title: Pulmonary hypertension in chronic dialysis patients with arteriovenous fistula: pathogenesis and therapeutic prospective.
abstract: OBJECTIVE
  End-stage renal disease patients receiving chronic haemodialysis via arteriovenous access often develop various cardiovascular complications, including vascular calcification, cardiac-vascular calcification and atherosclerotic coronary disease. This review describes recently published studies that demonstrate a high incidence of pulmonary hypertension among patients with end-stage renal disease receiving long-term haemodialysis via a surgical arteriovenous fistula. Both end-stage renal disease and long-term haemodialysis via arteriovenous fistula may be involved in the pathogenesis of pulmonary hypertension by affecting pulmonary vascular resistance and cardiac output.
  
  
  RESULTS
  Morbidity and mortality from cardiovascular disease are greatly increased in patients on maintenance haemodialysis therapy. Using Doppler echocardiography, we found a significant increase in cardiac output in 40% of chronic haemodialysis patients, probably related to the large arteriovenous access or altered vascular resistance as a result of the local vascular tone and function expressed by the imbalance between vasodilators such as nitric oxide, and vasoconstrictors such as endothelin-1.
  
  
  CONCLUSIONS
  We propose different potential mechanisms as explanations for the development of pulmonary hypertension. Hormonal and metabolic derangement associated with end-stage renal disease might lead to pulmonary arterial vasoconstriction and an increase in pulmonary vascular resistance. Pulmonary arterial pressure may be further increased by high cardiac output resulting from the arteriole-venous access itself, worsened by commonly occurring anaemia and fluid overload.
authors.affiliation: Department of Physiology and Biophysics, Rappaport Family Institute for Research in the Medical Sciences, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Technion City, Israel.
authors.forename: Zaid
authors.initials: Z
authors.lastname: Abassi
authors.forename: Farid
authors.initials: F
authors.lastname: Nakhoul
authors.forename: Eliyahu
authors.initials: E
authors.lastname: Khankin
authors.forename: Shimon A
authors.initials: SA
authors.lastname: Reisner
authors.forename: Mordechai
authors.initials: M
authors.lastname: Yigla
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D002114:Calcinosis / Q000209:etiology / Q000378:metabolism / Q000401:mortality / Q000473:pathology / Q000628:therapy; D002302:Cardiac Output; D015150:Echocardiography, Doppler / Q000379:methods; D019332:Endothelin-1 / Q000378:metabolism; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000378:metabolism / Q000401:mortality / Q000473:pathology / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000401:mortality / Q000473:pathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism / Q000503:physiopathology; D006435:Renal Dialysis / Q000009:adverse effects; D013997:Time Factors; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000378:metabolism; D014665:Vasodilator Agents / Q000378:metabolism
chemical_list: D019332:Endothelin-1; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide