This site became the new on June 19th. Learn more.
Show more Menu IMPORTANT: Listing of a study on this site does not reflect endorsement by the National Institutes of Health. Talk with a trusted healthcare professional before volunteering for a study. Read more... Menu IMPORTANT: Talk with a trusted healthcare professional before volunteering for a study. Read more... Menu
Give us feedback

The Effect of Blood Flow in the Maturing Arteriovenous Access for Hemodialysis on the Development of Pulmonary Hypertension.

This study has been completed.
Information provided by (Responsible Party):
Dr. Ilya Goldin, Shaare Zedek Medical Center Identifier:
First received: August 17, 2008
Last updated: December 12, 2013
Last verified: December 2013

Pulmonary hypertension (PHT) is an elevation of pulmonary arterial pressure (PAP) that can be the result of heart, lung or systemic disease. PHT also complicates chronic hemodialysis (HD) therapy immediately after the creation of an arteriovenous (AV) access, even before starting HD therapy. It tends to regress after temporary AV access closure and after successful kidney transplantation. Affected patients have significantly higher cardiac output. This syndrome is associated with a statistically significant survival disadvantage. The laboratory hallmark of this syndrome is reduced basal and stimulatory nitric oxide (NO) levels. It appears that patients with end-stage renal disease (ESRD) acquire endothelial dysfunction that reduces the ability of their pulmonary vessels to accommodate the AV access-mediated elevated cardiac output, exacerbating the PHT. Doppler echocardiographic screening of ESRD patients scheduled for HD therapy for the occurrence of PH is indicated. Early diagnosis enables timely intervention, currently limited to changing dialysis modality such as peritoneal dialysis or referring for kidney transplantation.An echocardiographic diagnosis of pulmonary hypertension (PHT) is made when the systolic pulmonary arterial pressure (PAP) exceeds normal values (30 mmHg). In mild PHT, PAP values range up to 45 mmHg, in moderate PHT, PAP is between 45 and 65 mmHg, and in severe PHT, PAP values are greater than 65 mmHg. Systolic PAP equals cardiac output times pulmonary vascular resistance (PVR), (i.e., PAP = cardiac output × PVR). Increased cardiac output by itself does not cause PH because of the enormous capacity of the pulmonary circulation to accommodate the increase in blood flow. Therefore development of PHT requires pathologic, marked elevation of pulmonary vascular resistance. The presence of PH may reflect serious pulmonary vascular disease, which can be progressive and fatal. Consequently, an accurate diagnosis of the cause of PHT is essential in order to establish an effective treatment program. Pulmonary hypertension can occur from diverse etiologies. In 1996 we first noted unexplained PH in some long-term hemodialysis (HD) patients during an epidemiologic study of this disorder (Nakhoul F and Yigla M Rambam Medical Cemter-Haifa). It was assumed that their PHT was related to end-stage renal disease (ESRD) or to long-term HD therapy via an arteriovenous (AV) access.

There are several potential explanations for the development of PHT in patients with ESRD. Hormonal and metabolic derangement associated with ESRD might lead to vasoconstriction of pulmonary vessels and increased pulmonary vascular resistance. Values of PAP may be further increased by high cardiac output resulting from the AV access itself, worsened by commonly occurring anemia and fluid overload. Despite almost five decades of HD therapy via a surgically created, often large, hemodynamically significant AV access the long-term impact of this intervention on the pulmonary circulation has received little attention.

RD versus AV HD via AV access

Proposed Mechanisms:

  1. Elevated Parathyroid hormone
  2. Metastatic Calcification due to the increase of the calcium-phosphor multiple
  3. High cardiac output
  4. Nitric oxide-endothelin metabolism
  5. A-v Access flow

These observations indicate a role for AV access-mediated elevations in cardiac output in the pathogenesis of PH. The correlation between access flow and PAP values has not yet been studied. Since patients undergoing HD therapy via AV access had PH that reversed after successful kidney transplantation and after short AV access compression, we concluded that both ESRD and AV access-mediated elevated cardiac output are required for the development PH. From a physiologic point of view, due to the enormous capacity of the pulmonary microcirculation, increased cardiac output by itself cannot cause PH. It is the inability of the pulmonary circulation of some ESRD patients to accommodate the AV access-mediated elevated cardiac output that leads to the development of PH.

Condition Intervention Phase
Pulmonary Hypertension Procedure: Primary arterio-venous vascular access creation Phase 1

Study Type: Interventional
Study Design: Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Basic Science
Official Title: The Effect of Blood Flow in the Maturing Arteriovenous Access for Hemodialysis on the Development of Pulmonary Hypertension.

Resource links provided by NLM:

Further study details as provided by Dr. Ilya Goldin, Shaare Zedek Medical Center:

Primary Outcome Measures:
  • Correlation between av access flow and development of pulmonary hypertension [ Time Frame: Study period ]

Enrollment: 50
Study Start Date: September 2011
Study Completion Date: April 2012
Primary Completion Date: April 2012 (Final data collection date for primary outcome measure)
Intervention Details:
    Procedure: Primary arterio-venous vascular access creation
    Primary arterio-venous vascular access creation, ECHO with pulmonary artery pressure measurements, Assessment of blood NO metabolite levels

Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No

Inclusion Criteria:

  • All new primary av access

Exclusion Criteria:

  • Preoperatively known pulmonary hypertension
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its identifier: NCT00739375

Shaare Zedek Medical Center
Jerusalem, Israel
Sponsors and Collaborators
Shaare Zedek Medical Center
Principal Investigator: Ilya Goldin, Dr Shaare Zedek Medical Center
  More Information

Responsible Party: Dr. Ilya Goldin, Dr, Shaare Zedek Medical Center Identifier: NCT00739375     History of Changes
Other Study ID Numbers: 112
Study First Received: August 17, 2008
Last Updated: December 12, 2013

Keywords provided by Dr. Ilya Goldin, Shaare Zedek Medical Center:
of av access

Additional relevant MeSH terms:
Hypertension, Pulmonary
Vascular Diseases
Cardiovascular Diseases
Lung Diseases
Respiratory Tract Diseases processed this record on August 18, 2017