INTRODUCTION
Cardiovascular disease is the leading cause of morbidity and mortality in dialysis patients, accounting for 50%of deaths. Pulmonary hypertension (PHT) comprises a group of clinical and pathophysiological entities with similar features but a variety of underlying causes. There are several etiologies for PHT. Pulmonary hypertension (PHT) can be the result of heart, lung or systemic disorders. Regardless of the etiology, morbidity and mortality from long-standing PHT exceed that expected from the causative condition.
PHT was frequently found in patients with chronic renal failure (CRF). Review of literature showed that in one study, PHT was found in 40% of patients with end stage renal disease (ESRD) on chronic hemodialysis therapy via arterio venous access. Adekunle et al. stated that PHT is an independent predictor of mortality in ESRD patients.
PHT involves vasoconstriction and obliteration of the lumen of small vessels in the lungs by plexiform lesions resulting in increased resistance to flow. Proposed mechanisms for the formation of the plexiform lesion included regulation of endothelial growth and angiogenic response to local
triggers. Hormonal and metabolic derangement associated with ESRD might lead to pulmonary arterial vasoconstriction and an increase of the pulmonary vascular resistance.
Pulmonary artery pressure (PAP) may be further increased by high cardiac output resulting from the arterio venousaccess itself and also worsened by commonly occurring anemia and fluid overload. Subclinical left ventriculardysfunction also occurs in patients with ESRD, and is evidenced as abnormal myocardial diastolic rather than systolic dysfunction.
Local vascular tone and function of pulmonary vessels are regulated by the balance between vasodilators, such as nitric oxide, and vasoconstrictors, such as thromboxane. Patients with CRF show an endothelial dysfunction related to defective nitric oxide activity, which is not corrected by hemodialysis (HD). Increased brain natriuretic hormone is associated with age, left ventricular hypertrophy, renal failure, and PHT. N-terminal pro-brain natriuretic peptide (NT-proBNP) is a byproduct of brain natriuretic peptide (BNP) that has been shown to be of prognostic value in PHT.
AIM :
In this study, we aim to find the prevalence of PHT in patients with ESRD and compare the incidence of PHT between those on hemodialysis and those on conservative management. We also compare the biochemical data of the patients with and without PHT to find out any possible associations.
METHODOLOGY :
Study Method :
The study was conducted on patients attending the in-patient/out-patient department of nephrology in PSG hospital. All patients with a diagnosis of ESRD where taken up for the study after the application of the inclusion and exclusion criteria and after obtaining consent. These patients were divided into two groups – those who receive dialysis and those on conservative management.
The biochemical data collected were the average of the last six readings .ECG, CXR and echocardiography to assess PHT were done to those patients who were selected to be included in the study.
Study Place : The study was conducted in PSG Hospitals, Coimbatore.
Study Population : Patients diagnosed with end stage renal disease presenting to PSG hospitals during a time period of 6 months were included in the study after the application of inclusion and exclusion criteria.
Study Period :
The study was conducted during the time period of April 2010 to October 2010. All patients with a diagnosis of ESRD attending the Nephrology department who gave consent to be included in the study were included during this time period. Total of 73 patients were studied.
Inclusion Criteria :
ESRD patients on HD or conservative management were selected. ESRD due to all etiologies and patients of all age groups were selected.
Exclusion Criteria :
COPD, Parenchymal Lung Disease, Chest Wall Disease, Previous history of PHT, Previous pulmonary embolism, Smoker ( >5 pack years), Collagen Vascular Disease, LV EF <50%, Significant mitral/aortic valve disease.
HD patients were being treated with standard bicarbonate dialysis for 4 hours, 3 times a week. Subjects gave their informed consent and the study protocol was approved by the institute’s Committee on Human Research.
RESULTS :
PHT is more common among those on hemodialysis than those who are on conservative management. The cause of a higher PAP in group 1 may be related to the process of HD or the hemodynamic changes caused by AVF. The process of HD itself may be a contributing factor for elevated PAP, but the exact cause is not known and vasoconstrictors such as endothelin may be involved. Microbubble emboli are another cause. In addition, HD causes recurrent episodes of hypoxemia due to partial blockage of the pulmonary capillary bed by white cells or silicone microemboli. Recurrent hypoxemia is associated with elevation of PAP.
CONCLUSION :
This study shows that PHT is very common in ESRD patients.
a. 31.5% of total patients (73) with ESRD had PHT,
b. 35% of 37 patients on HD had PHT,
c. 28% of 36 patients on conservative management had PHT.
Also, PHT is much more common in ESRD patients receiving HD than those on conservative management.
Since pulmonary arterial hypertension usually presents at a very late stage, early diagnosis is a key to proper management and a better outcome.
Estimation and follow-up of PAP using doppler echocardiography may be indicated in all patients with ESRD undergoing HD via an arteriovenous access
