotic tendencies. Screening for heart disease in this population relies mainly on dobutamine stress echocardiography or nuclear scintigraphy. The role of electron beam CT (EBCT) scanning is currently controversial. The indications for coronary angiography are the same for patients with CKD as for the general population, but patients with CKD are at greatly increased risk for contrast-associated nephropathy, the least controversial preventive therapy, which consists of isotonic saline and N-acetylcysteine. Finally, patients with CKD do not currently receive adequate medical therapy for prevention and treatment of heart disease.
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PMID:Cardiovascular risk in stage 4 and 5 nephropathy. 1521 84

Major causes of death in dialysis patients are heart failure, infection, cerebro-vascular accident, malignancy, myocardial infarction, and cardiovascular disturbance; they are 43.7% of all causes of death. Hyperphosphatemia and increased calcium-phosphorus product aggravate ectopic calcification, and raise mortality rate. According to statistical data from the Japanese Society for Dialysis Therapy, calcium and phosphate levels recently decreased, because of progress of therapeutic agents and increase in aged people. But extreme decreases of them are also the risk factors of mortality, so appropriate control into the recommended range is necessary.
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PMID:[Cause of death in dialysis patient--according to the survey of the Japanese Society for Dialysis Therapy]. 1557 59

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

The duration and frequency of hemodialysis was determined empirically when this therapy first came into use, and treatment was commonly three 8 h sessions per week by the end of the 1960s. Subsequently, however, the growing number of patients who required this therapy had to be reconciled with the shortage of equipment; therefore, dialysis time was decreased to three 4 h sessions per week. At the same time, on the basis of data from the first randomized controlled trial of dialysis -- the National Cooperative Dialysis Study -- Kt/V(urea) was devised as the optimum measure of dialysis adequacy. Nowadays, although Kt/V(urea) targets are fulfilled in an increasing number of patients, observational studies show that individuals on hemodialysis continue to experience a high rate of complications, including hypertension, left ventricular hypertrophy, cardiac failure, hyperphosphatemia, malnutrition and death. Although no randomized controlled trial has yet been published, observational data indicate that increasing hemodialysis time and/or frequency improves a number of these complications, especially the death rate. This Review outlines the advantages of longer and/or more frequent dialysis sessions and highlights the barriers to adoption of such regimens, which largely relate to economics, patient willingness, and organization of dialysis units.
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PMID:The advantages and challenges of increasing the duration and frequency of maintenance dialysis sessions. 1903 1

Cardiovascular disease is a frequent complication of renal failure and is the most common cause of death in patients with chronic kidney disease (CKD). Accelerated atherogenesis has been widely documented in CKD and diabetic nephropathy is the leading cause of renal failure worldwide. Furthermore, CKD promotes hypertension and dyslipidemia, which in turn may contribute to the progression of renal failure. All together, hypertension, dyslipidemia and diabetes are considered major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Elevated inflammatory mediators and activation of the renin-angiotensin system contribute through enhanced production of reactive oxygen species, to atherogenesis in CKD. Vascular calcification is also important. Calcification of arteries occurs in the intima in association with atherosclerosis, where it may contribute to plaque formation, and in the media, where it causes stiffening. Increased serum levels of calcification promoters, such as hyperphosphatemia, and a decrease in circulating and local inhibitors of calcification, favor vascular calcification. On the other hand, transdifferentiation of vascular smooth muscle cells to osteblast-like cells would be the pivotal event in calcification. Bone morphogenetic protein agonists and antagonists are playing a role in this osteogenic differentiation. Accelerated atherosclerosis and media calcification will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with CKD.
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PMID:[Vascular damage in chronic kidney disease]. 1930 81

Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with chronic kidney disease (CKD) and end-stage renal disease. LVH in CKD patients has generally a negative prognostic value, because it represents an independent risk factor for the development of arrhythmias, sudden death, heart failure and ischemic heart disease. LVH in CKD patients is secondary to both pressure and volume overload. Pressure overload is secondary to preexisting hypertension, but also to a loss of elasticity of the vessels and to vascular calcifications, leading to augmented pulse pressure. Anemia and the retention of sodium and water secondary to decreased renal function are responsible for volume overload, determining a hyperdynamic state. In particular, the correction of anemia with erythropoietin in CKD patients is advantageous, since it determines LVH reduction. Other risk factors for LVH in CKD patients are documented: some are specific to CKD, as mineral metabolism disorders (hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary hyperparathyroidism), others are non-traditional, such as increased asymmetric dimethylarginine, oxidative stress, hyperhomocysteinemia and endothelial dysfunction that, in turn, accelerates the process of atherogenesis, triggers the inflammation and pro-thrombotic state of the glomerular and the vascular endothelium and aggravates the process of both CKD and LVH.
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PMID:Hypertension, left ventricular hypertrophy and chronic kidney disease. 2111 11

Serum phosphorus abnormalities may pose a risk on the cardiovascular system. In heart failure (HF) phosphorus homeostatic mechanisms are altered and may be modified by modern HF therapy. The impact of therapy optimization on phosphorus abnormalities and related outcome remains unknown. In 722 patients with HF subjected to treatment up-titration we analyzed the prevalence of serum phosphorus abnormalities and their relation to HF severity on top of optimal treatment, and we assessed adjusted risk of phosphorus abnormalities at different stages of HF. We analyzed predictors of hypo- and hyperphosphatemia and relation to prognosis. Hypophosphatemia was associated with better response to therapy, was more prevalent in milder HF, and the association was independent of age, sex, BMI, etiology of HF, kidney function and the use of diuretics. Hypophosphatemic patients lost more phosphorus into urine. They had also less catabolic profile. Patients with hyperphosphatemia on top of optimal therapy responded worse to treatment. Hyperphosphatemia was more prevalent in advanced HF, but the effect was attenuated after adjustment for potential confounders. Clinical and biochemical profiles of hyperphosphatemics suggested domination of catabolism. Neither hypophosphatemia nor hyperphosphatemia modifies the outcome Serum phosphorus abnormalities are related to HF severity on top of optimal therapy. Hypophosphatemia occurring on HF up-titration therapy likely has a multifactorial pathophysiology comprising of urinary phosphorus wasting and refeeding effects. Hyperphosphatemia is linked to the catabolic profile but the effect of renal impairment can't be ruled out. The prognostic impact of serum phosphorus abnormalities remain to be established.
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PMID:Serum phosphorus level is related to degree of clinical response to up-titration of heart failure pharmacotherapy. 2549 88

Recent studies of myocardial infarction in secreted Frizzled-related protein 2 (sFRP2) knockout mice and our hamster heart failure therapy based on sFRP2 blockade have established sFRP2 as a key profibrotic cytokine in the heart. The failing hamster heart is marked by prominent fibrosis and calcification with elevated expression of sFRP2. Noting the involvement of tissue-nonspecific alkaline phosphatase (TNAP) in bone mineralization and vascular calcification, we determined whether sFRP2 might be an upstream regulator of TNAP. Biochemical assays revealed an approximately twofold increase in the activity of TNAP and elevated levels of inorganic phosphate (Pi) in the failing heart compared with the normal heart. Neither was this change detected in the liver or hamstring muscle nor was it associated with systemic hyperphosphatemia. TNAP was readily cloned from the hamster heart and upon overexpression increased the level of extracellular but not intracellular Pi, which is consistent with the cell surface location of the ectoenzyme. In line with the previous demonstration that sFRP2 blockade attenuated fibrosis, we show here that the therapy downregulated TNAP. This in vivo finding is corroborated by the in vitro study showing that cultured cardiac fibroblasts treated with recombinant sFRP2 protein exhibited progressive increase in the expression and activity of TNAP, which was completely abrogated by cycloheximide or tunicamycin. Induction of TNAP by sFRP2 is restricted to cardiac fibroblasts among the multiple cell types examined, and was not observed with sFRP4. The current work indicates that sFRP2 may promote cardiac fibrocalcification through coordinate activation of tolloid-like metalloproteinases and TNAP.
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PMID:Tissue-nonspecific alkaline phosphatase as a target of sFRP2 in cardiac fibroblasts. 2610 66


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