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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2020  |  Volume : 31  |  Issue : 5  |  Page : 927-936
Prevalence, Location, and Determinants of Valvular Calcifications in Congolese Patients on Chronic Hemodialysis: A Multicenter Cross-Sectional Study


1 Nephrology Unit, University Hospital of Kinshasa, Kinshasa, Democratic Republic of Congo
2 Cardiology Unit, University Hospital of Kinshasa, Kinshasa, Democratic Republic of Congo

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Date of Web Publication21-Nov-2020
 

   Abstract 


Valvular calcifications (VCs) are one of the major cardiovascular complications in patients on chronic hemodialysis (HD) due to its prevalence and predictive morbidity and mortality. The current study assessed the prevalence, location, and risk factors of VC among chronic HD Congolese patients in Kinshasa. This observational study involved three HD centers in Kinshasa between March and August 2016. Consecutive consenting adults on maintenance HD for at least six months were recruited. VCs were defined as a luminous echo on one or more cusps of the aortic or mitral valve. Risk factors of VC were determined by multivariate analysis. Sixty patients (mean age: 52.5 ± 15.9 years) were enrolled. The mean serum calcium and phosphorus were7.9 ± 1.3 mg/dL and 5.7 ± 1.7 mg/dL, respectively. VCs were encountered in 38% of the whole group in aortic and mitral valvular location in 64% and 23%, respectively. Hypertension, age >60 years, tobacco use, and hyperphosphatemia were independently associated with VC. Despite a young age of patients, VCs were a common finding and associated with both traditional and chronic kidney disease-specific risk factors.

How to cite this article:
Engole YM, Lubenga YN, Nlandu YM, R. Makulo JR, Mokoli VM, Kahindo CK, I. Mboliasa MF, Kadima EM, Longo AL, Nkodila A, Bukabau JB, Lepira FB, Nseka NM, Sumaili EK. Prevalence, Location, and Determinants of Valvular Calcifications in Congolese Patients on Chronic Hemodialysis: A Multicenter Cross-Sectional Study. Saudi J Kidney Dis Transpl 2020;31:927-36

How to cite this URL:
Engole YM, Lubenga YN, Nlandu YM, R. Makulo JR, Mokoli VM, Kahindo CK, I. Mboliasa MF, Kadima EM, Longo AL, Nkodila A, Bukabau JB, Lepira FB, Nseka NM, Sumaili EK. Prevalence, Location, and Determinants of Valvular Calcifications in Congolese Patients on Chronic Hemodialysis: A Multicenter Cross-Sectional Study. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2020 Dec 2];31:927-36. Available from: https://www.sjkdt.org/text.asp?2020/31/5/927/301199



   Introduction Top


Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in hemo-dialysis (HD). Mortality is 3 to 20 times higher than in the general population, due to many factors including the accelerated process of atherosclerosis, arteriosclerosis, arteriolosclerosis, and vascular calcifications in uremic patients.[1] HD is associated with an increased risk of CVD manifested in its subclinical phase as heart valvular calcifications (VCs).[2],[3] Indeed, it has been reported that heart VCs represent 38.4% of subclinical CVD in HD patients and are powerful predictors of CV morbidity and mortality.[4],[5] Pathogenetic pathways underlying VC in HD patients involve the interaction of both traditional (e.g., hypertension, diabetes, dyslipidemia, aging, and tobacco use) and uremia-specific risk factors (e.g., systemic inflammation, oxidative stress, protein-energy wasting, P-cresol, fetuin-A, osteopontin, osteoprotegerin, hyperphosphatemia, and high calcium × phosphorus product) resulting in vascular remodeling and accelerated atherosclerosis.[3],[4],[5],[6],[7],[8] Vascular complications may have different locations and types and include intimal artery calcification or medial artery calcification, cardiac valve calcification, calciphylaxis, and tumor calcinosis.[9] Therefore, early detection of VC and control of their underlying risk factors could help preventing or postponing the progression of accelerated atherosclerosis seen in HD patients. Echocardiography is a sensitive and specific method for the detection of VC.[10]

In the Democratic Republic of the Congo, the prevalence of chronic kidney disease in adult people is estimated to be 12%, with 0.2% of patients having end-stage renal disease (ESRD) requiring renal replacement therapy.[11] For 10 years, the activity of HD is growing in Kinshasa, the capital city, and associated with substantial mortality mainly of CV origin, with stroke and heart failure being the main underlying causes.[12] This observation highlights the need for identifying HD at increased risk for CVD, and early detection of VC can serve this purpose. Therefore, the aim of the present study was to assess the prevalence and location of VC as well as associated risk factors among Congolese chronic HD patients.


   Methods Top


We conducted a multicenter, descriptive, and analytical cross-sectional study including adult patients who are undergoing chronic HD three times a week for at least six months at the three HD centers (Kinshasa University Hospital, Ngaliema Medical Center, and Afia Medical Center) and performed Doppler transthoracic echocardiography between March and August 2016. For each patient, we analyzed demographic, clinical, biological data related to HD and echocardiography. Clinical data were retrieved from patients’ records and included age, sex, initial nephropathy, systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP). Data related to HD were vascular access, duration of HD (in months), interdialytic weight gain, and dialysis dose measured using Kt/V urea. Biological parameters were as follows: serum calcium, phosphorous, phosphorus-calcium product, urea, creatinine, uric acid, cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, triglycerides, hemoglobin, hematocrit, C-reactive protein (CRP), and 24-h proteinuria. For each of these parameters, the annual average value was calculated. HD was performed with acid concentrate (containing Na, K, Ca++, Mg++, glucose, etc.) and standard bicarbonate at least a week for 4 h. The dialysis dose was adequate for a weekly Kt/v urea value of ≥1.4. The dialysis schedule alternated conventional HD with hemodiafiltration using high-flux dialyzers. Doppler transthoracic echocardiography was performed 24h after the mid-week HD session using a VIVID 7 ultrasound system equipped with a 3.5 Hz transducer (General Electric, Boston, USA). All cardiac ultrasounds were performed by a unique cardiologist. This examination allowed to detect VC in cardiac valves, with continuous Doppler wave in large and minor axis parasternal incidence. The calcified heart valve was seen as a luminous echo of more than 1 mm on 1 or more cusps of the aortic or mitral valve.[13] We defined some conditions as follows: diabetes which had been diagnosed during past patient visits or concomitant use of antidiabetic medications,[14] hypertension (HTN), blood pressure ≥140/90 mm Hg in three successive samples in sitting position and after interval of 5 min between two consecutive measurements or current use of antihypertensive drugs,[15] dyslipidemia with total cholesterol >200 mg/dL, LDL >110 mg/dL, HDL <40 mg/dL, and triglycerides >150 mg/dL.[16]

The statistical analysis was carried out using IBM SSPS Statistics version 21.0 (IBM Corp., Armonk, NY, USA). Quantitative variables were expressed as mean ± standard deviation and qualitative variables as a percentage. Student's t-test and Chi-square were used to compare quantitative and qualitative variables, respectively. The determinants of VC in HD patients were identified using univariate and multivariate stepwise logistic regression analysis.

The study protocol was approved by the Clinical Research Ethics Committee of Kinshasa School of Public (number ESP/CE/ 013/2016).


   Results Top


Sixty patients (males: 71.6%) participated in the study. Their mean age and duration of HD were 52.5 ± 15.9 years (range: 18–82 years) and 15.1 ± 3.7 months, respectively. The mean SBP, DBP, and PP were156.6 ± 15.7 mm Hg, 86.8 ± 14.5 mm Hg, and 69.7 ± 15.6 mm Hg, respectively [Table 1]. The main causes of ESRD were diabetic nephropathy (35%), nephro-angiosclerosis (30%), and chronic glomerulonephritis (25%). Biochemical values are shown in [Table 2]. The mean serum calcium, phosphate, and phosphorus–calcium product levels were7.9 ± 1.3 mg/dL, 5.7 ± 1.7 mg/dL, and 44.7 ± 14.1 mg2/dL2, respectively. Only 6% of patients were taking phosphorus chelators and 37% received Vitamin D+ calcium carbonate. Only one patient in this study was receiving an antivitamin K. The anti-hypertensive drugs used were the following: calcium channel blockers (69%), angiotensin-converting enzyme inhibitors (29%), diuretics (22%), β-blockers (17%), and angiotensin receptor antagonists (10%). The antidiabetic agents included insulin (10%) and oral anti-diabetic agents (4%). The mean serum albumin, CRP, and total cholesterol were 35.9 ± 5.4 g/L, 12.5 (8–19) mg/L, and 176.9 ± 34.4 mg/dL, respectively. There was no significant difference for echocardiographic parameters between men and women except E / A which was higher in males (1.01 ± 0.6) vs (1.6 ± 1.2), P = 0.026) [Table 3].
Table 1: Clinical characteristics of the study population by sex.

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Table 2: Biological characteristics of the study population by sex.

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Table 3: Echocardiographic parameters of the study population by sex.

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VCs were encountered in 23 patients (38%) encompassing aortic (64%) and mitral (23%) valvular location [Figure 1]. Compared to patients without VC [Table 4], those having VC had a significantly higher proportion of participants aged >60 years (70% vs. 22%, P <0.0001) and, on average, a significantly higher PP (77.4 ± 15.2 vs. 64.9 ± 13.9 mm Hg, P <0.002), phosphate (6.5 ± 1.8 vs. 5.2 ± 1.5 mg%, P <0.005), and phosphorus–calcium product (41.7 ± 14.7 vs. 49.6 ± 11.9 mg2/dL2, P <0.035) levels. In contrast, their DBP (80.5 ± 13.0 vs. 90.7 ± 14.1 mm Hg, P <0.007) was significantly lower.
Figure 1: Location of valvular calcifications in the study populations.

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Table 4: General characteristics of the study population according to vascular calcifications status.

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[Table 5] shows that HTN [adjusted odds ratio (OR): 4; 95% confidence interval (CI) (1.24–15.7)], age >60 years [adjusted OR: 4; 95% CI (1.67–30.10)], tobacco use [adjusted OR: 5, 95% CI (1.15–13.36)], and phosphatemia [aOR to 2; 95% CI (1.83-5.65)] were independently associated with VCs.
Table 5: Uni- and multivariate factors associated with vascular calcifications using logistic regression analysis.

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   Discussion Top


The main findings of the present cross-sectional study are as follows: first, VC with mainly aortic and mitral location was a common finding in the present case series; second, traditional (mainly aging, tobacco use, and HTN) and uremia specific (phosphatemia) were both the main factors associated with VC. In the present study, VCs were seen in nearly four out of 10 HD patients. This frequency is within the range of VC prevalence reported in the literature.[17] It is somewhat higher than that of 14%–92% reported by several previous studies (Kaze et al,[18] Benamar et al,[1] Sayarlioglu et al,[19] Ezziani et al,[20] Ellouali et al,[21] Rosa-Diez et al,[22] Mihailescue,[23] Braun,[10] and Renaud).[17] This discrepancy can be justified by the low use of phosphorus chelators and the abusive use of Vitamin D + calcium carbonate without proper control of monitoring parameters. The dialysis itself may represent a certain risk with the occurrence of a metabolic alkalosis at each session of HD, which can promote the precipitation of calcium salts, decreasing the solubility of calcium in the extracellular space.[24] The use of calcium carbonate as a phosphorus chelator, combined with three standard dialysis sessions, which are insufficient to completely eliminate dietary phosphorus intake, contributes to calcification.[25] This value is, however, lower than 46% and 50% found by Selcoki et al in Turkey[26] and Sanchez-Perales et al in Spain, respectively.[27] In the present study, aortic and mitral valves were the most frequent location of VC, with aortic valve being mainly involved. Our finding agrees with previous reports by Cisse (aortic 10.5% vs. mitral 5.75%) and Rekik (aortic 52% vs. mitral 44.5%), who reported a higher frequency of aortic versus mitral VC.[28],[29] Indeed, aortic VC is the most common valvular abnormality in the general population as well as in patients on HD.[19] Aortic valves are submitted to cyclic mechanical stress related to pressure gradients and turbulent blood flow resulting from the high acceleration rate and peak velocity when blood flows through the aortic valve. Over the lifespan, the repetitive mechanical stress causes fatigue and re-arrangement of bio-elastomers, leading to microfractures in the biomaterials ultimately resulting in fibrosis and calcification.[30] Aortic stenosis was more common in calcified patients with a statistically significant difference, thus supporting Urena's et al study.[31] However, it is in disagreement with previous reports by Hayrire (aortic 21.7% vs. mitral 23.3%) and Sanchez (aortic 7.8% vs. mitral 15.2%) of a lower frequency of aortic versus mitral VC.[19],[27] Similar frequency of aortic and mitral VC (aortic 41.2% and mitral 41.2%) was reported by Samia.[32] The disparity between studies in VC frequency and location could be in part explained by the clinical profile of patients, their therapeutic background, the duration and type of HD as well as the definition used to define VC.[19] VC is potentially dangerous because of association with valvular dysfunction, myocardial ischemia, conduction defects, infectious endocarditis, and heart failure.[33] Calcification-related stiffness of vessels and valves reduce their compliance, contributing to left ventricular hypertrophy and increasing all-cause mortality.[34]

In the present study, traditional (aging, tobacco use, and HTN) as well as uremic-specific (hyperphosphatemia) risk factors were both associated with VC. Indeed, aging process is a well-known vascular risk factor through associated-insulin resistance and subsequent clustering of multiple risk factors to vascular wall remodeling.[35] HTN is an important risk factor for atherosclerosis, and its association with cardiac VC in HD patients has been already reported.[10],[26],[36] Tobacco use may induce vascular remodeling and subsequent atherosclerosis through oxidative stress and subsequent inflammation, activation of sympathetic nervous system, and renin–angiotensin system.[37] Frequent HTN in HD promotes phosphorus–calcium deposits in the tissues. The shear forces generated by arterial HTN are capable of inducing the synthesis of TGF-β1 by the vascular endothelium, which promotes the excessive elaboration of extracellular vascular matrix and the occurrence of calcifications.[38] Diabetes mellitus, the main nephropathy in our study, is known as a risk factor for valvular calcifications. A recent study has shown that hyperglycemia reduces the binding of Vitamin D to its receptor, which could interfere with osteocalcin synthesis and thus increase the risk of soft-tissue calcification.[39] As reported by Raggi et al,[40] Qunibi et al, and Kahnooj et al,[41],[42] our study found an association between a high phosphorus–calcium product and the occurrence of cardiac VC. In addition, hyperphosphatemia has been reported to be associated with the development of vascular calcifications and is a factor favoring cardiac fibrosis.[43] Indeed, observational studies in HD patients found a statistically significant increase in the risk of cardiovascular and all-cause mortality with a phosphorus level >6.5 to 6.6 mg/dL.[44]


   Limitations Top


Our study has some limitations that must be acknowledged. First, the limitation of the study to only three centers of HD leads to a selection bias and does not allow the generalization of our findings to all hypertensive people. Second, the cross-sectional design of our study precludes the establishment of any causal relationship. Third, the small sample size does not give enough power to statistical tests to detect potential associations. Fourth, VCs were assessed using echocardiography, a tool less sensitive than electron beam computed tomography, and do not allow precise quantitation of calcium deposited on the cardiac valves.[10] Fifth, VCs were assessed by only one investigator with subsequent risk of under or overestimation of measured values.


   Conclusion Top


Despite a relatively young age of patients, the prevalence of VC in Congolese HD patients remains high due to the traditional risk factors and HD session. Those factors may be preventable by moderate changes in diet, lifestyle, and adequate HD.

Conflict of interest: None declared.



 
   References Top

1.
Benamar L, Rhou H, Guerraoui MH, et al. Cardiovascular Calcifications in Chronic Hemodialysis: Prevalence and risk factors. Nephrology 2003;24:143-7  Back to cited text no. 1
    
2.
Rufino M, García S, Jiménez A, et al. Heart valve calcification and calcium x phosphorus product in hemodialysis patients: Analysis of optimum values for its prevention. Kidney Int Suppl 2003;63 Suppl 85:S115-8.  Back to cited text no. 2
    
3.
Simindokht M, Seyedehsara B, Mohsenikiac M, Najibpourb A. The Association of Calcium-Phosphorus Product With Cardiac Values Failure in Patients Under Chronic Hemodialysis Cardiol Res 2016;7:80-3.  Back to cited text no. 3
    
4.
Ribeiro S, Ramos A, Brandão A, et al. Cardiac valve calcification in haemodialysis patients: Role of calcium-phosphate metabolism. Nephrol Dial Transplant 1998;13:2037-40.  Back to cited text no. 4
    
5.
Goldsmith DJ, Covic A, Sambrook PA, Ackrill P. Vascular calcification in long-term hemo-dialysis patients in a single unit: A retrospective analysis. Nephron 1997;77:37-4.  Back to cited text no. 5
    
6.
Goodman WG, Goldin J, Kuizon BD, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med 2000;342: 1478-83.  Back to cited text no. 6
    
7.
Renaud H, Atik A, Hervé M, et al. Evaluation of vascular calcinosis risk factors in patients on chronic hemodialysis: Lack of influence of calcium carbonate. Nephron 1988;48:28-32.  Back to cited text no. 7
    
8.
Stenvinkel P, Carrero JJ, Axelsson J, Lindholm B, Heimburger O, Massy Z, Emerging biomarkers for evaluating cardiovascular risk in the chronic kidney disease patient: How do nez pieces fit into the uremic puzzle? Clin J Am Soc Nephrol 2008;3:505-21.  Back to cited text no. 8
    
9.
Wang AY, Woo J, Wang M, et al. Association of inflammation and malnutrition with cardiac valve calcification in continuous ambulatory peritoneal dialysis patients. J Am Soc Nephrol 2001;12:1927-36.  Back to cited text no. 9
    
10.
Braun J, Oldendorf M, Moshage W, Heidler R, Zeitler E, Luft FC. Electron beam computed tomography in the evaluation of cardiac calcification in chronic dialysis patients. Am J Kidney Dis 1996;27:394-401.  Back to cited text no. 10
    
11.
Sumaili EK, Krzesinski JM, Cohen EP, Nseka NM. Epidemiology of chronic kidney disease in the democratic republic of Congo: Review of cross-sectional studies from Kinshasa, the capital. Nephrol Ther 2010;6:232-9.  Back to cited text no. 11
    
12.
Nlandu Y, Lepira F, Makulo JR, et al. Reverse epidemiology of elevated blood pressure among chronic hemodialysis black patients with stroke: A historical cohort study. BMC Nephrol 2017;18:277.  Back to cited text no. 12
    
13.
Panuccio V, Tripepi R, Tripepi G, et al. Heart valve calcifications, survival, and cardiovascular risk in hemodialysis patients. Am J Kidney Dis 2004;43:479-84.  Back to cited text no. 13
    
14.
Grimaldi A. Treatise on diabetology, Medecine-Sciences. 1999-2000;114-39.  Back to cited text no. 14
    
15.
Gee ME, Campbell N, Sarrafzadegan N, et al. Standards for the uniform reporting of hypertension in adults using population survey data: Recommendations from the world hypertension league expert committee. J Clin Hypertens (Greenwich) 2014; 16:773-81.  Back to cited text no. 15
    
16.
Junquero D, Rival Y. Metabolic syndrome: what definition for which treatment? Medecines-Sciences 2005;21:1045-53.  Back to cited text no. 16
    
17.
Rojas-Campos E, Herrera-Llamas R, Montañez-Fernández JL, et al. Vascular calcification in Mexican hemodialysis patients. Arch Med Res 2013;44:628-32.  Back to cited text no. 17
    
18.
Kaze FF, Kengne AP, Aboubakar Djalloh AM, et al. Pattern and correlates of cardiac lesions in a group of Subsaharan African patients on maintenance hemodialysis. Pan Afr Med J 2014;17:3.  Back to cited text no. 18
    
19.
Sayarlioglu H, Acar G, Sahin M, et al. Prevalence and risk factors of valvular calcification in hemodialysis patients. Iran J Kidney Dis 2013;7:129-34.  Back to cited text no. 19
    
20.
Ezziani M, Najdi A, Mikou S, et al. Echocardiographic abnormalities in chronic hemodialysis patients: Prevalence and risk factors. Pan Afr Med J 2014;18:216.  Back to cited text no. 20
    
21.
Ellouali F, Berkchi F, Elhoussni S, et al. Evaluation of the effect of duration on dialysis on echocardiographic parameters: A preliminary study. Saudi J Kidney Dis Transpl 2015; 26:83-9.  Back to cited text no. 21
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22.
Rosa-Diez G, Bratti G, Filannino G, et al. Prevalence of factors related to vascular calcifications in patients with chronic kidney disease on dialysis. Medicina (B Aires) 2017; 77:207-13.  Back to cited text no. 22
    
23.
Mihailescu D, Velciov S. Features of phosphocalcic metabolism disorders in patients undergoing dialysis at a hemodialysis center located in West-Romania. J Exp Med Surg Res 2010;3:175-82.  Back to cited text no. 23
    
24.
Bosticardo G, Malberti F, Basile C, et al. Optimizing the dialysate calcium concentration in bicarbonate hemodialysis. Nephrol Dial Transplant 2012;27:2489-96.  Back to cited text no. 24
    
25.
Chen NC, Hsu CY, Chen CL. The strategy to prevent and regress the vascular calcification in dialysis patients. Biomed Res Int 2017; 2017:9035193.  Back to cited text no. 25
    
26.
Selcoki Y, Turgut F, Kanbay M, et al. Cardiac valve calcifications and predictive parameters in hemodialysis patients. CEJ Med 2007;2(3): 304-12.  Back to cited text no. 26
    
27.
Sanchez-Perales C, Ruiz de Castrovejo EV, Garcia-Cortes MJ, et al. Valvular calcifications at the start of dialysis predict the onset of cardiovascular events in the course of follow up. Nephrologia 2015;35:157-63.  Back to cited text no. 27
    
28.
Moustapha CM, Tall LA, Maria F, et al. Evaluation of cardiac complications among chronic hemodialysis in Dakar. Pan Afr Med J 2016;23:43.  Back to cited text no. 28
    
29.
Rekik H, Abid L, Abid D, et al. Valvular calcifications: Prevalence and predictive factors. 2012;5:26-9.  Back to cited text no. 29
    
30.
London GM, Pannier B, Marchais SJ, Guerin AP. Calcification of the aortic valve in the dialyzed patient. J Am Soc Nephrol 2000;11: 778-83.  Back to cited text no. 30
    
31.
Urena P, Malergue MC, Goldfarb B, Prieur P, Guedon Rapoud C, Petrover M. Evolutionary aortic stenosis in hemodialysis patients: Analysis of risk factors. Nephrology 1999; 20:217-25.  Back to cited text no. 31
    
32.
Faqih SA, Noto-Kadou-Kaza B, Abouamrane LM, et al. Valvular calcifications in a patient on hemodialysis in Morocco. Pan Afr Med J 2016;24:115.  Back to cited text no. 32
    
33.
Mazzaferro S, Coen G, Bandini S, et al. Role of aging, chronic renal failure and dialysis in the calcification of mitral annulus. Nephrol Dial Transpl 1993;8(4):335-40.  Back to cited text no. 33
    
34.
Demer LL, TintutY. Vascular calcification: Pathobiology of a multifaceted disease. Circulation 2008;117:2938-48.  Back to cited text no. 34
    
35.
Jonk AM, Houben AJM, Jongh RT, Serné EH, Schaper, NC, Stehouwer CD. Microvascular dysfunction in obesity: A potential mechanism in the pathogenesis of obesity-associated insulin resistance and hypertension, Physiopathology 2007;22:252-60.  Back to cited text no. 35
    
36.
Torun D, Sezer S, BaltaliM, et al. Association of cardiac valve calcification and inflammation in patients on hemodialysis. Ren Fail 2005; 27:221-6.  Back to cited text no. 36
    
37.
Middlekauff HR, Park J, Moheimani RS. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: Mechanisms and implications for cardiovascular risk. J Am Coll Cardiol 2014; 64:1740-50.  Back to cited text no. 37
    
38.
Megnien JL, SimonA, Lemariey M, Plainfossé MC, LevensonJ. Hypertension promotes coronary calcium deposit in asymptomatic men. Hypertension 1996;27:949-54.  Back to cited text no. 38
    
39.
Patel SR, Xu Y, Koenig RJ, Hsu CH. Effect of glucose on the function of the calcitriol receptor and vitamin D metabolism. Kidney Int 1997;52:79-86.  Back to cited text no. 39
    
40.
Raggi P, Boulay A, Chasan-Taber S, et al. Cardiac calcification in adult hemodialysis patients. A link between end-stage renal disease and cardiovascular disease? J Am Coll Cardiol 2002;39:695-701.  Back to cited text no. 40
    
41.
Qunibi WY, Nolan CA, Ayus JC. Cardiovascular calcification in patients with end-stage renal disease: A century-old phenomenon. Kidney Int Suppl 2002;82:S73-80.  Back to cited text no. 41
    
42.
Kahnooj M, Masoomi M, Naderinasab A, Zaeem A, Sheikhvatan M. Relationship between calcium-phosphorus product and severity of valvular heart insufficiency in patients undergoing chronic hemodialysis. J Tehran Heart Cent 2010;5:78-82.  Back to cited text no. 42
    
43.
Torres PU. Calcimimetics: Physiology, results of preclinical and clinical studies, and perspectives. Nephrol Ther 2011;7:99-104.  Back to cited text no. 43
    
44.
Brunet P. Chronic Renal Insufficiency: From bone disease to bone and vascular disease. Med Nucl 2009;33:33-3831.  Back to cited text no. 44
    

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Correspondence Address:
Yannick M Engole
Nephrology Unit, University Hospital of Kinshasa, Kinshasa
Democratic Republic of Congo
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DOI: 10.4103/1319-2442.301199

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