5 results match your criteria: "USA. Electronic address: msarnak@tuftsmedicalcenter.org.[Affiliation]"

Pulmonary Hypertension in Chronic Kidney Disease.

Cardiol Clin

August 2021

Department of Medicine, Tufts Medical Center, 800 Washington Street, Boston, MA 02111, USA; Division of Nephrology, Tufts Medical Center, Box 257, 800 Washington Street, Boston, MA 02111, USA. Electronic address:

There is a high prevalence of pulmonary hypertension in chronic kidney disease (CKD), with rates increasing as glomerular filtration rate declines. Pulmonary hypertension is associated with a higher risk of cardiovascular events and mortality in non-dialysis-dependent CKD stages 3 to 5, dialysis-dependent CKD, as well as kidney transplant recipients. The pathophysiology of pulmonary hypertension in CKD is multifactorial and includes higher pulmonary capillary wedge pressure caused by ischemic heart disease and cardiomyopathy, higher cardiac output caused by anemia and arteriovenous access used for hemodialysis, as well as potentially higher pulmonary vascular resistance.

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Chronic kidney disease (CKD) is a major risk factor for valvular heart disease (VHD). Mitral annular and aortic valve calcifications are highly prevalent in CKD patients and commonly lead to valvular stenosis and regurgitation, as well as complications including conduction system abnormalities and endocarditis. VHD, especially mitral regurgitation and aortic stenosis, is associated with significantly reduced survival among CKD patients.

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Angiotensin-converting enzyme inhibitors are beneficial in heart failure with reduced ejection fraction but are associated with acute declines in estimated glomerular filtration rate (eGFR). Prior studies evaluating thresholds of eGFR decline while using angiotensin-converting enzyme inhibitors in heart failure with reduced ejection have not taken into account this medication-driven decline. Here we used data from the Studies of Left Ventricular Dysfunction (SOLVD) trial of 6245 patients and performed Cox proportional hazards regression models to calculate hazard ratios of all-cause mortality and heart failure hospitalization-associated with percent eGFR decline at two- and six-weeks after randomization to enalapril versus placebo.

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Sleepless in CKD: a novel risk factor for CKD progression?

Kidney Int

June 2016

Renal Division, Department of Internal Medicine, University of New Mexico, Albuquerque, New Mexico, USA; Renal Section, Medicine Service, Department of Medicine, Raymond G. Murphy VA Medical Center, School of Medicine, University of New Mexico, Albuquerque, New Mexico, USA.

Disorders of sleep have been associated with adverse outcomes in both the general population and in patients with chronic kidney disease. McMullan et al. add to this literature by demonstrating an association between short sleep duration and more rapid decline in glomerular filtration rate.

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Background: Fibroblast growth factor 23 (FGF23) has emerged as a novel risk factor for mortality and cardiovascular events. Its association with the ankle-brachial index (ABI) and clinical peripheral artery disease (PAD) is less known.

Methods: Using data (N = 3143) from the Cardiovascular Health Study (CHS), a cohort of community dwelling adults >65 years of age, we analyzed the cross-sectional association of FGF23 with ABI and its association with incident clinical PAD events during 9.

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