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Pulmonary Hypertension in Patients With End-Stage Renal Disease^*

^* From the Departments of Nephrology (Drs. Nakhoul and Gorevich) and Cardiology (Dr. Reisner), Division of Pulmonary Medicine (Drs. Yigla, Sabag and Tov), Rambam Medical Center and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa; and Nephrology Research Laboratory (Dr. Abassi), Technion-Israel Institute of Technology, Haifa, Israel.

Correspondence to: Mordechai Yigla, MD, Division of Pulmonary Medicine, Rambam Medical Center, PO Box 9602, Haifa 31096, Israel; e-mail: m_yigla{at}rambam.health.gov.il

Background: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Key Words: arteriovenous access • end-stage renal disease • hemodialysis • pulmonary hypertension

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