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Abstract
The aims of this study were to evaluate the incidence of unexplained pulmonary hypertension
(PH) among patients with end-stage renal disease (ESRD) and to suggest possible etiologic
factors.
The incidence of PH was prospectively estimated by Doppler echocardiography in 58
patients with ESRD receiving long-term hemodialysis via arteriovenous access, and
in control groups of 5 patients receiving peritoneal dialysis (PD) and 12 predialysis
patients without a known other cause to suggest the presence of PH. Clinical variables
were compared between patients with and without PH receiving hemodialysis. Changes
in pulmonary artery pressure (PAP) values before and after onset of hemodialysis via
arteriovenous access, arteriovenous access compression, and successful kidney transplantation
were recorded.
PH > 35 mm Hg was found in 39.7% of patients receiving hemodialysis (mean +/- SD,
44 +/- 7 mm Hg; range, 37 to 65 mm Hg), in none of the patients receiving PD, and
in 1 of 12 predialysis patients. Patients with PH receiving hemodialysis had a significantly
higher cardiac output (6.9 L/min vs 5.5 L/min, p = 0.017). PH developed in four of
six patients with normal PAP after onset of hemodialysis therapy via arteriovenous
access. One-minute arteriovenous access compression in four patients decreased the
mean systolic PAP from 52 +/- 7 to 41 +/- 4 mm Hg (p = 0.024). PH normalized in four
of five patients receiving hemodialysis following kidney transplantation. Kaplan-Meier
survival analysis according to PAP values revealed significant survival differences
(p < 0.024).
This study demonstrates a surprisingly high incidence of PH among patients with ESRD
receiving long-term hemodialysis with surgical arteriovenous access. Both ESRD and
long-term hemodialysis via arteriovenous access may be involved in the pathogenesis
of PH by affecting pulmonary vascular resistance and cardiac output.