Close Association between parathyroid hormone and left ventricular function and structure in end-stage renal failure patients under maintenance hemodialysis

Authors

  • Hamid Nasri
  • Azar Baradaran

Abstract

Background: Cardiovascular risk factors are a sig­nificant burden in end-stage renal dis­ease patients under  hemodialysis and are the leading cause of death among these patients. The influence of parathyroid hormone (PTH) on myocardial function as a toxin of uremia is under more attention and evaluation becaue of growing evidence showing that the effects of PTH on cardiac function may be the most serious consequence of secondary hyperparathroism in renal failure.In this study we determined role of excess PTH in the development of left ventricilar (LV) hypertrophy as well as LV ejection fraction in patients with end-stage renal disease under regular hemodialysis.  Methods: This study  is cross-sectional that was done on  patients with end-stage renal disease (ESRD) undergoing maintenance  hemodialysis treatment. For patients, Calcium, Phosphorus, Alkaline phosphatase and Intact PTH (iPTH) were measured. Hypertensive patients were stratified into stages one to three. Ecocadiographies for LV hypertrophy and ejection fraction (%) were done and patients stratified into normal ,mild, moderate and severe LV hypertrophy. Results: The total patients were 73(F=28 M=45), consisting  of 58 non diabetic hemodialysis patients (F=22 M=36), and 15diabetic hemodialysis patients (F=6 M=9).The  mean age was 46.5±16 years. The  time on hemodialysis was 21.5±23.5months. The LV ejection fraction (EF%) were 51±8 percent. ‘iPTH’ of patients was 309±349 Pg/ml. ‘iPTH’  of diabetic and nondiabetic groups was 234±265 pg/ml and 329±368 pg/ml respectively. Serum alkaline phosphatase was 413±348 IU/L. Serum alkaline phosphatase of diabetic and nondiabetic groups were 295±179 IU/L and 443±375 IU/l respectively. Serum albumin was 4±0.75 g/dl. Serum albumin of diabetic and nondiabetic groups was 3.6±0.7 g/dl and  4.2±0.7 g/dl respectively. Significant inverse correlation of serum ALP with percent of LV ejection fracction and marginal positive correlation of serum ALP with LVH and also marginal correlation of serum iPTH with LVH were seen. Also  significant inverse correlation between serum iPTH with percent of LV ejection fraction in non diabetic heart patients was observed. Conclusions: Adverse effects of secondary hyperparathyroidism on LV function and structure in this study show  the role of excess PTH in the development of left ventricilar (LV) hypertrophy as well as low LV ejection fraction in patients with end-stage renal disease under hemodialysis  which   needs more attention to control of secondary hyperparathyroidism to reduce the risk of cardiovascular morbidity and mortality in dialysis patients . Keywords: Hemodialysis, Left ventricular hypertrophy, Ejection fraction ,Secondary hyperparathyroidism

References

Rahn KH, Barenbrock M, Kosch M, Suelak B,Witta J.Vessle wall alterations in patients with renal failure.Hypertens Res 2000;23(1):3-6.

Murphy SW, Foley RN. Cardiac disease in dialysis patients, Divalent Ion Abnormalities and Hyperparathyroidism In the Etiology of Cardiovascular Disease of Patients with Chronic Renal Failure. Seminars in Dialysis 1999;12(2):97-101.

Zoccali C, Benedetto FA , Mallamaci F, Tripepi G, Giacone G, Cataliotti A et al. Prognostic impact of the indexation of left ventricular mass in patients undergoing dialysis J AM Soc Nephrol 2001;12: 2768-74.

Norris KC. Avoiding the risk of secondary hyperparathyroidism in chronic renal failure:A new approach and a review. Dialysis & Transplantation 2001;30(6).

Dyadyk AI, Bagriy AE, Yarovaya NF. Left ventricular hypertrophy in chronic uremia (a review). Dialysis & Transplantation 2000;29(6).

Locatelli F, Bommer J, London GM, Martin-Malo A, Wanner C, Yaqoob M et al. Cardiovascular disease determinants in chronic renal failure: Clinical approach and Treatment. Nephrol Dial Transplant 2001;16:459-68.

Lopez-Gomez J.M, Jofre R, Cases A. Factores de riesgo cardiovascular en la enfermedad renal cronica. Nefrologia 2002;21:(suppl1).

London GM. Calcium-Phosphate disturbances andhyperpara-thyroidism.http://www.sin-italia.org/jnonline/Symposia/ Accord/LONDON/london.html.

Rostand SG. Coronary heart disease in chronic renal insufficiency :Some manengement consideration. J Am Soc Nephrol 2000;11:1948-56.

Bonisch S, Huge L.U, Amann K, Ritz E. Effect of PTH and ANG II on cardiac fibriblast in vitro. J Am Soc Nephrol 1999;10:616A.

The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure.Arch Intern Med 1997;157:2413-46.

Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL et al.The seventh report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. JAMA 2003;289:2560-71.

Salem MM, Hyperparathyroidism in hemodialysis population:A survey of 612 patients. Am J Kidney Dis 1997;29:862-8652.

Drueke T, Fauchet M, Fleury J, Toure Y. Lesourd P, Le Pailleure, Crosnier J. Effect of parathroidectomy on left ventricular function in hemodialysis patients. Lancet 1980;i:112-114.

Timio M. Cardiotoxicity of parathyroid hormone .It J Mineral Electrolyt Metab 1995;9:19-24.

Rostand SG, Drueke TB. Parathyroid hormone ,vitamin D,and cardiovascular disease in chronic renal failure.Kidnet Int1999;56:383-92.

Kyu Ha S, Park HS, Kim SJ, Park CH, Kim DS,Kim HS. Prevalence and patterns of left ventricular hypertrophy in patients with predialysis chronic renal failure.J Korean Med Sci1998;13:488-94.

Strozecki P, Adamovicz E, Odrowaz-Sypniewska G,wlodarczyk Z, Parathormon MJ. Calcium phosphorus and left ventricular structure and function in normotensive hemodialysis patients.Ren Fail 2001;23(1):115-26.

Wanic-Kossowska M, Lehmann P, Czekalski S. Left ventricular hypertrophy in patients with chronic renal failure treated by hemodialysis. Pol Arch Med Wewn 2002;107(6):539-46.

Massry SG, Smogorzewski M. Mechanisms through which parathyroid hormone mediates its deleterious effects on organ function in uremia. Semin Nephrol 1994;14:219-31.

Lowrie EG, Lew NL. Death risk in hemodialysis patients:The predicting value of commonly measured variables and the evaluation of death rate defferences between facilities.Am J Kid Dis 1990;5:458-82.

Foly RN,ParfreyPS, Harnett JD, Kent GM, Hu L, O"Dea R,et al. Hypocalcemia,morbidity and mortality in end-stage renal disease.Am J Nephrol 1996;16:386-93.

Harnett JD, Parfrey PS, Griffiths Sm,Gault MW, Barre PE, Guttmann RD. Left ventricular hypertrophy in end-stage renal disease. Nephron 1988;48:107-115.

Block GA, Hulbert-ShearonTE, Levin NW, Port FK. Association of serum phosphorus and calcium xphosphate product with mortality risk in chronic hemodialusis patients:A national study. Am J Kidney Dis 1998;31:607-17.

Hara S,Ubara Y, Arizono K, Ikeguchi H, Katori H, Yamada A. Relationship between parathyroid hormone and cardiac function in long-term hemodialysis patients. Min Electrolyte Metab 1995;21:67-71.

Nagashima M, Hashimoto K, Shinsato T, Ashida K, Kobayashi M, Yamashita H, et al. Marked improvement of left ventricular function after parathyroidectomy in a hemodialysis patient with secondary hyperparathyroidism and left ventricular dysfunction. Circ J 2003;67(3):269-72.

Park CW, OH YS,Shin YS. Intravenous calcitriolregress myocardial hypertrophy in hemodialysis patients with secondary hyperparathyroism. Am J Kidney Dis 1999;33:73-81.

Block GA, Port FK. Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients.Recomendation for a change in manengement.Am J Kidney Dis 2000;35:1226-37.

Drueke TB. Aspects of cardiovascular burden in pre-dialysis patients.Nephron 2000;85:9-14.

Issue

Vol. 16 No. 2 (2004): JOURNAL OF AYUB MEDICAL COLLEGE, ABBOTTABAD

Section

ORIGINAL ARTICLE

License

Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License  CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.

USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.

AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.