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

Chronic renal failure results in a variety of metabolic derangements that perturb glucose homeostasis. These may in part result from the fact that the kidney plays a prominent role in the metabolism of insulin as well as a number of other low-molecular-weight peptide hormones that affect carbohydrate metabolism. Specific abnormalities in glucose utilization that appear to be related to alterations in membrane receptors, resulting in increased glucagon sensitivity and decreased insulin action, are a newly recognized factor in intolerance to oral glucose. Glucose production and utilization are both abnormally increased in patients with chronic uremia, and these disturbances are only partially corrected by hemodialysis treatment. The mechanism(s) contributing to these changes is unclear, but seems to involve a combination of humoral and cellular factors. These include some degree of insulin resistance, probably inadequately modulated proteolytic responses to glucagon and parathyroid hormone, and a basic defect in energy production that alters intracellular concentrations of high-energy phosphate-containing nucleotides. It is unclear whether these changes in carbohydrate tolerance pose an increased risk for the premature development of cardiovascular disease in patients with renal failure, as they appear to do in the nonuremic population. The occasional patient with renal failure may develop clinical hypoglycemia when glucose utilization continues in a setting in which the hepatic capacity to produce glucose is reduced, probably as a consequence of altered substrate delivery and/or inhibition of one or more key gluconeogenic enzymes.
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PMID:Disorders of glucose metabolism in uremia. 11 52

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

Lipoadenoma is the accepted diagnosis of a single enlarged parathyroid gland that contains large quantities of mature fat cells and focal myxoid stroma, all widely separating small parenchymal cell nests in patients with hyperparathyroidism. Here we are reporting, for the first time, on five cases of hyperparathyroidism in which all four parathyroid glands are enlarged and each gland is noted to have an admixture of fat and parenchymal cells. We will introduce the descriptive diagnosis of lipohyperplasia to name this condition and keep it in perspective with other forms of parathyroid disease. All five patients were women between the ages of 36 and 62 years who underwent neck exploration, at which time four enlarged light-tan parathyroid glands were observed. Three and one half gland resections were performed, and all patients returned to a normocalcemic state except one who had borderline serum hypercalcemia after operation. Most of the resected parathyroid glands weighed in the range of 100 to 200 mg. The largest measured gland weighed 820 mg. Parathyroid histology showed an admixture of mature fat cells with parathyroid parenchymal cells often in a 1:1 ratio. One patient who had renal failure exhibited a lower ratio of fat cells. Two patients had chronic lymphocytic thyroiditis that was severe enough to require synthetic thyroid hormone therapy. Two patients had a history of urinary tract infections. Three patients had hypertensive cardiovascular disease, and several patients had arteriosclerotic cardiovascular disease. One patient had diabetes mellitus, one had a history of pituitary adenoma, and one had polydipsia. All of these patients were first seen with parathyroid glands measuring an average of five times normal size, yet they showed the usual 50% fat/50% parenchyma pattern of normal mature parathyroid glands. This means that the enlarged glands contain a 500% increase in parathyroid tissue, justifying the diagnostic term "lipohyperplasia." This easily represents enough parathyroid tissue to generate excessive parathyroid hormone production. At this time, there is no explanation of the pathogenesis of lipohyperplasia or how it varies from other previously described forms of parathyroid hyperplasia.
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PMID:Five cases of parathyroid lipohyperplasia. 664 2

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

The majority of hemodialysis patients die from cardiovascular disease. However, the contribution of myocardial infarction to mortality is relatively minor, despite the fact that coronary artery disease is common in uremic patients. Hypertension seems to be the major risk factor for the development of atherosclerosis in hemodialysis patients, although abnormalities of the lipid spectrum, characterized by an increase in triglycerides and very low density lipoprotein levels and a decrease in high-density lipoprotein levels, are frequent in hemodialysis patients. The existence of left ventricular (LV) hypertrophy is a serious risk factor for morbidity and mortality in hemodialysis patients. LV hypertrophy can present as a dilated cardiomyopathy or as concentric or asymmetric septal hypertrophy. Loss of myocardial contractility by coronary artery disease or carnitine deficiency can lead to systolic LV dysfunction with a compensatory dilated cardiomyopathy. Furthermore, the presence of a hypercirculation in uremic patients, resulting from anemia, the arteriovenous fistula, or fluid overload, can also lead to a dilated cardiomyopathy. Systolic LV dysfunction occurs when the increase in LV wall thickness is inadequate for the increase in LV radius, which might be caused by increased levels of parathyroid hormone. LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. Therefore, in uremic patients, anemia should be corrected and hypertension adequately treated early in the development of renal failure. Chronic fluid overload should be prevented by adequate estimation of optimal dry weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular aspects in renal disease. 792 20

A noninvasive method for the diagnosis of cardiac calcinosis, a life-threatening complication in hemodialysis patients with end-stage renal disease (ESRD), has not, as yet, been firmly established. We tested whether whole body scanning with 99m-technetium methylene diphosphonate (MDP) might visualize cardiac calcinosis. In 19 consecutive chronic hemodialysis ESRD patients (13 males and 6 females, aged 40-81, mean 63 +/- 8 years) with cardiovascular disease [mitral annular calcinosis and/or calcified aortic valve (n = 4), hemodialysis cardiomyopathy (n = 1), coronary artery disease (n = 9) and peripheral artery atherosclerotic disease (n = 6)], MDP uptake in the heart was compared to that in 7 non-ESRD controls with hyperparathyroidism due to adenoma. Cardiac and lung field MDP uptake was confirmed in only 3 (16%) and 5 (26%) of the 19 ESRD subjects, respectively, but was absent in controls. Positive cardiac uptake was related to cardiac calcified complications (mobile intracardiac calcinosis, myocardial calcinosis and mitral annular calcification) and the duration of hemodialysis (p = 0.015). While it was statistically insignificant, subjects showing MDP uptake were elder and had higher serum Ca or Ca x P product and lower intact parathyroid hormone levels. These results suggest that cardiac calcinosis in ESRD patients can be detected noninvasively by myocardial scintigraphy with 99m-technetium MDP.
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PMID:Detection of cardiac calcinosis in hemodialysis patients by whole-body scintigraphy with 99m-technetium methylene diphosphonate. 1097 Sep 80

The common carotid intima-media thickness (CC IMT) is a strong predictor for cardiovascular disease in patients with end-stage renal failure. However, little is known about possible associations between potential cardiovascular risk factors such as serum total homocysteine concentrations (tHcy) and the CC IMT. Thus, we investigated (a) the course of tHcy levels after renal transplantation (RTX) and (b) the relationship between CC IMT and tHcy in 53 renal allograft recipients with chronic renal failure before transplantation and 3, 6, and 12 months after transplantation. Exclusion criteria were volume overload, symptomatic coronary artery disease, symptomatic cerebrovascular disease, peripheral artery disease, heart failure, valvular heart disease, diabetes mellitus, severe hypercholesterolemia, and blood pressure above 159/89 mmHg at the time of the investigation. In all renal allograft recipients, a carotid high-resolution B-mode ultrasound measurement of the CC IMT was performed. Eighteen patients had normal ( < 20 micromol/L) pre-transplant (U0) tHcy, 25 had moderately elevated (20-40 micromol/L) pre-transplant (U0) tHcy, and 10 had severely elevated (> 40 micromol/L) pre-transplant (U0) tHcy. After 12 months of follow-up time (U12), no statistically significant differences concerning the tHcy levels could be detected between the groups (average serum tHcy 16.4 micromol/L +/- 1.1 micromol/L). The CC IMT did not differ significantly between the three tHcy groups at any time within the present follow-up. This was also true for the 'wall-to-lumen ratio'. A multiple forward stepwise regression analysis showed that the reduction of the CC IMT was positively correlated with gender (p < 0.01), glucose levels at U12 (p < 0.05; r2 = 0.96), systolic arterial blood pressure at U12 (p < 0.05; r2 = 0.97), and with the intact parathyroid hormone levels at U0 (p < 0.01; r2 = 0.98). In conclusion, (a) tHcy decreases significantly after RTX, but (b) does not influence the CC IMT thickness independently.
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PMID:Effect of homocysteine on carotid intima-media thickness after renal transplantation. 1112 8

Even though Mg is by far the least abundant serum electrolyte, it is extremely important for the metabolism of Ca, K, P, Zn, Cu, Fe, Na, Pb, Cd, HCl, acetylcholine, and nitric oxide (NO), for many enzymes, for the intracellular homeostasis and for activation of thiamine and therefore, for a very wide gamut of crucial body functions. Unfortunately, Mg absorption and elimination depend on a very large number of variables, at least one of which often goes awry, leading to a Mg deficiency that can present with many signs and symptoms. Mg absorption requires plenty of Mg in the diet, Se, parathyroid hormone (PTH) and vitamins B6 and D. Furthermore, it is hindered by excess fat. On the other hand, Mg levels are decreased by excess ethanol, salt, phosphoric acid (sodas) and coffee intake, by profuse sweating, by intense, prolonged stress, by excessive menstruation and vaginal flux, by diuretics and other drugs and by certain parasites (pinworms). The very small probability that all the variables affecting Mg levels will behave favorably, results in a high probability of a gradually intensifying Mg deficiency. It is highly regrettable that the deficiency of such an inexpensive, low-toxicity nutrient result in diseases that cause incalculable suffering and expense throughout the world. The range of pathologies associated with Mg deficiency is staggering: hypertension (cardiovascular disease, kidney and liver damage, etc.), peroxynitrite damage (migraine, multiple sclerosis, glaucoma, Alzheimer's disease, etc.), recurrent bacterial infection due to low levels of nitric oxide in the cavities (sinuses, vagina, middle ear, lungs, throat, etc.), fungal infections due to a depressed immune system, thiamine deactivation (low gastric acid, behavioral disorders, etc.), premenstrual syndrome, Ca deficiency (osteoporosis, hypertension, mood swings, etc.), tooth cavities, hearing loss, diabetes type II, cramps, muscle weakness, impotence (lack of NO), aggression (lack of NO), fibromas, K deficiency (arrhythmia, hypertension, some forms of cancer), Fe accumulation, etc. Finally, because there are so many variables involved in the Mg metabolism, evaluating the effect of Mg in many diseases has frustrated many researchers who have simply tried supplementation with Mg, without undertaking the task of ensuring its absorption and preventing excessive elimination, rendering the study of Mg deficiency much more difficult than for most other nutrients.
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PMID:The multifaceted and widespread pathology of magnesium deficiency. 1142 81

Elevated serum concentrations of 1-84 parathyroid hormone (PTH) after operation for sporadic parathyroid adenoma have been reported in previous studies, years after operation for primary hyperparathyroidism (pHPT). The cause and significance of this finding have not been elucidated. Primary hyperparathyroidism was diagnosed in 195 patients from January 1987 to December 1998. Operation for pHPT was performed in 124 patients. To evaluate long-term effects of elevated serum 1-84 PTH, biochemical variables and pre- and postoperative diseases were investigated from hospital case records. Of the 124 patients operated on, 103 had a solitary adenoma. Among these patients, 60 had normal serum concentrations of 1-84 PTH and calcium postoperatively, 38 patients had follow-up for more than 12 months (range 12-207 months-group A). Persistent elevated serum concentrations of 1-84 PTH and normocalcemia were found in 23 patients. Fourteen patients had follow-up for more than 12 months (range 15-76 months-group B). Two patients had persistent pHPT, and 18 were normocalcemic, but in this retrospective study data on serum 1-84 PTH were not available. No significant differences were found between groups A and B at the time of diagnosis concerning clinical characteristics. More that 12 months after operation for pHPT, the patients in group B, with persistent elevated serum concentrations of 1-84 PTH, had a significantly (c2 = 11, p = 0.005, and power of test 0.66) higher frequency of cardiovascular diseases from ischemic heart disease and hypertension. Persistent elevated serum concentrations of 1-84 PTH after operation for sporadic parathyroid adenoma may be associated with development of cardiovascular disease. This group of patients therefore needs lifelong control and, possibly, medical intervention.
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PMID:Normocalcemia and persistent elevated serum concentrations of 1-84 parathyroid hormone after operation for sporadic parathyroid adenoma: evidence of increased morbidity from cardiovascular disease. 1205 14


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