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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2008  |  Volume : 19  |  Issue : 2  |  Page : 189-193
Pulmonary Hypertension in Hemodialysis Patients


1 Department of Nephrology, Tehran University of Medical Sciences, Tehran, Iran
2 Department of Pulmonary Medicine, Iran University of Medical Sciences, Tehran, Iran
3 Department of Medicine, Iran University of Medical Sciences, Tehran, Iran
4 Department of Cardiology, Iran University of Medical Sciences, Tehran, Iran
5 Department of Nephrology, Iran University of Medical Sciences, Tehran, Iran

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   Abstract 

The aim of this study was to evaluate the prevalence of primary pulmonary hypertension (PHT) among hemodialysis patients and search for possible etiologic factors. The prevalence of PHT was prospectively estimated by Doppler echocardiogram in 62 long-term hemodialysis patients on the day post dialysis. PHT (> 35 mm Hg) was found in 32 (51.6%) patients with a mean systolic pulmonary artery pressure of 39.6 ± 13.3 mmHg. The hemoglobin and albumin levels were significantly lower in the PHT subgroup (11.1 ± 1.86 vs 9.8 ± 1.97 g/dL and 3.75 ± 0.44 vs 3.38 ± 0.32 g/dL, p = 0.01 and 0.02, respectively). Our study demonstrates a surprisingly high prevalence of PHT among patients receiving long-term hemodialysis. Early detection is important in order to avoid the serious consequences of the disease.

Keywords: Arteriovenous access; end-stage renal disease; hemodialysis; pulmonary hypertension

How to cite this article:
Mahdavi-Mazdeh M, Alijavad-Mousavi S, Yahyazadeh H, Azadi M, Yoosefnejad H, Ataiipoor Y. Pulmonary Hypertension in Hemodialysis Patients. Saudi J Kidney Dis Transpl 2008;19:189-93

How to cite this URL:
Mahdavi-Mazdeh M, Alijavad-Mousavi S, Yahyazadeh H, Azadi M, Yoosefnejad H, Ataiipoor Y. Pulmonary Hypertension in Hemodialysis Patients. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Nov 20];19:189-93. Available from: http://www.sjkdt.org/text.asp?2008/19/2/189/39028

   Introduction Top


Excess mortality rates due to cardiovascular disease in end-stage renal disease (ESRD) patients been described by epidemiological and clinical studies. It accounts for approxi­mately 50 percent of deaths in dialysis patients. [1] Although controversial, this may be due in part to the presence of excess vascular calcification (VC), particularly in the form of extensive coronary artery calcification (CAC), which can be observed even in very young dialysis patients. [2],[3],[4],[5]

It was suggested that abnormalities of the right ventricular function in patients with ESRD were largely due to pulmonary hypertension (PHT), which usually develops secondary to pulmonary artery calcifications (PAC). [6]

Pulmonary hypertension is present when mean pulmonary artery pressure (PAP) exceeds 30 mmHg. Regardless of the etiology, the mortality and the morbidity from long­standing PHT exceed that expected from the causative condition. The clinical manifes­tations of secondary PHT are frequently masked by the underlying etiology, and the diagnosis may be confirmed only after the onset of right ventricular failure. PAP may be further increased by high cardiac output resulting from the arteriovenous access itself, worsened by commonly occurring anemia and fluid overload. [7],[8],[9] Doppler echocardio­graphy has enabled non invasive accurate estimation of PAP in a large patient population [6] .

Prevalence of PHT ranges from 30-40% as detected by Doppler echocardiography in patients on chronic hemodialysis (HD) therapy. Early intervention to reduce the pressure in the pulmonary artery may prevent deterioration to heart failure and death.[10],[11],[12],[13]

The purpose of this study was to evaluate the prevalence of PHT in patients on main­tenance hemodialysis therapy in relation with possible etiological factors of this condition.


   Patients and Methods Top


We studied 62 patients who were main­tained on long-term regular hemodialysis therapy via arteriovenous fistulas or grafts three times per week in 4-h sessions in Hasheminejad Hospital and Emam Khomeni Hospital Tehran, Iran. The study was per­formed from January to December, 2006.

Patients with comorbid conditions and high probability of secondary PHT (cardiac disease, pulmonary disease, collagen vascular disease) were excluded.

Systolic PAP was estimated in the study patients with Doppler echocardiography that was performed on the day post dialysis. One cardiologist performed all the echo­cardiographical studies, using Esaote; Megas ultrasound machines (Connector EA 1 PA230E). A complete two dimensional, Doppler echocardiographic study was ob­tained on each patient. A tricuspid regur­gitation systolic jet was recorded from the parasternal or apical window with the continuous- wave Doppler echocardiographic probe. Systolic right ventricular (or pulmo­nary artery) pressure was calculated using the modified Bernoulli equation: PAP = tricuspid systolic jet (TR) + 10-15 mm Hg (estimated right atrial pressure: 15 mm Hg in dilated right atrium and 10 mmHg in normal or slightly enlarged right atrium). PHT was defined as a systolic PAP > 35 mmHg. Cardiac output was not estimated during this study.

The patients' data included age, sex, co­morbidities, medications, etiology of kidney disease, age at time of ESRD, duration of hemodialysis therapy, and blood access location.

Laboratory investigations included hemo­globin, hematocrit, calcium, phosphorus, and parathyroid hormone level. The results of the predialysis blood samples at time of the echocardiographical study and the mean of the preceding three months values were evaluated.

Patients with PHT (35 mmHg) were evaluated further by an experienced pulmo­nologist in order to uncover other potential causes of PHT. This assessment included chest radiography, chest computerized tomo­graphy (CT) scan, and complete pulmonary function tests.


   Statistical Analysis Top


The prevalence of PHT was calculated using the SPSS software. Clinical variables were compared between patients with and without PHT and within patients with PHT receiving hemodialysis using analysis of variance and "t" test. Values were expressed as mean ± Standard deviation (SD). All p values less than 0.05 were considered significant.


   Results Top


The PAP values of the study patients are presented in [Table - 1]. PHT was observed in 32 (52%) patients receiving hemodialysis, with a mean systolic PAP of 39.6 ± 13.3 mmHg. Patient characteristics are presented in [Table - 2]. The mean duration of hemo­dialysis therapy prior to the echocardiography study was 78.6 ± 73.8 months. The most common etiologies of renal failure were diabetes mellitus and arterial hypertension. Data on the 32 patients with PHT were compared with the 31 patients without PHT. The hemoglobin and albumin levels were significantly lower in the PHT subgroup (11.1 ± 1.86 g/dL vs 9.8 ± 1.97 g/dL and 3.75 ± 0.44 vs 3.38 ± 0.32, p = 0.012 and 0.02, respectively), but it did not show significant correlation with severity of PHT. Although ejection fraction was statistically significantly higher in the PHT than the non-PHT sub­group, it was not clinically significant.

The elevated ejection fraction in both sub­groups was not explained by the hemoglobin level as a covariant [Figure - 1]. Furthermore, there was no significant difference of mean duration of hemodialysis therapy in the PHT from that of the non-PHT subgroup (78.2 months vs 80.7 months). Other variables, such as anatomic location of the dialysis vascular access, lipid profile, parathyroid hormone activity, and calcium-phosphate product, did not differ between the normal patients and even patients with different severity of PHT.


   Discussion Top


In this study, the prevalence of PHT as defined by Doppler echocardiographic assess­ment of tricuspid valve was almost 50% in the HD patients, and 17 (26%) patients demonstrated moderately severe PHT (PAP greater than 45 mmHg). The reported preva­lence of PHT disease ranges from 26% to 40%. [4],[7],[10],[12]

We compared the clinical and metabolic variables of the patients with different seve­rity and without PHT. The patients with PHT had significantly lower hemoglobin and albumin levels than those without it. How­ever, we did not find any difference in age, duration of dialysis, or lipid profile between these sub-groups as reported elsewhere. [4],[10]

We could not show the effect of anatomic location of the dialysis vascular access such as Abolghasemi et al [12] , while Yigla et al suggested in their comprehensive studies that pathologic elevation of PAP occurs in those patients whose pulmonary circulation could not compensate for the arteriovenous (AV) access-related high cardiac output. They recommended surgical reduction of oversized AV accesses in patients with PHT who demonstrate high cardiac output; both cardiac output and PHT improved significantly following the temporary closure of the AV accesses in the echo laboratory. [7],[14] Increased stiffness of the pulmonary capillaries due to hyperparathyroidism and pulmonary vascular calcification is one possible expla­nation for the PHT. Akmal et al studied the role of excess parathyroid hormone in the genesis of pulmonary calcifications in dogs with experimental CRF. They proposed that the abnormalities in right ventricular function were largely due to pulmonary hypertension, which develops secondary to pulmonary calcification, since ESRD is associated with generalized calcification. [4],[15] It may appear that the disease process is driven by vaso­constriction, but it now appears that pulmo­nary vascular proliferation and remodeling are the prime forces of. In addition, endo­thelial dysfunction is a key element in the pathogenesis, which is marked by prolonged elevation of endothelin coupled with chronic reductions in nitric oxide and prostaglandin I2. Identification of these processes has allowed the development of specific pharma­cological targets. [6]

PHT has an insidious nature and results in extremely serious morbidity. Early detection of the disease is necessary before the deve­lopment of significant pathophysiological changes. Despite the possibility of common mediators for all the mechanisms of pulmo­nary hypertension, there are clear differ­rences observed in the potential reversibility of pathophysiological responses of the three components of pulmonary artery pressure that include volume of pulmonary blood flow, resistance in the pulmonary vascular bed and pulmonary venous pressure. [6]

Barak and Katz's hypothesized that micro­bubbles, which originate from the dialysis tubes or filter, may be trapped in the pulmonary circulation. Thus, hemodialysis patients may suffer lung injury due to the microbubble shower. Chronically, the recurrent ongoing microbubble-induced infla­mmatory response and lung injury may explain the high pulmonary morbidity, mani­fested as increased pulmonary artery pressure in the chronic hemodialysis patients. [16]

Based on the data presented, we conclude that a substantial number of ESRD patients have functional abnormality of pulmonary circulation. This unrecognized complication is not uncommon and is associated with reduced survival. Early detection is impor­tant in order to avoid the serious consequences of the disease.

 
   References Top

1.United States Renal Data System. Excerpts from USRDS 2005 Annual Data Report. U.S. Am J Kidney Dis 2006;47(Suppl 1):S1.  Back to cited text no. 1    
2.London GM, Guerin AP, Marchais SJ, Metivier F, Pannier B, Adda H. Arterial media calcification in end-stage renal disease: Impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant 2003;18 (9):1731-40.  Back to cited text no. 2    
3.Floege J. When man turns to stone: Extraosseous calcification in uremic patients. Kidney Int 2004;65(6):2447-62.  Back to cited text no. 3    
4.Floege J, Ketteler M. Vascular calcification in patients with end-stage renal disease. Nephrol Dial Transplant 2004;19(Suppl 5):v59-66.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Stompor T. An overview of the patho­physiology of vascular calcification in chronic kidney disease. Perit Dial Int. 2007 Jun;27 Suppl 2:S215-22.  Back to cited text no. 5    
6.Galie N, Manes A, Branzi A: Evaluation of pulmonary arterial hypertension. Curr Opin Cardiol. 2004 Nov;19(6):575-81  Back to cited text no. 6    
7.Yigla M, Nakhoul F, Sabag A, et al. Pulmonary hypertension in patients with end-stage renal disease. Chest 2003;123 (5):1577-82.  Back to cited text no. 7    
8.Yigla M, Abassi Z, Reisner SH, Nakhoul F. Pulmonary hypertension in hemodialysis patients. Semin Dial 2006;19(5):353-7.  Back to cited text no. 8    
9.Berger, M, Haimowitz, A, Van Tosh, A, et al. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985; 6:359.  Back to cited text no. 9    
10.Amin M, Fawzy A, Abdel Hamid M, Elhendy A. Pulmonary hypertension in patients with chronic renal failure: Role of parathyroid hormone and pulmonary artery calcifications . Chest 2003;124(6):2093-7.  Back to cited text no. 10    
11.Bossone E, Bodini BD, Mazza A, Allegra L. Pulmonary arterial hypertension: The key role echocardiographty. Chest 2005;127 (5):1836-43.  Back to cited text no. 11    
12.Abolghasemi R, Sang-Sefidi J, Miri R, Soluki M: Pulmonary Hypertension in Chronic Hemodialysis patients; Iranian Journal of Kidney Diseases, Vol 1, Supp.1 2007:9  Back to cited text no. 12    
13.Reisner SA, Azzam Z, Halmann M, et al. Septal to free wall curvature ratio: A non­invasive index of pulmonary arterial pressure. J Am Soc Echocardiogr 1994;7(1):27-35.  Back to cited text no. 13    
14.Abassi Z, Nakhoul F, Khankin E, Reisner SH, Yigla M. Pulmonary hypertension in chronic dialysis patients with arteriovenous fistula. Curr Opin Nephrol Hypertens 2006;15(4):353-60.  Back to cited text no. 14    
15.Akmal M, Barndt RR, Ansari AN, Mohler JG, Massry SG. Excess PTH in CRF induces pulmonary calcification, Pulmonary hyper­tension and right ventricular hypertrophty. Kidney Int 1995;47(1):158-63.  Back to cited text no. 15    
16.Barak M, Katz Y. Microbubbles: Patho­physiology and clinical implications. Chest 2005;128(4):2918-32.  Back to cited text no. 16    

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Correspondence Address:
Mitra Mahdavi-Mazdeh
Associate Professor of Nephrology, Tehran University of Medical Sciences, Tehran
Iran
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PMID: 18310865

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