| [Download PDF]
|Year : 2007 | Volume
| Issue : 1 | Page : 4--6
Clinical and biochemical parameters in chronic kidney disease with pulmonary hypertension
P Patel1, G Abraham1, B Pratap1, R Ramalakshmi1, M Mathew1, JM Jeevan1, TR Muralidharan1, A Moorthy1, N Leslie2,
1 Department of Medicine, Sri Ramachandra Medical College, Chennai, India
2 Madras Medical Mission Hospital, Chennai, India
Sri Ramachandra Medical College and Research Institute, Porur, Chennai - 600 116
Background: Pulmonary hypertension is said to be present when the systolic and mean pressures in the pulmonary artery exceeds 30 and 20 mmHg, respectively. There is a paucity of data on the incidence and prevalence of pulmonary hypertension in chronic kidney disease (CKD) in Indian patients. Materials and Methods: A total of 100 CKD patients (male 69, female 31), who were on conservative management, hemodialysis, or continuous ambulatory peritoneal dialysis at a tertiary care center, were studied for the presence of pulmonary hypertension. None of the patients were smokers. The variables studied were hypertension, diabetes, and duration of dialysis, and the hemoglobin, blood urea nitrogen (BUN), creatinine, and serum bicarbonate levels. Results: Forty-one percent of the patients had pulmonary hypertension, 96% had anemia (Hb<10 gm/dl), and 85% had metabolic acidosis. The dialysis vintage was less than 10 months in 29% of the patients. Conclusion: The prevalence of pulmonary hypertension was highest in the hemodialysis group (33%). Multivariate regression analysis showed that age, duration of renal failure, vintage of dialysis, hemoglobin, BUN, serum creatinine, and bicarbonate levels were all positively correlated with pulmonary hypertension; in all cases, the correlation was statistically significant.
|How to cite this article:|
Patel P, Abraham G, Pratap B, Ramalakshmi R, Mathew M, Jeevan J M, Muralidharan T R, Moorthy A, Leslie N. Clinical and biochemical parameters in chronic kidney disease with pulmonary hypertension.Indian J Nephrol 2007;17:4-6
|How to cite this URL:|
Patel P, Abraham G, Pratap B, Ramalakshmi R, Mathew M, Jeevan J M, Muralidharan T R, Moorthy A, Leslie N. Clinical and biochemical parameters in chronic kidney disease with pulmonary hypertension. Indian J Nephrol [serial online] 2007 [cited 2022 Dec 7 ];17:4-6
Available from: https://www.indianjnephrol.org/text.asp?2007/17/1/4/35012
Chronic kidney disease (CKD) leads to many comorbidities that affect patients at all stages of the disease. The complications of CKD are due to the disease itself as well as the mode of renal replacement therapy (RRT). Kidney function can only be partly replaced by maintenance dialysis, which provides only 5-10% of excretory renal function.  At present, out of the three modalities of treatment-conservative management, hemodialysis (HD), and peritoneal dialysis-about 82% of patients are on HD.  Cardiovascular morbidity and mortality is highest in the dialysis population. Recently, an association has been found between RRT and the development of pulmonary hypertension.
The normal pulmonary artery pressure in a person living at sea level has a peak systolic value of 18-25 mmHg. Definite pulmonary hypertension is present when pulmonary artery systolic and mean pressures exceed 30 and 20 mmHg, respectively. The normal pulmonary vascular bed offers less than one-tenth of the resistance to flow offered by the systemic bed. Pulmonary artery pressure and pulmonary vascular resistance increase with advancing age. Reduced compliance of the pulmonary vascular bed, secondary to intimal fibrosis or increased wall thickness in the muscular pulmonary arteries, is a possible cause for this. It is also possible that some of the changes in the pulmonary arteries are related to the reduced compliance to left ventricular filling, which is passively reflected on the pulmonary vascular bed.  The majority of the patients with CKD have hypertension with diastolic dysfunction, arteriovenous fistulas (AV fistulas), anemia, uremic lung, volume overload with interstitial pulmonary edema, and a high cardiac output state, all of which can lead to increased pulmonary vascular pressures. ,
The following study was done to find out the prevalence of pulmonary hypertension in a cohort of CKD patients at a tertiary care center. We also examined the correlation of pulmonary hypertension with the duration of renal failure, HD, continuous ambulatory peritoneal dialysis (CAPD), various biochemical parameters, hemoglobin, systemic hypertension, and diabetes mellitus.
Materials and Methods
We studied a total of 100 CKD patients in a tertiary care center after obtaining written consent. The group included 25 on conservative management (male 18, female 7), 65 on HD (male 44, female 21), and 10 on CAPD (male 7, female 3). The mean age of the patients on conservative management was 52 ± 13 years, that in the HD group was 48 ± 12 years, and in the CAPD group it was 57.5 ± 12 years. Duration of renal failure, duration of dialysis [Table 1], and the presence or absence of an arteriovenous fistula was noted. Known cases of coronary artery disease and pulmonary disease (including smokers) were excluded. The selected subjects underwent a detailed clinical examination and the relevant biochemical investigations were done. The two comorbid conditions which were taken into consideration were diabetes mellitus and hypertension, and their distribution in the study group is shown in [Table 2].
All patients had a 2D-echocardiogram done by an experienced cardiologist and the findings were confirmed by a second blinded cardiologist. Pulmonary artery systolic pressure was recorded by tricuspid regurgitation jet method [Figure 1]. In HD patients the echocardiogram was done on the day after dialysis; in CAPD patients there was no such specification. Once the data was collected, it was analyzed by the Chi-square test. The relationships of all the variables to pulmonary hypertension in CKD were assessed by multivariate regression analysis.
Ninety six percent of the patients had a hemoglobin value below 10 gm/dl and 98% had a hematocrit 20 mg/dl and in 36% the creatinine was >5 mg/dl. Metabolic acidosis was present in 85% (serum HCO 3 ,,,,, At the ultrastructural level, these changes include swelling of the pulmonary capillary endothelial cells, thickening of the basal lamina, and wide separation of groups of connective tissue fibrils, all indicative of interstitial edema. With persistent edema, there is proliferation of the reticular and elastic fibrils leading to dense connective tissue infiltration in the alveolar capillaries.  Structural changes in the small pulmonary arteries, arterioles, and venules include medial hypertrophy and intimal fibrosis. Many patients with left ventricular diastolic dysfunction exhibit increased pulmonary vascular resistance and moderately severe pulmonary hypertension.
In our study, we found that hemoglobin and hematocrit were negatively correlated with pulmonary hypertension. However, Nissenson et al . has recommended optimization of the hematocrit to maximize the blood oxygen carrying capacity and minimize the impact of arterial hypoxemia.  It has been found that repeated episodes of hypoxia during and/or after HD lead to the development of pulmonary hypertension and cause morphological changes in the lung. ,,
We also found that as the duration of renal failure increased so did the chances of developing pulmonary hypertension. Braunwald has stated, 'Relieving the downstream obstruction results in the normalization of pulmonary artery pressure… this has been believed to be related to the chronicity of the active pulmonary hypertension, leading to irreversible vascular changes.'  One of the recent observations as to why pulmonary hypertension occurs in CKD patients has to do with the role of the parathyroid hormone. A study found that in patients with hyperparathyroidism there is an increase in the intracellular calcium in the pulmonary vessels, causing increased pulmonary pressures.  However, the study failed to prove this theory and could not show any correlation between this variable and pulmonary hypertension.
In our study, the prevalence of pulmonary hypertension was highest in the HD group, which is not surprizing, as these patients had AV fistulas; lower hemoglobin, hematocrit, and serum bicarbonate values and higher BUN and serum creatinine levels. CAPD patients had the least evidence of pulmonary hypertension. Hence, it seems that CAPD may be the better RRT if development of pulmonary hypertension is to be prevented. A recent report by Gueraoui et al . in 1994 showed that 48% of chronic HD patients had pulmonary hypertension.  Patients on dialysis, especially those on HD, need to be evaluated for cardiac function with 2-D echocardiography. Severe pulmonary hypertension in these patients can be ameliorated by banding of the fistula to reduce the high output state, thereby reducing left ventricular end diastolic pressure. Additional strategies include management of anemia with recombinant erythropoietin and iron, correction of metabolic acidosis with sodium bicarbonate, and increasing the frequency of dialysis and renal transplantation.
|1||Gokul R. Replacement therapy by dialysis. Oxford textbook of medicine, 3 rd ed. Weatherall DJ, Ledingham JG, Warrell DA, editor. Oxford University Press: Oxford; 1996. p. 3306.|
|2||Rich S, Chomka E, Hasara L, Hart K, Drizd T, Joo E, et al . The prevalence of pulmonary hypertension in the United States. Chest 1989;96:236-41.|
|3||Okura H, Takatsu Y. High-output heart failure as a cause of pulmonary hypertension. Intern Med 1994;33:363-5.|
|4||Guazzi MD, Polese A, Bartonelli A, Loaldi A, Fiorentini C. Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: A possible role of intracellular calcium. Circulation 1982;66:881-6.|
|5||Clarkson MR, Giblin L, Brown A, Little D, Donohoe J. Reversal of pulmonary hypertension after ligation of a brachiocephalic arteriovenous fistula. Am J Kidney Dis 2002;40:E8.|
|6||Walker JF, Lindray RM, Driedger AA, Sibbald WJ, Linton AL. Hemodialysis commonly causes pulmonary hypertension. Kidney Int 1984;25:195.|
|7||Gueraoui A, Pengloan J, Birmele B, Moline J, Patat F, Nivet H. Pulmonary hypertension in chronic hemodialysis patients: A prospective study. J Am Soc Nephrol 1994;5:450.|
|8||Faishter RD, Vaziri ND, Mirahmadi MK. Lung pathology in chronic hemodialysis patients. Int J Artif Organs 1982;5:97-100.|
|9||Akmal M, Barndt RR, Ansari AN, Mohler JG, Massary SG. Excess PTH in CRF induces pulmonary calcification, pulmonary hypertension and right ventricular failure. Kidney Int 1995;47:158-63.|
|10||Walker JF, Lindsay RM. Acute pulmonary hypertension, leucopenia and hypoxia in early dialysis. Proc Eur DN Transplant Asso Eur Ren Asso 1985;21:135-42.|
|11||Harris P, Heath D. The human pulmonary circulation. 3 rd ed. Churchill Livingstone: New York; 1986. p. 702.|
|12||Nissenson AR, Fine RN. Dialysis Therapy, 3 rd ed. Nissenson AR, Fine RN, editors. Hanley and Belfus: California; 2001. p. 98-9.|
|13||Dhakal MP, Kallay MC, Shelly MA, Taley TE. Post-hemodialysis hypoxia occurs in both biocompatible and bioincompatible dialyzers. Dialysis Transplant 1999;28:666-72.|
|14||Aurigemma NM, Feldman NT, Gottlieb M, Ingram RH Jr, Lazarus JM, Lowrie EG. Arterial oxygenation during hemodialysis. N Eng J Med 1977;297:871-3.|
|15||Igarishi H, Kiois A, Gejyo F, Arakawa M. Physiologic approach to dialysis induced hypoxemia. Nephron 1985;41:62-9.|
|16||Braunwald E, Rich S, Grossman W. Heart disease: A textbook of cardiovascular medicine, 5 th ed, ed. Braunwald E, WB Saunders Co: Philadelphia; 1997. p. 796.|
|17||Amin M, Fawzy A, Hamid M, Elhendy A. Pulmonary hypertension in patients with CRF: Role of PTH and pulmonary artery calcification. Chest 2003;124:2093-7.|