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ORIGINAL ARTICLE
Year : 2018  |  Volume : 5  |  Issue : 4  |  Page : 134-139

Study of some electrocardiographic and echocardiographic data in toddelers and children with primary glomerulonephropathy


Department of Pediatrics, Faculty of Medicine, Tanta University, Tanta, Gharbia, Egypt

Date of Web Publication27-May-2019

Correspondence Address:
Dr. Mohamed Abdelaziz El-Gamasy
Department of Pediatric, Tanta University Hospital, El Giesh Street, Tanta, Gharbia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jina.jina_36_17

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  Abstract 


Background and Objective: Primary glomerulonephropathy mainly acute poststreptococcal glomerulonephritis (APSGN) is the most common cause of hypertensive heart failure in the pediatric age as APSGN may involve various systems including cardiovascular system. There are few research publications on electrocardiographic (ECG) and echocardiographic (two-dimensional [2D]-echo) data in childrenwith primary glomerulonephropathy. The aim is to study some ECG and 2D-echo data in Egyptian pediatric patients with ANS). Subjects and Methods: Sixty children with ANS were included and subjected to clinical, laboratory, ECG for corrected QT (QTc) interval and 2D echocardiographic study on admission and repeated at 6 and 12 weeks using GE Vivid 7 (GE Medical System, Horten, Norway with a 3.5-MHz multifrequency transducer) to measure left ventricular ejection fraction (LVEF), left atrium to aorta ratio and E/A ratio. Results: Prolonged QTc interval was reported in 22 patients (37%), of whom 18 had hypertension. Fourteen of the 60 children had LVEF <60%. The same children also had left atrium/aorta ratio >2 and E/A ratio more than two. LVEF became within normal values by 1½ month (6 weeks) in 12 patients, two become normal by three months of follow-up. Four (28.6%) from 14 children with low LVEF had normal arterial blood pressure. All the 14 children had completely recovered on follow-up period of 3 months. Conclusion: Changes in ECG and echo data which were reported in the acute phase of ANS appear to be temporary (transient) as they became within normal values in almost all children by 12 weeks period of follow-up. Although elevated blood pressure was the most common etiology of congestive heart failure in children with ANS, the impact of primary myocardial functional disturbance could also be put into consideration.

Keywords: Electrocardiographic, primary glomerulonephropathyechocardiographic, toddelers and children


How to cite this article:
El-Gamasy MA, El-Shehabi W. Study of some electrocardiographic and echocardiographic data in toddelers and children with primary glomerulonephropathy. J Integr Nephrol Androl 2018;5:134-9

How to cite this URL:
El-Gamasy MA, El-Shehabi W. Study of some electrocardiographic and echocardiographic data in toddelers and children with primary glomerulonephropathy. J Integr Nephrol Androl [serial online] 2018 [cited 2019 Jun 26];5:134-9. Available from: http://www.journal-ina.com/text.asp?2018/5/4/134/259162




  Introduction Top


Primary glomerulonephropathy in childhood mainly presented as Acute nephritic syndrome (ANS), which is defined as a syndrome of acute onset of gross or microscopic hematuria, proteinuria, oliguria, hypertension, generalized edema, and azotemia.[1] In pediatric age, the most common type is postinfectious by Group A of beta-hemolytic streptococcal infection of throat or skin.[2] Acute post-streptococcal glomerulonephritis (APSGN) remains a frequent and urgent health hazard in developing Arab countries like Egypt.[3] In spite that the long-term sequelae of ANS in Pediatric age is favorable, it may be associated with dangerous complications which may result in fatal sequelae in the early phases of the disease. Congestive heart failure (CHF) is one of these horrible complications. CHF may complicate up to one-eighth to half of the patients with ANS, resulting in unfavorable even fatal sequelae.[4],[5] The heart-related complications may be presented in early phases of illness. CHF in acute kidney injury (AKI) may be attributed to salt and water retention which results from AKI, hypertensive pressure overload on the left ventricle, or hyperkalemia.[4] Recent previous publications have reported that some patients with ANS may be complicated by CHF in the absence of hypertension and or hyperkalemia or other electrolytes abnormalities.[4],[5] In these patients, it was supposed that primary or idiopathic disturbances in cardiac muscles function were the underlying etiology precipitating CHF. In spite of the commonality of association between ANS and CHF, there was no enough previous research works to discuss different clinical, electrocardiographic (ECG) and echo data in pediatric patients with ANS.[4],[5]

Aim of the work

To study some ECG and two-dimensional echocardiogram (2D-echo) data in Egyptian pediatric patients with ANS and to evaluate their relationship with clinical and laboratory findings of patients.


  Subjects and Methods Top


Design of the study and setting

After research ethics committee approval and informed written or oral consents obtained from all participants in this research; this prospective, randomized controlled study was carried out during the period from December 2015 to December 2017 on 60 children with a diagnosis of APSGN which was the most common form of ANS. Patients were under follow-up at Pediatric Nephrology, Pediatric intensive care unit and Cardiology units of the Pediatric Department of Tanta University Hospital (TUH).

The inclusion criteria

Children with APSGN as the most common form of ANS with age ranged between 1 year and 12 years. AGN which was defined by acute onset of edema, oliguria, and hematuria (gross or microscopic) with antecedent streptococcal infection as indicated by either a history of sore throat or pyoderma and raised antistreptolysin O (ASO) titer >200 Todd units or anti-deoxyribonuclease B (anti-DNase B) >170 U. Patients were diagnosed to have hypertension if their blood pressure exceeded the 95th percentile for age, gender and height, and severe hypertension if their blood pressure exceeded the 99th percentile.[6]

Protocol of management of patients

All patients received salt and potassium restricted diet and fluid restriction. Patients with hypertension received a loop diuretic and furosemide. An antihypertensive, nifedipine, was added if blood pressure was not controlled despite these measures. All patients received a single dose of benzathine penicillin. The patients were monitored daily for weight, intake and output, blood pressure, and signs of heart failure.

The exclusion criteria

The exclusion criteria were patients with preexisting cardiac problems (cardiomyopathy, congenital, or rheumatic heart disease) or chronic renal problems.[6]

Methods

All children participating in the study were subjected to:

  • Careful history taking about demographic data, course, and outcome from case record forms
  • Full clinical examination including full cardiac examination
  • Laboratory investigations which were also performed on admission
  • They included complete blood count, ASO, and anti-DNase B serum electrolytes, serum complement C3 levels, urine analysis, blood urea nitrogen, and serum creatinine. Serum C3 was repeated at 8 weeks.


An electrocardiographic and two-dimensional echocardiogram

An electrocardiographic and two-dimensional echocardiogram were performed in all patients at admission and repeated at 6 weeks and 12 weeks, if abnormal. Corrected QT interval (QTc) in the ECG was derived from the nomogram based on Bazzet's formula. Prolonged QT interval was defined by a value >0.40 s. Parameters studied on 2D-echo were left ventricular ejection fraction (LVEF), left atrium/aortic root (LA/AO) ratio, and E/A ratio. Left ventricular systolic function was assessed using the LVEF. LVEF >60% was considered as normal. The LA/AO ratio was measured as an indication of left atrial enlargement, values >2 being considered as abnormal. The E/A ratio, i.e., the ratio of passive filling of the ventricle, the early E wave and active filling due to atrial systole, the atrial A wave, was also determined, a normal ratio ranging from 1 to 2. Diastolic dysfunction was diagnosed in patients presenting with heart failure and having a reversal of the E/A ratio.[7]

Echocardiography was performed in pediatric cardiology unit of the Pediatric department of TUH using GE Vivid 7 (GE Medical System, Horten, Norway with a 3.5-MHz multifrequency transducer). The echocardiography imaging included the two-dimensional study including E/A ratio will be based on the average of the six regional values.

Echo imaging took place in the left lateral decubitus position. Besides the standard parasternal (long and short axis) and apical (two- and four-chamber) images, additional apical (four-chamber) images were obtained that included the interventricular septum, the apex and the right ventricular (RV) free wall up to tricuspid annulus. Images were digitally stored in the cine-loop format for off-line analysis. Longitudinal strain was assessed off-line, on the four-chamber cine-loop that included the RV free wall, using speckle-tracking analysis.[8]

Statistical analysis

Statistical analysis was performed with statistical package for social science SPSS version 17 for windows(SPSS, Inc., Chicago, IL, USA). Means and standard deviations of quantitative data the studied groups were calculated and compared using Student's t-test. P < 0.05 was considered as statistically significant. Correlation between variables was evaluated using Pearson's correlation coefficient.[9]


  Results Top


A total of 60 patients with confirmed diagnosis of ANS were enrolled in this work.

The demographic, clinical, and laboratory parameters of the studied patients were summarized in [Table 1]. The male-to-female ratio was 3:2. 42 (70%) of 42 (70%) of patients were >6 years old and 18 (30%) of the patient were from 1 to 5 years of age. Forty (66.7%) patients were presented with hypertension, 10 (22.2%) with CHF, and 4 (6.7%) with hypertensive emergency in the form of encephalopathy. Twenty-four (40%) of patients had preceding upper respiratory tract infection and 20 (33.4%) had preceding skin infection. Four of the 10 children with CHF were with normal arterial blood pressure. Sixty children (100%) had a hypocomplementaemia C3 which returned to normal value in 2 months follow-up duration. 6 (10%) of children had hyponatremia and 4 (6.7%) had hyperkalemia. All 60 patients received protocol of treatment in the form of fluid and Na restriction and furosemide as loop diuretic. The 40 (66.7%) of patients with hypertension also received nifedipine as a direct arterial vasodilator.
Table 1: Demographic, clinical and laboratory data of the studied patients with acute nephritic syndrome

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[Table 2] summarizes the results of ECG and 2D-echo. ECG findings were tachycardia relative to age in 14 (23.3%) and prolonged QT interval in 22 (36.7%) of patients, which returned to normal values by one and half month follow-up duration. Fourteen (23.3%) patients had a low LVEF on echocardiography at presentation which returned to normal values in one and half month follow-up duration in 12 (20%) of patients. The remaining two patients had a normal ejection fraction by 3 months duration of follow-up. Four of 14 patients with low LVEF were with normal blood pressure. The LA/aorta ratio was abnormal in 14 (23.3%) children suggestive of left atrial enlargement. The E/A ratio was abnormal in 14 (23.3%) patients suggestive of diastolic dysfunction. None of the patients with low LVEF had abnormal serum electrolytes.
Table 2: Some ECG & Echo.data at admission and follow up

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[Table 3] summarizes the relation of the ECG and echo parameters with the studied clinical and laboratory data. Prolonged QTc interval was reported in 22 (36.7%) patients. All the children with prolonged QTc had normal serum total and ionized calcium levels. 12 of these patients had hypertension and two had elevated serum potassium level.
Table 3: Relation of electrocardiographic and echocardiographic findings and demographic, clinical and laboratory data of the studied patients with the acute nephritic syndrome

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  Discussion Top


In this work, 10 of the 60 studied children were presented with heart failure. Fourteen children had a reduced LVEF at time of clinical presentation suggestive for a reduction in left ventricular function (LVF). These results became within normal values in 12 children at 6 weeks. In the remaining children, LVF return to normal values at 3 months. Ten out of the 14 pediatric patients had elevated arterial blood pressure as the most possible etiology for disturbed LVF. The remaining four children were normotensive indicating the possibility of primary myocardial disturbed function in ANS.

A previous similar research work was conducted by Singh et al. in 34 children with APSGN.[5] In their study, CHF was present in 9 patients. Three patients had decreased LVF on echocardiography of which two were with normal blood pressure. In a previously published article conducted by Banapurmath et al., 13 out of 50 patients had CHF.[4] Twelve of these patients had hypertension. One child was with normal blood pressure and was presumed to be having noninfective myocarditis as proofed by auscultation of muffled cardiac sounds and low-voltage complexes on ECG. The most common cause of CHF in patients with ANS was hypertension. However, some previously published articles have concluded a poor a weak correlation between hypertension and signs of CHF (P > 0.05).[4],[5] Moreover, cases of ANS with cardiomegaly but without hypertension have also been reported.[10] Apart from hypertension, other possible etiologies of CHF in ANS included circulatory congestion, hyperkalemia, administration of excessive amounts of intravenous fluids, especially if patients were presented by oligoanuria leading to cardiac muscle injury.[4] Gore and Saphir have observed significant patchy areas of myocardial damage in autopsies examination in 16 out of 160 studied cases who died after AGN.[11] As regard to therapy of ANS, they recommended cautious administration of intravenous fluids. In studies performed by Manhas et al. and Puri et al., 83% and 50% of patients, respectively, with CHF were normotensive, and they lacked evidence of myocarditis.[12],[13]

Kaplan et al. have reported temporary vasculitic phenomena which affect multiple organs, including that of the central nervous system, in ANS.[14] It was likely that vasculitic phenomena involving the myocardial tissue may explain the decreased LVF in some patients of ANS who were normotensives.

In the present study, 36 children (60%) had evidence of ECG abnormalities, which was within the range of 5%–75% reported in various previous publications.[4],[12],[13],[15] The ECG changes seen in our work were tachycardia in 14 (23.3%) and prolonged QTc interval in 22 (36.7%). Prolonged QTc was recorded in 22 patients (36.6%), 18 (30%) of whom had hypertension. Eight (13.3%) patients with prolonged QTc were normotensive and had decreased LVEF and tachycardia, suggesting myocardial dysfunction. Two (3.3%) patients with prolonged QTc had hyperkalemia. A previous similar study performed by Banapurmath et al. found tachycardia in 11 cases, of whom eight had hypertension.[4] In their study, prolonged QTc interval was seen in 11 children, nine of whom had hypertension.

The other ECG abnormalities observed in the study were bradycardia, prolonged PR interval, ST-segment elevation and depression, tall T-wave, inverted T wave, U wave, low voltage complexes, right axis deviation, and left axis deviation. Another study performed by Singh et al. reported 19 patients out of 34 (55.9%) with prolonged QTc. Five out of these patients were normotensive with decreased LVF suggesting myocardial dysfunction.[5]

There were many previous studies about cardiac dysfunction and its significance in chronic kidney diseases, but only seldom data exist regarding the involvement of heart in acute glomerular diseases.[4],[5] Kamisago and Hirayama studied left ventricular hemodynamics using M-mode and pulsed Doppler echocardiography in 18 patients with APSGN during the acute phase.[16] The results reported that in the acute phase of APSG left ventricular preload, contractility, and afterload was increased mainly due to circulatory congestion. In the present work, 14 (23.3%) patients had evidence of increased LA/AO ratio, thereby suggesting left atrial enlargement due to circulatory congestion. Sieck et al. described a after ensuring that the patient consent form has been obtained 16-year-old adolescent male with APSGN whose echocardiography showed marked impairment of LV systolic and diastolic function with apical thrombus. Serial echo examinations showed improvement over three weeks with treatment.[17] In our work, 14 children had reversal of the E/A ratio and decreased LVEF on echocardiography indicating the presence of systolic and diastolic dysfunction. Ten out of these 14 patients had hypertension. The remaining four children were within normal blood pressure suggesting primary myocardial involvement. The systolic and diastolic function in our patients became within normal values by 12 weeks of follow-up period.

Limitation of the study

One of the limitations of this work was a small sized sample of subjects so further studies on a wider scale of children will be hoped to clarify the possibility of effects of primary myocardial dysfunction in the pathophysiology and etiology of heart failure in pediatric patients with ANS.


  Conclusion Top


This work has reported that abnormalities in ECG and or ECHO were frequent in the acute phase of ANS. These abnormalities were reported in some children even in the presence of normal arterial blood pressure and normal serum sodium and potassium levels.

Elevated arterial blood pressure was the most common predisposing agent in the etiology of hypervolemia of circulatory system in ANS. However, fewer children presented by CHF without elevated blood pressure thus primary or idiopathic disturbed myocardial function might be the underlying etiology of CHF in these patients. Children with ANS might be presented by systolic and or diastolic myocardial dysfunction which was proofed by echo data. The abnormalities in ECG and echo data were temporary (transient) meaning that they returned to normal values in the majority of children by 12 weeks duration of follow-up.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rodriguez-Iturbe B, Mezzano S. Acute postinfectious glomerulonephritis. In: Avner ED, Harmon WE, Niaudet P, Yoshikawa N, editors. Pediatric Nephrology. 6th ed. Berlin, Heidelberg: Springer-Verlag; 2009. p. 743-55.  Back to cited text no. 1
    
2.
Sepahi MA, Shajari A, Shakiba M, Shooshtary FK, Salimi MH. Acute glomerulonephritis: A 7 years follow up of children in center of Iran. Acta Med Iran 2011;49:375-8.  Back to cited text no. 2
    
3.
Becquet O, Pasche J, Gatti H, Chenel C, Abély M, Morville P, et al. Acute post-streptococcal glomerulonephritis in children of French Polynesia: A 3-year retrospective study. Pediatr Nephrol 2010;25:275-80.  Back to cited text no. 3
    
4.
Banapurmath CR, Zacharias TS, Somashekhar KS, Abdul Nazer PU. Congestive cardiac failure and electrocardiographic abnormalities in acute glomerulonephritis. Indian Pediatr 1996;33:589-92.  Back to cited text no. 4
    
5.
Singh H, Chugh JC, Srivastava RN, Benmussa AA, Shembesh AA, Mehta HC, et al. Cardiac status in post-streptococcal acute glomerulonephritis. Indian Pediatr 1999;36:911-3.  Back to cited text no. 5
    
6.
Falkner B, Daniels SR. Summary of the fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Hypertension 2004;44:387-8.  Back to cited text no. 6
    
7.
Muraru D, Cucchini U, Mihăilă S, Miglioranza MH, Aruta P, Cavalli G, et al. Left ventricular myocardial strain by three-dimensional speckle-tracking echocardiography in healthy subjects: Reference values and analysis of their physiologic and technical determinants. J Am Soc Echocardiogr 2014;27:858-710.  Back to cited text no. 7
    
8.
Mor-Avi V, Lang RM, Badano LP, Belohlavek M, Cardim NM, Derumeaux G, et al. Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography. Eur J Echocardiogr 2011;12:167-205.  Back to cited text no. 8
    
9.
Khothari CR, editor. Research Methodology, Methods and Techniques. 2nd ed. New Delhi: New Age International; 2012. p. 95-7.  Back to cited text no. 9
    
10.
Defazio V, Christensen RC, Regan TJ, Baer LJ, Morita Y, Hellems HK, et al. Circulatory changes in acute glomerulonephritis. Circulation 1959;20:190-200.  Back to cited text no. 10
    
11.
Gore I, Saphir O. Myocarditis associated with acute and subacute glomerulonephritis. Am Heart J 1948;36:390-402.  Back to cited text no. 11
    
12.
Manhas RS, Patwari A, Raina C, Singh A. Acute nephritis in Kashmiri children – A clinical and epidemiological profile (a study of 350 cases). Indian Pediatr 1979;16:1015-21.  Back to cited text no. 12
    
13.
Puri RK, Khanna KK, Raghu MB. Acute glomerulonephritis in children. Indian Pediatr 1976;13:707-11.  Back to cited text no. 13
    
14.
Kaplan RA, Zwick DL, Hellerstein S, Warady BA, Alon U. Cerebral vasculitis in acute post-streptococcal glomerulonephritis. Pediatr Nephrol 1993;7:194-5.  Back to cited text no. 14
    
15.
Berry S, Prakash K, Srivastava G, Gupta S. Acute glomerulonephritis in children. Indian Pediatr 1971;8:198-200.  Back to cited text no. 15
    
16.
Kamisago M, Hirayama T. Echocardiographic evaluation of left ventricular hemodynamics in children with post-streptococcal acute glomerulonephritis. Nihon Ika Daigaku Zasshi 1994;61:306-14.  Back to cited text no. 16
    
17.
Sieck JO, Awad M, Saour J, Ali H, Qunibi W, Mercer E, et al. Concurrent post-streptococcal carditis and glomerulonephritis: Serial echocardiographic diagnosis and follow-up. Eur Heart J 1992;13:1720-3.  Back to cited text no. 17
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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