Search

An increase in pulse pressure is a risk factor for death in patients with kidney failure who receive dialysis, according to a study of 37,069 hemodialysis patients. Pulse pressure is a different way of measuring blood pressure. It involves subtracting diastolic pressure from systolic pressure to measure the actual pulse of blood flow every time the heart contracts., Context: Although increased blood pressure is associated with adverse outcomes in the general population, elevated blood pressure is associated with decreased mortality in patients with end-stage renal disease undergoing maintenance hemodialysis. Recent investigations in the general population have demonstrated the predictive utility of pulse pressure (systolic minus diastolic blood pressure), a measure reflecting the pulsatile nature of the cardiac cycle. Objectives: To estimate the relationship between pulse pressure and mortality in patients undergoing maintenance hemodialysis and to test our hypothesis that an increasing pulse pressure would be associated with increased risk of death up to 1 year despite the inverse relationship between conventional blood pressure measures and mortality in patients with end-stage renal disease. Design, Setting, and Patients: Retrospective cohort investigation of patients with end-stage renal disease undergoing maintenance hemodialysis at 782 hemodialysis facilities throughout the United States. Of 44 069 eligible patients as of January 1, 1998, 37069 with complete demographic data were included in the analyses of clinical and laboratory data collected from October 1 through December 31, 1997. Patients were followed up through December 31, 1998. Main Outcome Measures: The primary study outcome was death at 1 year. A secondary outcome was the magnitude of the pulse pressure. Results: The final patient cohort was similar to national averages with respect to age, sex, race, and diabetic status. Mean (SD) pulse pressures before dialysis were 75.0 (15.0) mm Hg and 66.9 (13.9) mm Hg after dialysis. By the end of the 1-year follow-up, 5731 patients (18.4%) died. After adjusting for level of systolic blood pressure, multivariable Cox proportional hazards modeling showed a direct and consistent relationship between increasing pulse pressure and increasing death risk. Each incremental elevation of 10 mm Hg in postdialysis pulse pressure was associated with a 12% increase in the hazard for death (hazard ratio, 1.12; 95% confidence interval, 1.06-1.18). Postdialysis systolic blood pressure was inversely related to mortality with a 13% decreased hazard for death for each incremental elevation of 10 mm Hg (hazard ratio, 0.87; 95% confidence interval, 0.84-0.90). In a multivariable linear regression model, important variables directly associated with elevated pulse pressure included age, diabet es, white race, female sex, and number of years receiving dialysis (all P Conclusions: Pulse pressure is associated with risk of death in a large, nationally representative sample of patients undergoing maintenance hemodialysis. The recognition of pulse pressure as an important correlate of mortality in patients receiving dialysis highlights the need to investigate the relationship between potential therapeutic implications of conduit vessel function and clinical outcomes in patients with end-stage renal disease.

Presents letters to the editor pertaining to medical topics and research as of March 13, 2002. Efficacy of intranasal corticosteroids for acute sinusitis; Time of day of hemodialysis and effect on survival; Inappropriate prescribing for elderly patients; Sexual orientation and suicide risk among teenagers; Circadian variability in hemorrhagic stroke.

Analyzes the use of calcium salts in the management of phosphorus among dialysis patients. Two pathologic sites of occurrence of vascular calcification; Techniques used for measuring vascular calcification; Need for exploring the pathogenesis of vascular calcification.

Derangements of mineral metabolism occur during the early stages of chronic kidney disease (CKD). Hyperphosphatemia develops in the majority of patients with ESRD and has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy. More recent observational data have associated hyperphosphatemia with increased cardiovascular mortality among dialysis patients. Adequate control of serum phosphorus remains a cornerstone in the clinical management of patients with CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduce the risk for vascular calcification and cardiovascular mortality. These measures include dietary phosphorus restriction, dialysis, and oral phosphate binders. Dietary restriction is limited in advanced stages of CKD. Phosphate binders are necessary to limit dietary absorption of phosphorus. Aluminum hydroxide is an efficient binder; however, its use has been nearly eliminated because of concerns of toxicity. Calcium salts are inexpensive and have been used effectively worldwide as an alternative to aluminum. Concerns of calcium overload have led to the investigation of alternatives. Currently, only two Food and Drug Administration-approved noncalcium, nonaluminum binders are available. Sevelamer hydrochloride is an exchange resin and was not as effective as calcium acetate in meeting new guideline recommendations in one double-blind clinical trial. Lanthanum carbonate is a rare earth element and has been studied less extensively. Concerns of long-term administration and toxicity exist. Furthermore, these agents are significantly more expensive than calcium salts, which may contribute to patient noncompliance.

Secondary hyperparathyroidism (HPTH) was initially viewed as a disorder of the skeletal system; however, recent population-based data have associated markers of HPTH with an increased cardiovascular mortality among patients with end-stage renal disease (ESRD). This has stimulated much interest in further evaluating secondary HPTH as a cardiovascular disease risk factor, as well as the putative role of its therapy. This article explores the current state of scientific evidence concerning the pathophysiology of cardiovascular disease among the ESRD population and potential risk factors for its development, including markers of HPTH, and its therapies., (Copyright 2002 by the National Kidney Foundation, Inc.)