Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 683 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 

Table of Contents   
ORIGINAL ARTICLE  
Year : 2021  |  Volume : 32  |  Issue : 1  |  Page : 92-100
Prevalence of Cardiac Abnormalities in Children with Chronic Kidney Disease: A Cross-sectional Study from a Developing Country


1 Department of Pediatric Nephrology, Sindh Institute of Urology and Transplantation, Karachi, Pakistan
2 Department of Cardiology, Sindh Institute of Urology and Transplantation, Karachi, Pakistan

Click here for correspondence address and email

Date of Web Publication16-Jun-2021
 

   Abstract 


Improved therapeutic modalities in chronic kidney diseases (CKD) children and consequent extension of life expectancy, draws more attention towards secondary complications. Cardiovascular adaptations precipitating such terminal events, begin in pre-dialysis CKD. Hence, it’s imperative to identify modifiable risk factors to direct care and resources in haltering CKD progression, evade long-term dialysis and anticipate kidney transplantation to avert cardiac complications in predialysis period. One hundred and six pre-dialysis patients aged one year to 15 years, with estimated glomerular filtration rate of <90 mL/min/1.73 m2 and proteinuria were included. Patient’s history, weight, height and blood pressures (BPs) performed. Left ventricular mass index (LVMI) calculated to correct for patient height to determine raised values of >38.6 g/m2.7 and of left ventricular hypertrophy (LVH) >55 g/m2.7. Shortening fraction and ejection fraction measured to assess systolic function. Diastolic function assessed by Doppler measuring the mitral inflow (e/a) ratio. Hemoglobin, calcium phosphorous product, parathyroid hormone and hypertension measured to assess cardiac risk factor. The total prevalence of cardiac abnormality was found in 66.9% (95% confidence interval [CI] 57.6%–75.2%. Raised LVMI was seen in 64%, among which 34.9% had LVH. Diastolic and systolic dysfunction was found in 12.2% and 11.3% respectively. The cardiac abnormality was more prevalent in CKD grade IV and V. The independent risk factors were anemia and abnormal diastolic BP index which increase the risk for LVH by 3-fold and 5-fold respectively. Proportion of cardiac abnormalities were more prevalent in CKD IV and V. Anemia and diastolic hypertension were independent risk factors for LVH.

How to cite this article:
Ehsan A, Aziz M, Lanewala AA, Mehmood A, Hashmi S. Prevalence of Cardiac Abnormalities in Children with Chronic Kidney Disease: A Cross-sectional Study from a Developing Country. Saudi J Kidney Dis Transpl 2021;32:92-100

How to cite this URL:
Ehsan A, Aziz M, Lanewala AA, Mehmood A, Hashmi S. Prevalence of Cardiac Abnormalities in Children with Chronic Kidney Disease: A Cross-sectional Study from a Developing Country. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2021 Nov 30];32:92-100. Available from: https://www.sjkdt.org/text.asp?2021/32/1/92/318553



   Introduction Top


The association between chronic kidney disease (CKD) and cardiovascular disease (CVD) follow a dose-response relationship. There is a 3 to 30-fold higher risk of mortality in CKD patients which is approximately 15 times higher than the general population.[1],[2],[3]

In 1998, the National Kidney Foundation Task Force on CVD declared an epidemic of cardiac disease in end stage renal disease patients and later raised questions regarding pediatric age group. Parekh et al used the United States Renal Data System database to evaluate the risk of cardiac death in children and young adults (aged 0–30 years) in 2002 and recorded 23% cardiac disease specific mortality in six years.[4]

CKD risk factors like anemia, fluid retention and hypertension increase cardiac preload whereas deregulated metabolism of calcium/ phosphate, inflammation raises the after load. As a result, left ventricle increases its output which progressively leads to hypertrophy, systolic and diastolic dysfunction. Diastolic dysfunction usually appears earlier than systolic dysfunction.[5] Left ventricular hypertrophy (LVH) can develop even with mild CKD and is known to progress with overall prevalence of up to 17%.[6] Literature revealed that masked hypertension is present in 25% of patients with stage 2–4 CKD, and that the presence of masked hypertension is associated with a two-fold increase in frequency of LVH at time of initial examination.[7]

Elevated parathyroid hormone (PTH) and calcium phosphorous product (Ca×P) might contribute to progression of LVH in children with stage 2–4 CKD. Risk factors for diastolic and systolic dysfunction specific to CKD include blood pressure (BP), anemia and inflammatory state while systolic dysfunction, oxidative stress and electrolyte imbalance.[8] The level of urinary protein excretion is independently and significantly associated with left ventricular mass in patients with CKD. This relationship is independent of BP.[9]

Although most pediatric studies evaluating CKD associated CVD are cross-sectional and include few patients, it is well established that cardiovascular alterations begin in predialysis era and these subtle changes can be detected by sensitive diagnostic methods. This study is aimed to assess the extent of the problem in predialysis period. To the best of our knowledge and literature search there has been no data available in Pakistan pertaining to this subject. Belonging to a resource poor country, we are required to identify the modifiable risk factors of CVD (such as anemia, hypertension, abnormal calcium and phosphate metabolism, secondary hyperparathyroidism and proteinuria) at the earliest, with the notion to direct resources using a targeted approach.


   Materials and Methods Top


This prospective observational study took place at Sindh Institute of Urology and Transplantation Karachi, Pakistan from March 2018 to February 2019. Native ethical review board approval was acquired before starting the study (Reference no. SIUT-ERC-2018/A-121).

Sample size calculation was based on assumption that 15.7% of subjects in the population have the factor of interest based on a previous study.[4] Thus, the study required a sample size of 106 for estimating the expected proportion with 7% absolute precision and 95% confidence.

Patients aged between one year and 15 years diagnosed as CKD were recruited in their pre dialysis period. CKD was classified on basis of cause, estimated glomerular filtration rate (eGFR) <90 mL/min/1.73 m2 (I-V) and albuminuria, based on Kidney Disease: Improving Global Outcomes (KDIGO) 2017 CKD–mineral and bone disorder guidelines.[10] After obtaining informed consent the history was taken and physical examination was performed (weight, height and blood pressure percentiles). The average BP obtained via three clinical visits was divided by the 95th percentile for the corresponding gender, age and height percentile to determine the systolic and diastolic blood pressure indices (SBPI and DBPI). The BP index <1 is considered as controlled hypertension.[11]

The cardiac abnormalities included abnormal/ raised left ventricular mass index (LVMI), LVH, systolic dysfunction and diastolic dysfunction. LVM calculated using measurements obtained by two-dimensional echocardiography. LVMI was calculated to correct for patient height by using formula: LVMI = LV mass/height2.7 (value of 38.6 g/m2.7 denotes 95th percentile). Raised LVMI refers to values >38.6 g/m2.7 while LVH is defined as LVMI >55 g/m2.7.[11],[12] Systolic dysfunction denoted by shortening fraction (SF) and ejection fraction (EF) was measured using M-mode echocardiography. The EF was considered normal if >55% and SF >25%. Diastolic function was assessed by Doppler, measuring the mitral inflow (e/a) which is the ratio between early (e; passive ventricular filling) and late (a; active atrial contraction) diastolic flow velocities. Diastolic function was considered normal when the E/A ratio ranged between 0.9 and 1.5, abnormal with a delayed relaxation pattern when the E/A ratio was <0.9 and restrictive when E/A ratio was >2.[5]

Laboratory investigation included renal function tests, electrolytes, hemoglobin, calcium, phosphorous and parathyroid hormone (iPTH). To analyze a relationship of biochemical abnormality leading to LVH the parameters like hemoglobin, calcium and phosphorous, time-averaged was calculated to assess the time integrated burden instead of a single random value. This avoided the inaccuracy of comparing raw data. Guidelines from KDIGO 2017 CKD and National Kidney Foundation Kidney Disease Outcomes Quality Initiative were used to acquire all normal and abnormal reference range values to define CKD grades (I-V), anemia (<10.5 g/dL), abnormal Cap (>55 mg2/dL2), raised iPTH (>88 pg/mL).[13],[14]


   Statistical Methods Top


Data were entered and analyzed by IBM SPSS Statistics version 20.0 (IBM Corp., Armonk, NY, USA). Categorical variables were presented in terms of frequencies and percentages. Mean and standard deviation was computed for normal continuous variables while median with interquartile range was taken for skewed continuous variables. Normality of data was checked by Shapiro-Wilk test using P = 0.05 as significant difference value. To observe difference between more than two groups, One-way Anova was applied for normally distributed continuous variables (age), while Kruskal–Wallis test was used for asymmetric continuous variables. To measure the association of risk factors of cardiac abnormalities univariate and multivariate analysis was performed. For univariate analysis Chi-square test was performed, P <0.005 was considered significant. Multivariate analysis was done by multi-nominal logistic regression, odds ratio (OR) was calculated for independent risk factors.


   Results Top


A total of 106 CKD patients were included in the study out of which 64 (60%) were males. The mean age was 10.5 ± 3.4 years. CKD stage III accounted for 19 (18%), 34 (32%) had stage IV and 53 (50%) had stage V CKD. The underlying renal diseases were: small sized kidneys 28 (26%), glomerular diseases 23 (21%), obstructive uropathy 14 (13.2%), bladder outflow obstruction 17 (16%) solitary functioning kidney 15 (14%) and reflux disease 5 (5%). The demographic and clinical characteristic details are described in [Table 1].
Table 1: Baseline demographics and clinical characteristics.

Click here to view


The total prevalence of cardiac abnormality was found in 66.9% [95% confidence interval (CI) 57.6%–75.2%] patients. The echocardiographic findings showed that among all CKD grades, the total number of patients with raised LVMI were 68 (64%). Patients with LVH were 37 (34.9%). Diastolic dysfunction was found in 13 (12.2%) patients while systolic dysfunction in 12 (11.3%) patients [Table 2]. Cardiac abnormalities were seen more in CKD stage IV and V as compared to IIIa and IIIb. The prevalence of raised LVMI in each CKD group is shown in [Table 2] which tends to increase with the progressing stage of CKD and is also statistically significant among CKD groups (P = 0.02). LVH was found as a prominent CVD abnormality in CKD V 26 (49%) followed by CKD IV 10 (29.4%) thus showing a statistically significant inverse relationship to eGFR (P = 0.001). However, systolic dysfunction was observed more in CKD Stage V than Stage IV (11.7% vs. 15%) but statistically not significant. Diastolic dysfunction was comparatively more prevalent in CKD IV than V (17.6% vs. 13.2%) but of no statistically significant value among CKD groups, (17.6% vs. 13.2%) [Table 2]. Among patients with LVH, 29.7% (P <0.001) had systolic dysfunction and 13.5% (P <0.001) had diastolic dysfunction.
Table 2: Cardiac parameters according to chronic kidney disease grades.

Click here to view


Among the risk factors of cardiac abnormalities, anemia and abnormal DBPI was associated with raised LVMI and LVH and was also statistically significant (P = 0.05, 0.01) on univariate analysis. However, no risk factors were associated with systolic and diastolic dysfunction [Table 3].
Table 3: Correlation of cardiac abnormalities with risk factors.

Click here to view


On multivariate analysis, the independent risk factors for raised LVMI and LVH were anemia and abnormal DBPI. Raised LVMI was three times higher in patients with anemia [OR=3.02 CI (1.07–8.5) P = 0.03] as compared to normal LVMI. Similarly, LVH is 3.5 times higher in patients with anemia [OR = 3.5 CI (1.2–9.8) P = 0.02] as compared to normal LVMI. Whereas, LVH is five times more in patients with abnormal DBPI [OR=5.08 CI (1.6–16.1) P = 0.006] as compared to normal LVMI, but there was no association of abnormal DBPI with raised LVMI as compared to normal LVMI [Table 4].
Table 4: Multivariate analysis for independent risk factors of cardiovascular disease.

Click here to view



   Discussion Top


We found quite a high proportion of cardiac abnormalities in our study population (66.9%) indicating compromised cardiac function in pre-dialysis period. Among cardiac abnormalities raised LVMI was observed in 64% children and LVH was documented in 34.9%. LVH is frequently reported in CKD children starting in the early stages. Mencarelli et al reported almost the same percentage (38%) of ventricular hypertrophy with deteriorating renal functions.[5] We found LVH more frequently present in higher CKD grades (5.9%–49.1% in III and V respectively) owing to its association with the ongoing uremic milieu with declining eGFR. Similarly, there has been a single-center experience of Chavers and Herzog, reporting an LVH prevalence of 20% in CKD stage II and 70% in CKD stage V patients.[15] This prevalence is also known to increase to 80% in dialysis patients.[16] There is still a dearth of global multicenter evidence of the cardiac abnormalities associated with CKD and its risk factors. The baseline data of the largest ongoing multicenter longitudinal study the CKD (the 4C study), suggests that the prevalence of LVH was higher with each CKD stage, from 10.6% in CKD III to 48% in CKD V. This is quite comparable with our observation of LVH in 5.9%–49.1% in CKD III through V respectively.[17]

In a prospective longitudinal study in children with CKD (n = 31), eventually, 32% children with initially normal LVM developed LVH at a two year follow-up and at the initiation of dialysis 69%–82% of patients had LVH.[18] We found 45.6% of patients to have raised LVMI alone and this subclinical dysfunction poses a great risk for cardiac morbidity during dialysis and warrants timely recognition. This also leaves us with a dire need to follow these patients to the dialysis initiation period and determine the percentage of conversion rates of this subtle abnormality to complete ventricular hypertrophy and dysfunction. There is a clear void incomparable data of cardiac abnormalities in CKD children in our region. However, Ali et al reported 56.3% LVH in adult CKD patients compared to 34.9% of our pediatric study population. This high percentage owes to the additional risk factors, for example, (smoking, diabetes, hypertension and dyslipidemia) most prevalent in adults.[19]

Evaluation of cardiac function has directed the clinician’s attention to diastolic dysfunction which precedes systolic dysfunction. Johnstone et al[20] suggest an increase incidence of diastolic dysfunction in dialysis patients with LVH and a reversal of this abnormality in the transplanted patients however the clinical significance of diastolic dysfunction in pediatric patients is not certain and longitudinal studies are required to assess the effect of this dysfunction on cardiac morbidity. They found that none of the CKD patients had e/a ratio <1 but an increase in A wave velocity was found in all CKD and peritoneal dialysis groups (which in turn is supposed to cause reduction in e/a ratio). We found only one patient each in CKD grade IV and V (2.9% vs. 1.9%, CKD) with delayed relaxation pattern of diastolic dysfunction and none of the patients with normal e/a ratio had peaked A wave. This low prevalence may be due to the method we used to measure mitral inflow. Recent studies focused on the use of TDI indices in comparison to e/a ratio which is less load dependent and more accurate measure of diastolic function. Hence recent studies documented diastolic dysfunction in CKD patients employing this method.[21],[22] For future studies it is important to imply this method for the detection of diastolic dysfunction.

In our patients with LVH, 29.7% had systolic dysfunction and 13.5% had diastolic dysfunction. Studies suggest an increase incidence of diastolic dysfunction in dialysis patients with LVH and a reversal of this abnormality in the transplanted patients. We did not find a significant systolic dysfunction in our patients supporting the known fact that systolic LV function in children with CKD is usually preserved.[20] Weaver et al[23] assessed subclinical systolic dysfunction in children by (n = 57) by measuring the mid-wall SF (mwSF) instead of conventional measurement of shortening fraction (eSF). There were no differences in mwSF when control subjects were compared with patients with CKD stages II to IV. However, the patients undergoing dialysis had significantly reduced mwSF. It is also postulated that the measurement of eSF may be confounded by LVH and diastolic dysfunction and requires further prospective trials. No significant association of systolic and diastolic dysfunction with anemia, hypertension (SBPI, DBPI) was found in our patients unlike other studies.[11]

The prevention of CVD mortality in CKD includes the identification of modifiable risk factors. We found anemia in 72% of patients with cardiac abnormality rendering it the most common modifiable CVRF. Similarly, Mudi et al[24] and CKid study[12] found anemia to be the most common cardiac risk factor (39.6% and 45%, respectively). We observed a comparatively high percentage in our population which may be attributed to undernutrition, low access to erythropoietin due to financial constraints or secondary hyperparathyroidism. Anemia was found to increase the risk of LVH by three times in our study. Previously, a remarkable reduction in LMVI is reported by Morris et al[25] with the correction of anemia in dialysis patients. Although we provide S/C erythropoietin free of cost and encourage its use in early CKD stages, this modifiable risk factor is prevalent due to poor compliance, infections, dysentery, and iron deficiency anemia in our patients.

The second significant independent risk factor found was diastolic hypertension (abnormal DBPI) which is responsible for 5 times increased risk of LVH compared to those with normal LVMI. Systolic hypertension (abnormal SBPI) was recorded in 27% patients with LVH. The CKiD data[12] found confirmed hypertension (conventional BP measurement) in 18% and masked systolic or diastolic hypertension (Ambulatory BP monitoring) in 38% of subjects with CKD. The importance of ambulatory BP monitoring has been stressed upon previously,[26],[27] which we currently lack in our setup. The higher percentage of hypertensive patients identified through ambulatory BP monitoring in previous studies suggests the need for this method in our center. Nevertheless, the baseline observation of the ongoing CKD 4C study[17] showed strong linear relationship with BP measured by office reading with LVH and abnormal carotid intimal thickness.

A recent meta-analysis of long-term outcome studies performed in adults demonstrated the absence of cardiovascular risk associated with the mean 24-h ambulatory measurement.[28] There is an evident need for the homogeneity of diagnostic criteria for blood pressure monitoring in CKD children as observed in adults.

Elevated PTH was prevalent in a higher percentage in patients with cardiac abnormalities as compared to normal individuals but was not significant a risk factor for cardiac dysfunction. Previous studies confirmed the association of hyperparathyroidism with LVH.[11] Indirectly the increased calcium phosphorous product and increased carotid intimal thickness (CIMT) leads to hypertension and consequently LVH.[24] For better understanding we aim to direct studies to determine the adverse vascular outcome associated with CVD with hyperparathyroidism.

Despite a reasonable sample size, the study contained a very small number of early CKD grades. This is owing to the delayed referrals to the tertiary care hospitals in our setting. Although this creates a selection bias in terms of sampling technique, it does not affect the results because the risk factors related to cardiac abnormalities are more pronounced in higher CKD grades like IV and V. We found a very low proportion of diastolic dysfunction in our patients, but there is a possibility that this is an underestimation of the actual percentage. In future, we aim to use the TDI method to determine the diastolic dysfunction, as it provides more accurate results. Investigations regarding vascular abnormalities like increased carotid intimal thickness and vascular elasticity were also not assessed in the current study and could have strengthened the scope of this study. Another limitation of the study is the absence of long-term follow-up which is planned in the future as an update to this study but could not be feasible at this time. We also plan to investigate coronary vasculature and electrophysiological changes in future updates of this study to better understand etiology and forecast preventive measures in pediatric CKD patients.


   Disclosure Top


No funding or benefit of any kind was received or distributed to anyone during the study. Patients did not bear the cost of any additional investigation other than the routine.


   Conclusions Top


This study supported the notion that the risk of cardiac abnormalities increases with advancing CKD grades and is more pronounced in CKD grade IV and V in the pediatric population. Furthermore, variables like anemia, high CaP Product, raised PTH and hypertension (systolic and diastolic) are directly related to LVH in CKD patients (especially higher CKD grades). Keeping these relationships in mind, routine cardiovascular assessment should be enforced in all CKD grade patients to ensure preventive measures. Further studies pertaining to vascular changes and abnormalities in cardiac electrophysiology are warranted on larger sample sizes of the pediatric population with CKD. Further studies should be conducted to see the impact of the management of these risk factors.


   Acknowledgment Top


I am highly grateful to Almighty Allah, the most gracious and the most merciful, who bestowed upon me knowledge, wisdom, and power of communication. I thank to my supervisor for their guidance and supervision which made this project possible. I am grateful to my colleagues, seniors, and juniors alike who co-operated in the compilation of my project. I am in debt to my mother and my beloved husband for their motivation, cooperation and affection in overcoming my difficulties and enabling me to complete this research work. Last but not the least; I would like to mention Dr. Dhanvanti Dileep and Mr. Iqbal Mujtaba who helped with statistical analysis during this research. The primary investigator or patients did not have any conflict of interest during this research project.

Conflict of interest: None declared.



 
   References Top

1.
Ritz E. Minor renal dysfunction: an emerging independent cardiovascular risk factor. Heart 2003;89:963-4.  Back to cited text no. 1
    
2.
Ronco C, Cruz DN, Ronco F. Cardiorenal syndromes. Curr Opin Crit Care 2009;15:384-91.  Back to cited text no. 2
    
3.
Muntner P, He J, Hamm L, Loria C, Whelton PK. Renal insufficiency and subsequent death resulting from cardiovascular disease in the United States. J Am Soc Nephrol 2002;13:745-53.  Back to cited text no. 3
    
4.
Parekh RS, Carroll CE, Wolfe RA, Port FK. Cardiovascular mortality in children and young adults with end-stage kidney disease. J Pediatr 2002;141:191-7.  Back to cited text no. 4
    
5.
Mencarelli F, Fabi M, Corazzi V, et al. Left ventricular mass and cardiac function in a population of children with chronic kidney disease. Pediatr Nephrol 2014;29:893-900.  Back to cited text no. 5
    
6.
Mitsnefes MM. Cardiovascular disease in children with chronic kidney disease. J Am Soc Nephrol 2012;23:578-85.  Back to cited text no. 6
    
7.
Mitsnefes M, Flynn J, Cohn S. Left Ventricular Hypertrophy and Masked Hypertension: A Report from the Chronic Kidney Disease in Children (CKiD) Cohort. Poster Presented at: American Society of Nephrology Renal Week;2008. p. 4-9.  Back to cited text no. 7
    
8.
Freundlich M, Lipshultz SE, Filler G. Chronic kidney disease and cardiac morbidity – What are the possible links? Prog Pediatr Cardio 2016;41:89-95.  Back to cited text no. 8
    
9.
McQuarrie EP, Patel RK, Mark PB, et al. Association between proteinuria and left ventricular mass index: A cardiac MRI study in patients with chronic kidney disease. Nephrol Dial Transplant 2011;26:933-8.  Back to cited text no. 9
    
10.
Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) Guideline Update: what’s changed and why it matters. Kidney Int 2017;92:26-36.  Back to cited text no. 10
    
11.
Rinat C, Becker-Cohen R, Nir A, et al. A comprehensive study of cardiovascular risk factors, cardiac function and vascular disease in children with chronic renal failure. Nephrol Dial Transplant 2010;25:785-93.  Back to cited text no. 11
    
12.
Wong CJ, Moxey-Mims M, Jerry-Fluker J, Warady BA, Furth SL. CKiD (CKD in children) prospective cohort study: A review of current findings. Am J Kidney Dis 2012;60:1002-11.  Back to cited text no. 12
    
13.
National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003;42:S1-201.  Back to cited text no. 13
    
14.
National Kidney Foundation K/DOQI Clinical Practice Guidelines for managing Dyslipidemi as in Chronic Kidney Disease. Am J Kidney Dis 2003;41 Suppl 3:S1-91.  Back to cited text no. 14
    
15.
Chavers BM, Herzog CA. The spectrum of cardiovascular disease in children with predialysis chronic kidney disease. Adv Chronic Kidney Dis 2004;11:319-27.  Back to cited text no. 15
    
16.
Shroff R, Weaver Jr. DJ, Mitsnefes MM. Cardiovascular complications in children with chronic kidney disease. Nat Rev Nephrol 2011;7:642-9.  Back to cited text no. 16
    
17.
Schaefer F, Doyon A, Azukaitis K, et al. Cardiovascular phenotypes in children with CKD: The 4C study. Clin J Am Soc Nephrol 2017;12:19-28.  Back to cited text no. 17
    
18.
Mitsnefes MM, Kimball TR, Kartal J, et al. Progression of left ventricular hypertrophy in children with early chronic kidney disease: 2-year follow-up study. J Pediatr 2006;149:671-5.  Back to cited text no. 18
    
19.
Ali T, Idrees MK, Shoukat, Akhtar SF. Left ventricular hypertrophy among predialysis chronic kidney disease patients: Sindh institute of urology and transplantation experience. Saudi J Kidney Dis Transpl 2017;28:1375-80.  Back to cited text no. 19
[PUBMED]  [Full text]  
20.
Johnstone LM, Jones CL, Grigg LE, Wilkinson JL, Walker RG, Powell HR. Left ventricular abnormalities in children, adolescents and young adults with renal disease. Kidney Int 1996;50:998-1006.  Back to cited text no. 20
    
21.
Mitsnefes MM, Kimball TR, Border WL, et al. Impaired left ventricular diastolic function in children with chronic renal failure. Kidney Int 2004;65:1461-6.  Back to cited text no. 21
    
22.
Mitsnefes MM. Cardiovascular complications of pediatric chronic kidney disease. Pediatr Nephrol 2008;23:27-39.  Back to cited text no. 22
    
23.
Weaver DJ Jr., Kimball T, Witt SA, et al. Subclinical systolic dysfunction in pediatric patients with chronic kidney disease. J Pediatr 2008;153:565-9.  Back to cited text no. 23
    
24.
Mudi A, Dickens C, Levy C, Ballot D. Cardiovascular risk factors and mortality in children with chronic kidney disease. S Afr Med J 2017;107:710-4.  Back to cited text no. 24
    
25.
Morris KP, Skinner JR, Hunter S, Coulthard MG. Cardiovascular abnormalities in end stage renal failure: the effect of anaemia or uraemia? Arch Dis Child 1994;71:119-22.  Back to cited text no. 25
    
26.
Rostand SG, Drüeke TB. Parathyroid hormone, Vitamin D, and cardiovascular disease in chronic renal failure. Kidney Int 1999;56:383-92.  Back to cited text no. 26
    
27.
ESCAPE Trial Group, Wühl E, Trivelli A, et al. Strict blood-pressure control and progression of renal failure in children. N Engl J Med 2009;361:1639-50.  Back to cited text no. 27
    
28.
Li Y, Thijs L, Boggia J, et al. Blood pressure load does not add to ambulatory blood pressure level for cardiovascular risk stratification. Hypertension 2014;63:925-33.  Back to cited text no. 28
    

Top
Correspondence Address:
Afshan Ehsan
Department of Pediatric Nephrology, Sindh Institute of Urology and Transplantation, Karachi
Pakistan
Login to access the Email id


DOI: 10.4103/1319-2442.318553

PMID: 34145118

Rights and Permissions



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
   
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
   Introduction
    Materials and Me...
   Statistical Methods
   Results
   Discussion
   Disclosure
   Conclusions
   Acknowledgment
    References
    Article Tables
 

 Article Access Statistics
    Viewed962    
    Printed10    
    Emailed0    
    PDF Downloaded106    
    Comments [Add]    

Recommend this journal