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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 21  |  Issue : 3  |  Page : 124-129

Correlation of parathyroid hormone level with left ventricular mass in patients with end-stage kidney disease on hemodialysis


1 Department of Nephrology, Damanhour Nephrology Institute, Damanhour, Egypt
2 Department of Cardiovascular Medicine, Faculty of Medicine, Tanta University, Tanta, Egypt
3 Department of Internal Medicine, Faculty of Medicine, Tanta University, Tanta, Egypt
4 Department of Internal Medicine and Nephrology, Faculty of Medicine, Tanta University, Tanta, Egypt

Date of Submission01-Jan-2021
Date of Acceptance01-Apr-2021
Date of Web Publication09-Aug-2021

Correspondence Address:
Dr. Mohamed S Aboelnasr
Internal Medicine; Department of Internal Medicine and Nephrology, Faculty of Medicine, Tanta University, Tanta, 31666
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jesnt.jesnt_1_21

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  Abstract 


Background Patients with end-stage kidney disease (ESKD) on hemodialysis (HD) have a high prevalence of left ventricular hypertrophy (LVH), which is associated with increased cardiovascular risk. Hyperparathyroidism in these patients plays a key role in the development of LVH. The aim of this study was to evaluate the correlation of parathyroid hormone (PTH) level with left ventricular mass in patients with ESKD on HD. Other factors that contribute to the development of LVH were also included.
Patients and methods This study included 40 patients with ESKD at our dialysis unit. Patients were classified into two groups: group I included 20 patients with LVH and group II included 20 patients without LVH. Patients were defined as having LVH if they had left ventricular mass index more than 95 g/m2 in women and more than 115 g/m2 in men.
Results There was a statistically significant increase in PTH in patients in group I than group II (P=0.009). Hemoglobin % was significantly lower in patients in group I than group II (P=0.042). Left ventricular mass index showed a significant positive correlation with PTH and a significant negative correlation with hemoglobin %.
Conclusion Hyperparathyroidism and anemia are the two major contributors to the development of LVH in patients with ESKD on HD.

Keywords: anemia, end-stage kidney disease, hemodialysis, hyperparathyroidism, left ventricular hypertrophy


How to cite this article:
Shaltout AH, Samir S, Lashin FI, Sherif MH, Aboelnasr MS. Correlation of parathyroid hormone level with left ventricular mass in patients with end-stage kidney disease on hemodialysis. J Egypt Soc Nephrol Transplant 2021;21:124-9

How to cite this URL:
Shaltout AH, Samir S, Lashin FI, Sherif MH, Aboelnasr MS. Correlation of parathyroid hormone level with left ventricular mass in patients with end-stage kidney disease on hemodialysis. J Egypt Soc Nephrol Transplant [serial online] 2021 [cited 2021 Oct 17];21:124-9. Available from: http://www.jesnt.eg.net/text.asp?2021/21/3/124/323527




  Introduction Top


Patients with chronic kidney disease (CKD)/end-stage kidney disease (ESKD) suffer disproportionately from cardiovascular CVD [1], which is the most common cause of death in these patients [2],[3],[4].

Patients with CKD/ESKD have a high prevalence of left ventricular hypertrophy (LVH), which is associated with increased cardiovascular risk [5] that may be reduced with LVH regression [6].

Parathyroid hormone (PTH) has been identified as an important cardiotoxin in patients with CKD/ESKD [7]. Severe LVH was found in 70% of patients with ESKD, with elevated plasma PTH levels [8].


  Aim Top


The aim of this study was to evaluate the correlation of PTH level with left ventricular mass in patients with ESKD on hemodialysis (HD). Other factors that may predict LVH in our patients were also included e.g. anemia.


  Patients and methods Top


This study included 40 patients with ESKD at our dialysis unit. Patients were classified into two groups: group I included 20 patients with LVH and group II included 20 patients without LVH. Patients were defined as having LVH if they had left ventricular mass index (LVMI) more than 95 g/m2 in women and more than 115 g/m2 in men [9].

All participants were subjected to the following:
  1. Thorough assessment of history and complete physical examination.
  2. Laboratory investigations including the following:
    1. PTH.
    2. Ionized calcium.
    3. Serum phosphorus.
    4. Hemoglobin% (Hb%).
    5. Serum albumin.
    6. Urea reduction ratio.
  3. ECG.
  4. Echocardiography.


Echocardiographic evaluation was performed using standard M mode and two-dimensional images (Vivid 7 Dimension-GE Healthcare Ultrasound; GE Healthcare, Waukesha, Wisconsin, USA). Images were digitally stored and analyzed by an independent experienced cardiologist. Offline analysis was carried out using the workstation Echopac PC’08 version 7.0.0 GE Vingmed Ultrasound (GE Healthcare). In end diastole, the diastolic septal wall thickness, posterior LV wall thickness, and left ventricular internal diameter (LVIDd) were measured on the two-dimensional echo recordings. LVMI (g/m2) was calculated using the following equation: LVMI=[0.832×[(diastolic septal wall thickness+LVIDd+posterior LV wall thickness)3−(LVIDd)3]×0.6/body surface area. Patients were classified as having LVH if they had LVMI more than 95 g/m2 in women and more than 115 g/m2 in men [9].

Inclusion criteria: patients with ESKD on HD for more than 3 months were included in this study.

Exclusion criteria

  1. Recent acute coronary syndrome within the last 3 months.
  2. Active or chronic infection.
  3. Patients with the following echocardiography findings:
    1. Severe coronary artery disease with resting regional wall motion abnormality.
    2. Severe valvular heart disease.
    3. Dilated cardiomyopathy.
    4. Poor echogenicity.
    5. Pericarditis or pericardial effusion.
  4. Patients with atrial fibrillation and left bundle branch block.


Ethical considerations

The study protocol was approved by the local ethical committee. Informed consents were obtained from all patients after a complete explanation of the benefits and risk was provided. The privacy of all patients’ data was ensured and there was a code number for every patient file that includes all investigations.

Statistical analysis

Statistical analysis was carried out using the Statistical Package for Social Sciences (SPSS), version 22 (SPSS Inc., Chicago, IL, USA). For quantitative data, the Shapiro–Wilk test for normality was performed. For data that followed a normal distribution, values were expressed as mean±SD. Comparisons between the two groups were carried out using the independent samples t test. For data that did not follow a normal distribution, the median and range were calculated. The Mann–Whitney and Kruskal–Wallis tests were used to compare between two or three groups, respectively. For qualitative data, the variables were summarized as frequencies (count and percentage). Correlations between numerical variables were tested using Spearman’s rank-order correlation. Pearson’s χ2 test for independence, Fisher’s exact test, or the Fisher–Freeman–Halton exact test was used to examine the association between two categorical variables as appropriate. Significance was considered at P value less than 0.05 for interpretation of test results [10].


  Results Top


A comparison of basic demographic and clinical parameters of patients in both groups is shown in [Table 1]. There were no statistically significant differences between both groups in age, sex, BMI, body surface area, presence of hypertension, diabetes mellitus, hepatitis C virus seropositivity, or duration of dialysis.
Table 1 Comparison of the basic demographic and clinical parameters of both groups

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Comparison of laboratory parameters in the study groups is shown in [Table 2]. There was a statistically significant increase in PTH in patients in group I than group II (P=0.009). Hb% was significantly lower in patients in group I than group II (P=0.042). The correlation of LVMI with different parameters is shown in [Table 3]. This correlation is significantly positive with PTH and significantly negative with Hb%.
Table 2 Comparison of laboratory parameters of both groups

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Table 3 Correlation of the left ventricular mass index with different parameters

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  Discussion Top


It is well known that patients with CKD/ESKD are predisposed to CVD that manifests clinically as coronary artery disease, atrial or ventricular arrhythmias, myocardial infarction, stroke, or congestive heart failure [11].

LVH represents the key feature in uremic cardiomyopathy [12]. The prevalence of LVH is estimated to be between 16 and 31% in individuals with a GFR more than 30 ml/min; it increases to 60–75% before starting renal replacement therapy, and increases to 90% after the initiation of dialysis [13].

Vitamin D deficiency, secondary hyperparathyroidism, and hyperphosphatemia were the main factors contributing to high cardiovascular risks in patients with CKD/ESKD [14]. The pathogenesis of CKD-mineral bone disease has always been ascribed to a decrease in 1,25-dihydroxyvitamin D3 levels leading to increases in serum PTH and subsequent alterations in calcium and phosphorus metabolism [15],[16].

The role of PTH in the pathogenesis of LVH was confirmed in patients without renal disease. A study examined the relation between PTH and LVH in a general population and found that PTH is an independent predictor of left ventricular mass by height in males older than 59 years and females younger than 60 years [17]. Piovesan et al. [18] confirmed the high prevalence of LVH in patients with primary hyperparathyroidism, an effect that was even found in a group of patients with an asymptomatic clinical presentation. The surgical resolution of primary hyperparathyroidism was followed by a reduction in LVH.

Anemia is a common complication in patients with ESKD [19]. A meta-analysis showed how LV mass was reduced by anemia correction in patients who had severe anemia at baseline [20]. The role of hyperparathyroidism in the pathogenesis of anemia in patients with ESKD is well established [21].

This study included 40 patients with ESKD at our dialysis unit. Patients were classified into two groups: group I included 20 patients with LVH and group II included 20 patients without LVH. Our study showed that PTH was significantly higher and Hb% was significantly lower in patients with LVH. Also, there was a statistically significant positive correlation between LVMI and PTH.

Similar to our findings, Al-Hilali et al. [22] found that LVMI values correlated positively with PTH. They reviewed charts of 130 patients on HD for at least 6 months. Also, Çiçekçioğlu et al. [23] found that high levels of PTH contributed significantly to LVH in HD patients. A 2-year prospective study including 53 patients on HD found a significant positive correlation between concentrations of serum PTH and LVMI [21]. Randon et al. [24] found a significant positive association between LVMI and PTH. Similar to our findings, LVMI was inversely associated with Hb [24].

Stróżecki and colleagues found a statistically significant positive correlation between PTH and LVMI. There was a moderate but statistically insignificant negative correlation between Hb and LVMI [24]. A prospective and comparative study including 50 patients on HD found that LVH was present in 36/50 patients in the study group. LVH was significantly related to anemia and hyperparathyroidism [25].

Ali et al. [26] found that serum PTH was higher in patients with LVH. However, the difference was not statistically significant. Compared with our study, Ali et al. [26] included a larger number of patients (153 patients). Their study included patients with CKD (not on dialysis). In their study, LVH was significantly higher in stage 4 CKD and was related to the duration of CKD.

In contrast to our findings, Ahmed et al. [27] found that uncontrolled secondary hyperparathyroidism in patients on HD is not associated with the development of LVH. The study included 86 patients with ESKD on maintenance HD. This discrepancy may be related to the parameters that they used to define LVH. In their study, they defined LVH as having LVMI of 132 g/m2 for men and 100 g/m2 for women, while in our study, patients were classified as having LVH at a lower threshold (LVMI>95 g/m2 in women and >115 g/m2 in men).

Fujii et al. [28] carried out a study on a total of 81 patients who received chronic dialysis treatment. They found that LVMI was significantly higher only in patients with markedly elevated PTH levels (>500 pg/ml). In our study, the median (interquartile range) levels of PTH were 589 pg/ml (255.5–870.0 pg/ml) and 238.5 pg/ml (103.5–381.0 pg/ml) in group 1 and group 2, respectively.

Our study confirmed the role of hyperparathyroidism and anemia in the development of LVH, with a potential impact on cardiovascular outcome for patients on HD. Further studies including larger numbers of patients are needed. Also, prospective studies are needed to examine the impact of correction of anemia and PTH reduction on LVH and whether this could translate to better cardiovascular and/or mortality outcome in patients on HD in our locality.

Our study results are limited by the small number of patients and its cross-sectional design.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation 2003; 108:2154–2169.  Back to cited text no. 1
    
2.
de Jager DJ, Grootendorst DC, Jager KJ, van Dijk PC, Tomas LM, Ansell D et al. Cardiovascular and noncardiovascular mortality among patients starting dialysis. JAMA 2009; 302:1782–1789.  Back to cited text no. 2
    
3.
Saran R, Robinson B, Abbott KC, Agodoa LY, Albertus P, Ayanian J et al. US renal data system2016 annual data report: epidemiology of kidney disease in the United States. Am J Kidney Dis 2017; 69:A7–A8.  Back to cited text no. 3
    
4.
Roberts MA, Polkinghorne KR, McDonald SP, Ierino FL. Secular trends in cardiovascular mortality rates of patients receiving dialysis compared with the general population. Am J Kidney Dis 2011; 58:64–72.  Back to cited text no. 4
    
5.
Nardi E, Mulè G, Giammanco A, Mattina A, Geraci G, Nardi C et al. Left ventricular hypertrophy in chronic kidney disease: a diagnostic criteria comparison. Nutr Metab Cardiovasc Dis 2020; 31:137–144.  Back to cited text no. 5
    
6.
McCullough PA, Chan CT, Weinhandl ED, Burkart JM, Bakris GL. Intensive hemodialysis, left ventricular hypertrophy, and cardiovascular disease. Am J Kidney Dis 2016; 68:S5–S14.  Back to cited text no. 6
    
7.
Stróżecki P, Adamowicz A, Nartowicz E, Odrowąż-Sypniewska G, Włodarczyk Z, Manitius J. Parathormon, calcium, phosphorus, and left ventricular structure and function in normotensive hemodialysis patients. Ren Fail 2001; 23:115–126.  Back to cited text no. 7
    
8.
Barletta G, De Feo ML, Del Bene R, Lazzeri C, Vecchiarino S, La Villa G et al. Cardiovascular effects of parathyroid hormone: a study in healthy subjects and normotensive patients with mild primary hyperparathyroidism. J Clin Endocrinol Metab 2000; 85:1815–1821.  Back to cited text no. 8
    
9.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart Jo 2015;16:233–271.  Back to cited text no. 9
    
10.
Hinkle DE, Wiersma W, Jurs SG. Applied statistics for the behavioral sciences. 5th edition. Boston, Massachusetts: Houghton Mifflin College Division; 2003.  Back to cited text no. 10
    
11.
Tonelli M, Karumanchi SA, Thadhani R. Epidemiology and mechanisms of uremia-related cardiovascular disease. Circulation 2016; 133:518–536.  Back to cited text no. 11
    
12.
Di Lullo L, Gorini A, Russo D, Santoboni A, Ronco C. Left ventricular hypertrophy in chronic kidney disease patients: from pathophysiology to treatment. Cardiorenal Med 2015; 5:254–266.  Back to cited text no. 12
    
13.
Di Lullo L, Floccari F, Polito P. Right ventricular diastolic function in dialysis patients could be affected by vascular access. Nephron Clin Pract 2011; 118:c257–c261.  Back to cited text no. 13
    
14.
Bhuriya R, Li S, Chen SC, McCullough PA, Bakris GL. Plasma parathyroid hormone level and prevalent cardiovascular disease in CKD stages 3 and 4: an analysis from the Kidney Early Evaluation Program (KEEP). Am J Kidney Dis 2009; 53:S3–S10.  Back to cited text no. 14
    
15.
Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006; 69:1945–1953.  Back to cited text no. 15
    
16.
Moe S, Drüeke T, Block G, Cannata-Andía J, Elder G, Fukagawa M et al. Kidney Disease: Improving Global Outcomes CKD-MBDWG: KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl 2009; 113:S1–S130.  Back to cited text no. 16
    
17.
Saleh FN, Schirmer H, Sundsfjord J, Jorde R. Parathyroid hormone and left ventricular hypertrophy. Eur Heart J 2003; 24:2054–2060.  Back to cited text no. 17
    
18.
Piovesan A, Molineri N, Casasso F, Emmolo I, Ugliengo G, Cesario F et al. Left ventricular hypertrophy in primary hyperparathyroidism. Effects of successful parathyroidectomy. Clin Endocrinol (Oxf) 1999; 50:321–328.  Back to cited text no. 18
    
19.
Thomas R, Kanso A, Sedor JR. Chronic kidney disease and its complications. Prim Care 2008; 35:329–344.  Back to cited text no. 19
    
20.
Parfrey PS, Lauve M, Latremouille-Viau D, Lefebvre P. Erythropoietin therapy and left ventricular mass index in CKD and ESRD patients: a meta-analysis. Clin J Am Soc Nephrol 2009; 4:755–762.  Back to cited text no. 20
    
21.
Mousavi SSB, Shahbazian H, Tamadon MR. Association of secondary hyperparathyroidism with anemia in patients with end-stage renal disease; a review on current knowledge. J Parathyroid Dis 2016; 4:48–53.  Back to cited text no. 21
    
22.
Al-Hilali N, Hussain N, Ataia A, Al-Azmi M, Al-Helal B, Johny K. Hypertension and hyperparathyroidism are associated with left ventricular hypertrophy in patients on hemodialysis. Indian J Nephrol 2009; 19:153–157.  Back to cited text no. 22
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23.
Çiçekçioğlu H, Ergün İ, Uçar Ö, Yüksel C, Azak A, Abayli E et al. Cardiac complications of secondary hyperparathyroidism in chronic hemodialysis patients. Turk J Med Sci 2011;41:789–794.  Back to cited text no. 23
    
24.
Randon RB, Rohde L, Comerlato L, Ribeiro JP, Manfro RC. The role of secondary hyperparathyroidism in left ventricular hypertrophy of patients under chronic hemodialysis. Braz J Med Biol Res 2005; 38:1409–1416.  Back to cited text no. 24
    
25.
Rasic S, Kulenovic I, Haracic A, Catovic A. Left ventricular hypertrophy and risk factors for its development in uraemic patients. Bosn J Basic Med Sci 2004; 4:34–40.  Back to cited text no. 25
    
26.
Ali T, Idrees MK, Akhtar SF. Left ventricular hypertrophy among predialysis chronic kidney disease patients: Sindh institute of urology and transplantation experience. Saudi J Kid Dis Transplant 2017; 28:1375.  Back to cited text no. 26
    
27.
Ahmed HA, Yassein YS, Elzorkany KM, Abouseriwa AT. Influence of secondary hyperparathyroidism on left ventricular function in maintenance hemodialysis patients. Menouf Med J 2019; 32:922.  Back to cited text no. 27
    
28.
Fujii H, Kim JI, Abe T, Umezu M, Fukagawa M. Relationship between parathyroid hormone and cardiac abnormalities in chronic dialysis patients. Intern Med 2007; 46:1507–1512.  Back to cited text no. 28
    



 
 
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