Extraskeletal calcification in patients with chronic kidney failure.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S G Rostand.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Parathyroid hormone and vitamin D have been shown to influence cardiac and vascular growth and function experimentally in human subjects with normal renal function. Because of the increased prevalence of hyperparathyroidism and altered vitamin D status in chronic renal failure, these alterations have been considered to contribute to the increased prevalence of cardiovascular disease and hypertension seen in this patient population. Methods and Results. In this article, we review experimental and clinical literature on the cardiovascular effects of parathyroid hormone and vitamin D and relate them to the development of cardiac and vascular dysfunction in uremia, such as: cardiomyopathy, myocardial hypertrophy, and fibrosis, as well as to myocardial ischemia; uremic glucose intolerance, dyslipidemia, and atherosclerosis; hypertension; and vascular and cardiac calcifications. CONCLUSIONS: The hyperparathyroid state and altered vitamin D status found in uremia contribute to the cardiovascular pathology seen clinically in uremia and also to the excess mortality from cardiovascular causes found in this patient group. The therapeutic implications of these observations are also discussed.
Explore the source record for details and available documents.
Mean systolic and diastolic pressures and the prevalence of hypertension vary throughout the world. Published data suggest a linear rise in blood pressure at increasing distances from the equator. Similarly, blood pressure is higher in winter than summer. Blood pressure also is affected by variations in skin pigmentation. Altered calcium, vitamin D, and parathyroid hormone status is associated with hypertension and may vary with latitude and season. Since changes in UV light affect vitamin D and parathyroid hormone status and UV light intensity are influenced by seasonal change and latitude, these disparate observations suggest an association between blood pressure and ultraviolet light. This discussion presents the hypothesis that reduced epidermal vitamin D3 photosynthesis associated with high skin melanin content and/or decreased UV light intensity at distances from the equator, alone or when coupled with decreased dietary calcium and vitamin D, may be associated with reduced vitamin D stores and increased parathyroid hormone secretion. These changes may stimulate growth of vascular smooth muscle and enhance its contractility by affecting intracellular calcium, adrenergic responsiveness, and/or endothelial function. Thus, UV light intensity and efficiency of epidermal vitamin D3 photosynthesis may contribute to geographic and racial variability in blood pressure and the prevalence of hypertension.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We analyzed the records of all residents of Jefferson County, Alabama, accepted for renal replacement therapy between 1982 and 1987 and compared them with those accepted between 1974 and 1978 to determine any changes in the distribution and frequency of end-stage renal disease (ESRD) due to hypertension (H-ESRD). H-ESRD increased from 6.4 to 9.6 per 100,000 in blacks and from 0.36 to 0.62 per 100,000 in whites. Smoothed age- and race-specific yearly H-ESRD rates decreased in blacks under age 50. Peak incidence of H-ESRD shifted from age 40 to 49 in 1974 through 1978 to age 50 to 59 in 1982 through 1987 (P less than 0.0001). Blacks were referred for care with significantly higher blood pressure levels and serum creatinine concentrations than whites, and had more severe retinal vascular disease. Factors significantly associated with a shorter time from referral to renal replacement therapy were black race, female gender, blood urea nitrogen and serum creatinine concentrations, carbohydrate intolerance, and the use of alpha-agonist and/or angiotensin-converting enzyme (ACE) inhibitor. We conclude that racial distribution and risk for H-ESRD have not changed. Peak rates of H-ESRD have been delayed nearly a decade, suggesting a possible effect of better awareness and treatment of hypertension.
Cardiovascular diseases are a leading cause of death in end-stage renal disease (ESRD) largely as a result of the progressively increasing age of ESRD patients and the broad constellation of uremia-associated factors that can adversely affect cardiac function. Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. In addition to impairing the coronary microcirculation, hypertension may contribute to the development of atherosclerotic coronary artery disease, particularly in the presence of the many lipid abnormalities observed in ESRD. These patients have reduced high-density lipoprotein cholesterol and increased plasma triglyceride concentrations, and there is a defect in cholesterol transport. Other abnormalities that may contribute to atherosclerotic coronary artery disease in ESRD are reduced high-density lipoprotein cholesterol synthesis and reduced activity of the reverse cholesterol pathway. Treatment with fibric acids, nicotinic acids, and lovastatin may be useful in lowering cholesterol and triglyceride concentrations in some of these patients. The incidence of coronary artery disease in ESRD populations is difficult to determine. About 25 to 30% of ESRD patients with angina have no evidence of significant coronary artery disease, and an undetermined number have silent coronary disease. The presence of resting electrocardiographic abnormalities caused by hypertension or conduction defects makes it difficult to accurately diagnosis coronary artery disease in ESRD populations by noninvasive methods, including exercise testing and thallium scintigraphy with or without the use of dipyridamole. Hypotension is a frequent complication of the dialytic process. Many factors have been implicated, including autonomic neuropathy. There is no consensus on the function of the efferent limb of the sympathetic nervous system. The afferent limb (arterial baroreflex function) is felt to be impaired. Further, there may be defects in the ability of the cardiovascular system to respond to sympathetic nerve activity. Most studies of autonomic function have used indirect measurements. Studies are underway that use techniques to assess sympathetic function directly. Such experiments with microneuropathy suggest greater skeletal sympathetic muscle discharge in uremic patients than in normal patients.
Our approach to the clinical management of uremic and dialysis-associated pericarditis has been presented previously and is outlined in Figure 1. In hemodynamically stable patients with no effusion and in those with small to medium effusions, we recommend initial therapy with intensified dialysis. Close monitoring, perhaps every third day, with echocardiography should be carried out. If pericardial effusion progressively increases or if a large pericardial effusion fails to resolve after 7 to 10 days of intensive dialysis, the pericardial effusion may be drained by subxiphoid pericardiotomy or by pericardiectomy. Similarly, if hemodynamic evidence of cardiac pretamponade or tamponade appears, surgical drainage also should be carried out. If the echocardiogram is inadequate for interpretation but tamponade physiology is present, we recommend confirmation by cardiac catheterization before surgical drainage is attempted, recognizing that there may be circumstances such as left ventricular failure and pulmonary hypertension that may complicate the interpretation of the catheterization data. The type of invasive pericardial procedure chosen is determined by local experience. As stated, we prefer not to perform pericardiocentesis before surgery unless tamponade-induced hypotension is so severe that an adequate blood pressure cannot be maintained by means of plasma volume expansion. Under these circumstances, we prefer that pericardiocentesis be performed in the operating room immediately before the induction of anesthesia for the definitive surgical procedure. Although pericardiectomy is a definitive procedure for pericarditis with effusion in the uremic patient, the procedure has substantial morbidity. The results of subxiphoid pericardiotomy are encouraging, and it is clear that it can be carried out safely in patients who are debilitated or who are at increased risk from general anesthesia and major surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
We analyzed the clinical courses of 94 patients with treated primary hypertension and initially normal serum creatinine concentrations (less than or equal to 133 mumol per liter [less than or equal to 1.5 mg per deciliter]) who were followed for a mean (+/- SD) of 58 +/- 34 months (range, 12 to 174) to determine the frequency with which renal function deteriorated and the factors associated with deterioration. Fourteen patients (15 percent) had an increase in serum creatinine concentrations (greater than or equal to 35 mumol per liter [greater than or equal to 0.4 mg per deciliter]); in 16 percent of the 61 patients with apparently good control of blood pressure, the serum creatinine concentration rose 59 +/- 33 mumol per liter (0.67 +/- 0.38 mg per deciliter). Despite good control of diastolic blood pressure (less than or equal to 90 mm Hg), black patients were twice as likely as white patients to have elevations in serum creatinine (23 percent vs. 11 percent). Stepwise discriminant function analysis showed that a significant rise in the serum creatinine concentration was most likely to occur in association with older age, black race, a higher number of missed office visits, and employment as a laborer. We conclude that although renal function was preserved in 85 percent of patients with treated hypertension, it may deteriorate in some patients despite good blood-pressure control. Our observations may partly explain why hypertension, particularly among black persons, remains a leading cause of renal disease in the United States.
PURPOSE: Myocardial calcium content may have clinical importance in end-stage renal disease (ESRD), but it is difficult to detect during life. Our goal was to assess the effect of myocardial calcium content on left ventricular ejection fraction (LVEF) in uremic patients undergoing dialysis. PATIENTS AND METHODS: Energy subtraction radiography of the chest was used to measure myocardial calcium content in 43 patients undergoing dialysis, in 32 control subjects, and in nine patients with advanced cardiomyopathy. LVEF and left ventricular end-diastolic dimension were measured by two-dimensional echocardiography. The concentration of parathyroid hormone was measured by radioimmunoassay; calcium-phosphorus product, alkaline phosphatase, and serum bicarbonate were also assessed. RESULTS: Patients undergoing dialysis had a greater myocardial calcium content than control subjects [262 +/- 15.4 (mean +/- SE) versus 187 +/- 8 mg/cm2, p less than 0.05]. Ten patients with the highest myocardial calcium content (Group I) had the lowest LVEF values and highest left ventricular end-diastolic dimension. Significant inverse linear associations between LVEF and myocardial calcium content (r = -0.425, p = 0.013) and between parathyroid hormone concentration and LVEF (r = -0.352, p = 0.047) were noted. There was no association between parathyroid hormone concentration and myocardial calcium content. Stepwise regression analysis showed a strong positive correlation between myocardial calcium content and calcium-phosphorus product, vascular calcification, race (black), and parathyroidectomy. Similar analysis shows that LVEF was significantly associated with myocardial calcium content, lung calcium, calcium-phosphorus product, and race (black). CONCLUSION: We suggest that increased myocardial calcium content results from poor calcium and phosphorus control and may be enhanced by parathyroid hormone hyperactivity. Increased myocardial calcium content is strongly associated with myocardial dysfunction in patients undergoing dialysis.
We examined the results of coronary artery bypass grafting (CABG) in patients with end-stage renal disease and symptomatic ischemic heart disease who had significant arteriosclerotic narrowing of one or more coronary vessels between 1970 and 1984. Twenty-four such patients underwent bypass grafting, 20 dialysis patients and four who had been transplanted. Bypass grafting completely or partially relieved symptoms in 83%. The hospital mortality associated with this surgery for the 20 dialysis patients was 20% compared with a lower overall hospital mortality for bypass grafting in nondialysis patients of 1.3%. Greater hospital mortality was noted for patients over age 60 undergoing bypass grafting, 33.3% v 1.9% in nondialysis patients. In this study, the most significant factor associated with mortality was older age. We conclude that bypass grafting has an acceptable mortality in younger end-stage renal disease patients anticipating or having had renal transplantation, but it is associated with a high hospital mortality in older dialysis patients.
Hypertension occurs more frequently in U.S. blacks than whites and is more severe. Blacks represent a disproportionate percentage of patients receiving dialysis treatment. This disproportion raises the question of whether the renal circulation of blacks is more sensitive to the damaging effects of elevated intraarterial pressure or whether it is structurally different in ways that would render it more prone to damage. The first part of the question has not been conclusively answered although some data support the hypothesis. For the second part, it is clear that malignant nephrosclerosis of blacks is different from that of whites in an absence of fibrinoid necrosis of arterioles and glomeruli and the presence of musculomucoid intimal hyperplasia of small arteries. Whether this is a genetically determined reaction to damage has not been determined. It is a widely held belief that the kidney is the cause of much essential hypertension. In fact 6 cases of essential hypertension in blacks have been "cured" by renal transplantation, strongly supporting the belief. Also blacks differ from whites in 2 ways that could be relevant for their increased prevalence of hypertension: they excrete sodium loads more slowly and have a markedly lower urinary kallikrein. The former could be responsible for the predominance of salt-dependent hypertension in blacks and the latter could reflect a racial deficiency in a naturally occurring vasodilator system.
Pericarditis occurred 161 times in 136 of 1,058 patients undergoing chronic dialysis during a period of 13.7 years. Cardiac tamponade occurred during 27 episodes, while pretamponade occurred in 30. Tamponade was less frequent and resolution of pericarditis without invasive intervention more frequent when pericarditis occurred within 2 weeks of initiation of chronic dialysis. Similarly, resolution with conservative therapy was more frequent with first episodes than with recurrences, and when pericarditis occurred within 3 months of initiation of chronic dialysis. The overall survival was 89.7% and was the same irrespective of the duration of dialysis or whether the pericarditis was a first episode or a recurrence. We recommend that patients with pericarditis and no hemodynamic alterations receive intensive hemodialysis, with careful hemodynamic and echocardiographic monitoring, as primary treatment. Invasive intervention is indicated if cardiac tamponade or pretamponade develops, if a pericardial effusion increases progressively in size, or if a large effusion persists after ten to 14 days of intensive dialysis. In our experience, the invasive intervention of choice is either formal pericardiectomy or subxiphoid pericardiotomy with intrapericardial steroid instillation. In our experience, pericardiocentesis has proven to be a high-risk procedure. It is reserved for emergency circumstances, and then is preferably performed in the operating room just prior to induction of anesthesia for definitive surgical drainage.
We report a case of a 55-year-old woman with end-stage renal disease undergoing intermittent peritoneal dialysis who developed peritonitis secondary to an infection with Pasteurella multocida resulting from a cat bite or cat scratch penetrating her peritoneal dialysis tubing. This case points out the potential importance of household pets as a source of peritoneal contamination.