BACKGROUND: The syndrome of pulmonary hypertension (PHT) in end-stage renal disease (ESRD) has been described in patients on chronic hemodialysis (HD) therapy via arterial-venous (A-V) access. However, the exact timing for the development of the PHT is unknown. This study was designed to evaluate changes in pulmonary artery pressure (PAP) following creation of the vascular access. PATIENTS AND METHODS: PAP and cardiac-output (CO) values were recorded in 12 pre-dialysis patients without PHT a few months after the access formation, before treatment with HD was started, and the prevalence of PHT was calculated. Clinical data was compared between patients with and without PHT. RESULTS: The systolic PAP values were increased in "ve of the 12 pre-dialysis patients (42%) by 21+/-9 mm Hg to more than 35 mm Hg. Patients with and without PHT differed only in that CO was signi"cantly higher among the former. CONCLUSIONS: The development of PHT following access formation represents a failure of the pulmonary circulation to accommodate the access-mediated elevated CO. Pre-dialysis patients scheduled for access formation should be screened for the presence of sub-clinical PHT. "Positive" patients should proceed to peritoneal dialysis or advance to kidney transplantation; rather than getting access and HD therapy.
BACKGROUND: The syndrome of pulmonary hypertension (PHT) in end-stage renal disease (ESRD) has been described in patients on chronic hemodialysis (HD) therapy via arterial-venous (A-V) access. However, the exact timing for the development of the PHT is unknown. This study was designed to evaluate changes in pulmonary artery pressure (PAP) following creation of the vascular access. PATIENTS AND METHODS: PAP and cardiac-output (CO) values were recorded in 12 pre-dialysis patients without PHT a few months after the access formation, before treatment with HD was started, and the prevalence of PHT was calculated. Clinical data was compared between patients with and without PHT. RESULTS: The systolic PAP values were increased in "ve of the 12 pre-dialysis patients (42%) by 21+/-9 mm Hg to more than 35 mm Hg. Patients with and without PHT differed only in that CO was signi"cantly higher among the former. CONCLUSIONS: The development of PHT following access formation represents a failure of the pulmonary circulation to accommodate the access-mediated elevated CO. Pre-dialysis patients scheduled for access formation should be screened for the presence of sub-clinical PHT. "Positive" patients should proceed to peritoneal dialysis or advance to kidney transplantation; rather than getting access and HD therapy.
Authors: Melissa C Caughey; Randal K Detwiler; Joseph A Sivak; Lisa J Rose-Jones; Abhijit V Kshirsagar; Alan L Hinderliter Journal: Transplantation Date: 2020-10 Impact factor: 5.385