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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access.

BACKGROUND: We recently have shown a high incidence of unexplained pulmonary hypertension ( PHT) in end-stage renal disease (ESRD) patients on chronic haemodialysis (HD) therapy via arterio-venous (A-V) access. This study evaluated the possibility that PHT in these patients is triggered or aggravated by chronic HD via surgical A-V access, and the role of endothelin-1 (ET-1) and nitric oxide (NO) in this syndrome. METHODS: Forty-two HD patients underwent clinical evaluation. Pulmonary artery pressure (PAP) was evaluated using Doppler echocardiography. Levels of ET-1 and NO metabolites in plasma were determined before and after the HD procedure and were compared between subgroups of patients with and without PHT. RESULTS: Out of 42 HD patients studied, 20 patients (48%) had PHT (PAP = 46+/-2; range 36-82 mmHg) while the rest had a normal PAP (29+/-1 mmHg) (P<0.0001). HD patients with PHT had higher cardiac output compared with those with normal PAP (6.0+/-1.2 vs 5.2+/-0.9 l/min, P<0.034). HD patients, with or without PHT, had elevated plasma ET-1 levels compared with controls (1.6+/-0.7 and 2.4+/-0.8 fmol/ml vs 1.0+/-0.2, P<0.05) that remained unchanged after the HD procedure. HD patients without PHT and control subjects showed similar basal plasma levels of NO2 + NO3 (24.2+/-5.2 vs 19.7+/-3.1 microM, P>0.05) that was significantly higher compared with HD patients with PHT (14.3+/-2.3 microM, P<0.05). HD therapy caused a significant increase in plasma NO metabolites that was greater in patients without PHT (from 24.2+/-5.2 to 77.1+/-9.6 microM, P<0.0001, and from 14.3+/-2.3 to 39.9+/-11.4 microM, P<0.0074, respectively). Significant declines in PAP (from 49.8+/-2.8 to 38.6+/-2.2 mmHg, P<0.004) and cardiac output (CO) (from 7.6+/-0.6 to 6.1+/-0.3 l/min, P<0.03) were found in 11 HD patients with PHT that underwent successful transplantation. Similarly, temporary closure of the A-V access by a sphygmomanometer in eight patients with PHT resulted in a transient decrease in CO (from 6.4+/-0.6 to 5.3+/- 0.5 l/min, P = 0.18) and systolic PAP (from 47.2+/-3.8 to 34.6+/-2.8 mmHg, P<0.028). CONCLUSIONS: This study demonstrates a high prevalence of PHT among patients with ESRD on chronic HD via a surgical A-V fistula. In view of the vasodilatory and antimitogenic properties of NO, it is possible that the attenuated basal and HD-induced NO production in patients with PHT contributes to the increased pulmonary vascular tone. Furthermore, the partial restoration of normal PAP and CO in HD patients that underwent either temporal A-V shunt closure or successful transplantation indicates that excessive pulmonary blood flow is involved in the pathogenesis of the disease.[1]


  1. The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access. Nakhoul, F., Yigla, M., Gilman, R., Reisner, S.A., Abassi, Z. Nephrol. Dial. Transplant. (2005) [Pubmed]
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