American Journal of Pediatrics

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American Journal of Pediatrics

American Journal of Pediatrics


 
A Clinical Profile and Immediate Outcome of Acute Glomerulonephritis (AGN) in Hospitalized Children

A. N. M. Shahidul Islam Bhuiyan1, *, Zahangir Alam2, Khondaker Zahirul Hasan2, Md Mostafa Zaman3, Md Zakaria4

1Department of Paediatrics, Cumilla medical college, Cumilla, Bangladesh
2Department of Paediatrics, Abdul Malek Ukil Medical College, Noakhali, Bangladesh 3Department of Paediatrics, M Abdur Rahim Medical College, Dinajpur (MARMC), Bangladesh 4Department of Paediatrics, Sunamgong Sadar Hospital, Sunamgong, Sylhet, Bangladesh

 


Email address:*Corresponding author

To cite this article:

ANM Shahidul Islam Bhuiyan, Zahangir Alam, Khondaker Zahirul Hasan, Md Mostafa Zaman, Md Zakaria. A Clinical Profile and Immediate Outcome of Acute glomerulonephritis (AGN) in Hospitalized Children. American Journal of Pediatrics.
Vol. 6, No. 4, 2020, pp. 448-454. doi: 10.11648/j.ajp.20200604.20
 
Received: July 26, 2020; Accepted: October 13, 2020; Published: November 4, 2020

 
Abstract: Introduction: Acute glomerulonephritis includes renal diseases in which immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, proliferation of mesangium, capillary endothelium. Objectives: The objective of this study is to know the clinical profile and immediate outcome of acute glomerulonephritis in hospitalized children. Material & Methods: The study was done in Chittagong Medical College Hospital Pediatric Unit during the period of June 2007 to February 2008. All patients admitted with AGN, with or without complications were included in this study. Diagnostic criteria were scanty urine (infrequent and less than normal in amount as stated by the parents), swelling, high colored urine with or without albuminuria, no past history of similar attack and microscopic or naked eye haematuria. Criteria of discharge from the hospital were absence of puffiness and oedema, adequate urine formation, absence of heart failure and hypertensive encephalopathy. These were taken as clinical recovery. No long-term follow up was done. Results: Seventy-eight cases of acute glomerulonephritis (AGN) in children under 12 years of age were studied. Male to female ration 3:2. Scanty urine (84.0%), puffy face (88.5%) h, haematuria (80.0%), hypertension (82.5%), heart failure (11.5%) convulsion (14%) anuria (3.8%), RBC (92.3%), RBC cast (41%), albumin one (+) (52.6%) two + (14.1%) three + (14.1%), raised s. creatinine was (25.6%), blood urea (26.9%). Four patients were died. Among them three was due to hypertension and heart failure. One due to the development of acute renal failure. History of skin infection like scabies was present in 61.4% patient. Conclusion: Skin infection is the commonest cause of acute glomerulonephritis. Nephritic presentation (scanty urine oedema, haematuria, hypertension and heart failure) was the commonest mode of presentation. Immediate prognosis was excellent- Long term follow up is recommended.
Keywords: Acute Glomerulonephritis, Skin Infection, Hospitalized Children, Pediatric, Haematuria
 
 

1. Introduction

Acute glomerulonephritis includes renal diseases in which immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, proliferation of mesangium, capillary endothelium. Hippocrates originally described the manifestation of back pain and hematuria, which lead to
oliguria or anuria. With the development of the microscope, Langhans was later able to describe these pathophysiologic glomerular disorder affecting children and also is an important cause of hospital admission in peadiatric unit. Acute glomerulonephritis, particularly acute poststreptococcal glomerulonephritis, in children is a common condition caused due to bacterial infection with group-A beta hemolytic streptococcus typically involving a

 

throat, upper respiratory tract and skin [1]. Acute post streptococcal glomerulonephritis affects children between the ages of five and twelve years and usually rare before the age of three [2]. Most research focuses on the post-streptococcal origin. Acute glomerulonephritis is defined as the sudden onset of hematuria, proteinuria, and red blood cell casts. The clinical picture is often accompanied by hypertension, edema, and impaired renal function. glomerulonephritis refers to groups of renal disease characterized by inflammation of glomerulus manifested by proliferation of cellular elements secondary to immunogenic mechanism. Secondary forms of glomerulonephritis are much more common in the topics than in the industrialized countries [3]. It is more prevalent among the population particularly where poverty  overcrowding,  poor hygiene living is prevailing, this particular disease contributes to a significant amount of disease burden particularly on hospital admission and the major primary cause is infection [4]. Some of the other less common infective agents have also been identified, such as Streptococcus, schistosomiasis and malaria. Others are only speculative, being suspected from the strikingly high prevalence of proliferative glomerulonephritis, the prototype lesion of such etiology. The clinical picture is quite obvious but laboratory evidences of recent streptococcal infection by finding of elevated anti-streptococcal antibodies  and reduction in serum complement levels due to its consumption in antigen-antibody interaction in the kidneys lend additional diagnostic support. Regarding management and  prognosis, the immediate outcome is rather good in children, but the long-term prognosis is poor. Mortality in acute stage varies and they result from circulatory congestion due to heart failure hypertensive encephalopathy and acute renal failure [6]. The glomerular infection and extension damages the microcirculation, by dipping the glomerular filtration rate (GFR) and generally causes an increase in BUN and creatinine. This decrease in GFR, sequentially leads to the preservation of salt and water and produce fluid  overload. The amount of fluid overload in AGN might be differ from substantially. In severe circumstances, it might be visible by serious hypertension and pulmonary edema. Impulsive determination of the clinical indicators is mostly quick: diuresis commonly results in within 1-2 weeks, and the  serum creatinine concentration returns to base line within 4 weeks. The degree at which point urinary abnormalities dissolve is not less inconstant. Hematuria generally resolves by 6 months, but insignificant proteinuria is existent in 15% of patients after 3 years and in 2% of patients after 10 years. [6]
 

2. Objectives

General objective
To assess the clinical profile and immediate outcome of acute glomerulonephritis in hospitalized children.
Specific Objectives
1. To know presenting features of acute GN.
2. To assess the course of disease among hospitalized
acute glomerulonephritis patients
3. To ascertain the immediate outcome among hospitalized acute glomerulonephritis patients.
4. To assess the socio demographic pattern of these children.
 

3. Methodology and Materials

The study was done in Chittagong Medical College Hospital Pediatric Unit during the period of June 2007 to February 2008. All patients admitted with AGN, with or without complications were included in this study. Recruited sample size was 83, five of the patients were excluded from the analysis due to incompleteness of the data hence 78 cases were selected for analysis. Diagnostic criteria were scanty urine (infrequent and less than normal in amount as stated by the parents), swelling, high colored urine with or without albuminuria, no past history of similar attack and microscopic or naked eye haematuria. Criteria of discharge from the hospital were absence of puffiness and oedema, adequate urine formation, absence of heart failure and hypertensive encephalopathy. These were taken as clinical recovery. No long-term follow up was done.
Inclusion Criteria
1. Children admitted with Acute glomerulonephritis in to paediatric unit of CMCH
2. Stayed in the hospital and received at least 7 days treatment
3. Willing to participate in the study Exclusion Criteria
1. Patients with other systemic disease unrelated to acute glomerulonephritis
2. Not willing to participate
 

4. Results

Table 1 shows the distribution of the respondents by age. Among the acute glomerulonephritis patients 9.0% aged less than 3 years, 20.5% aged between 4 – 6 years, and 39.7% aged between 7 – 9 years and another 30.8% were aged between 10 – 12 years. Figure 1 shows the distribution of the study patients by sex. Among the children with acute glomerulonephritis 60% were male and 40% were female. Figure 2 show the distribution of the study patients by place of residence. Among the acute glomerulonephritis patient 58% were from urban place of residence, 23% were from semi urban back ground and 19% were from rural areas. Figure 3 illustrates the distribution of the study patients by their socioeconomic status. Most of the (59%) patients belong to the Low socioeconomic status, 17.9% were with middle socioeconomic status and only 23.1% share high socioeconomic status. Among the acute glomerulonephritis patients in the study 42.1% provided the history of Sore throat, 61.4% provided the history of infected scabies and 19.3% reported previous exposure to both Sore throat & skin infection. ‘Multiple response analysis’ was performed to find out the prevalence of individual presenting feature among the acute glomerulonephritis patients. Among the most striking

 
 

features puffy face (88.5%), Hematuria (80.7%) and Scanty micturition (84.0%) were most prevalent in different combination. Of the total patients (23.1%) had respiratory distress, 24.4% had cough, and other complications were- headache (17.9%), vomiting (14.1%), chest pain (14.1%), convulsion (14.1%). Among the other generalized features fever (7.7%), abdominal pain (2.6%) were also reported. Presenting general examination finding of the acute glomerulonephritis patient reported in paediatric hospital were tabulated in Table 4. Of the total participants pallor was found in 57.0% patients, oedema was found in 63.5% children with acute glomerulonephritis and hypertension was found in 82.5% patients. 11.5% had enlarged liver, 14.1% Lung crepitations, and 6.3% had engorged neck vein. Table 5 shows the urinary findings of acute glomerulonephritis patients. Regarding, urinary manifestations among the study patients in 24  hours 3.8% had  anuria.  Urinary volume   was
<250ml in 10.3% patients. 250-500ml 9.0%, 500-750ml- 39.7R and above 750ml in 37.2% cases. Urinary protein was measured and in 19.2% patient no protein was detected. In 52.6% patient protein content was One + in 14.1% protein content was ‘two +’ and in 14.1% patient protein content was ‘three +’. Following routine microscope examination RBC was detected in 92.3% patients, Pus cell was detected in 20.5% patient, RBC cast was detected in 41.0% patient, granular cast was found in 17.9% patients and Hyaline cast was detected 5.1% patient. Culture of urine revealed no growth in 91.03% cases and growth of E coli was found in 8.97% cases. Erythrocyte sedimentation rate (ESR) examination revealed > 20 mm in 1st hour in 87.2% of the subjects. Raised ASO titre (> 200 IU) was found in 52.6% patients, raised urea in blood (>60 mg/dl) was found in 26.9% patients, raised serum creatinine (>1 mg/dl) was found in 25.6% patients. Throat swab culture in 80.8% cases no growth was found, in 5.1% cases Streptococcus þ - hemolyticus growth was found and in 14.1% growth of normal flora was found. Following Skin culture in 91.0% cases no growth was found, in 9% cases Streptococcus þ- hemolyticus was isolated. Figure 4 shows the distribution of the time required to subside the oedema in patients with acute glomerulonephritis. Among the 54 patients, in 17.9% case oedema was subsided within 5 days, in 7.7% cases oedema was subsided between 6 – 10 days, in 15.4% cases oedema was subsided between 11-15 days in 2.6% cases oedema was subsided between 16-20 days and in 2.6% cases oedema was still persistent at discharge. Figure 5 shows the distribution of the time required to control the hypertension in patients with acute glomerulonephritis. Among the 64 patients with hypertension, in 1.3% case hypertension was subsided within 5 days, in 20.5% cases hypertension was subsided between  6
– 10 days, in 12.8% cases hypertension was subsided between 11 – 15 days in 26.9% cases hypertension was subsided between 16 – 20 days and in 1.3% cases hypertension was still persistent at discharge. Figure 6 depicts the distribution of the time required to subside hematuria. Among the patients with Hematuria on admission in 55% cases haematuria was subsided in between 6 – 10 days. In 28% cases haematuria was subsided in between 11 –
15   days  and   in  11%  cases  haematuria   was  subsided  in
between 16 – 20 days. In 6% cases haematuria was persistent during the discharge. Length of hospital stay for the event of illness or episode of acute glomerulonephritis is illustrated in Table 8. Among the acute glomerulonephritis patient survived the illness episode 14.1% had to stay in hospital for
< 1 week, 24.4% had to stay in hospital for 1 – 2 weeks, 39.7% had to stay in hospital for 2 – 3 weeks, and 21.8% had to stay in hospital 3 - 4 weeks. Immediate outcome of the acute glomerulonephritis was tabulated in Table 9, Among the 78 Acute glomerulonephritis patients 57.7% had compete recovery on discharge, 1.28% Acute renal failure (ARF), 11.5% Heart failure, 14.1% Hypertensive encephalopathy, 10.3% Discharge own risk bond and 5.1% Death.

 
  American Journal of Pediatrics
American Journal of Pediatrics 
Figure 1. Distribution of the study subjects by sex. (78).

 
  American Journal of Pediatrics
 
Figure 2. Distribution of the study subjects by place of residence.(n=78).

 
  American Journal of Pediatrics
 
Figure 3. Distribution of the study subjects by Socio economic status. (n=78).
 
Table 1. Distribution of the study subjects by age. (n=78).
 
   Age
< 3 Years
Frequency
7
%
9.0
4 – 6 Years 16 20.5
7 – 9 Years 31 39.7
10 – 12 Years 24 30.8
Total 78 100.0

 
 
American Journal of Pediatrics American Journal of Pediatrics

Figure 4. Period of subsiding Oedema. (n=78).
 
Table 2. Distribution of past history of risk factor exposure. (n=78).
 
History of infection Frequency %
Skin infection 24 42.1%
Sore throat 24 42.1%
Infected scabies 35 61.4%
Both Sore throat & skin infection 11 19.3%
  94 164.9%
* Percentage exceeds 100 dues to multiple responses.

 
  American Journal of Pediatrics
 
Figure 5. Period of controlling hypertension. (n=78).
Figure 6. Period of disappearing heamaturia. (n=78).
 
Table 3. Distribution of presenting features. (n=78).
 
   Presenting featuresa
Puffy face
Frequency
69
%
88.50
Scanty micturition 65 84.00
Hematuria 62 80.70
Respiratory Distress 18 23.10
Cough 19 24.40
Headache 14 17.90
Vomiting 11 14.10
Chest Pain 11 14.10
Convulsion 11 14.10
Fever 6 07.70
Abdominal pain 2 02.60
* Percentage exceeds 100 due to multiple responses.
 
Table 4. Distribution of Clinical features found in general examination. (n=78).
 
Clinical feature Frequency %
Pallor 45 57.0%
Oedema 40 63.5%
Hypertension 64 82.5%
Enlarged Liver 09 11.5%
Lung crepitations 11 14.1%
Engorged Neck Vein 04 06.3%
* Percentage exceeds 100 due to multiple responses.

 
Table 5. Distribution of urine analysis findings. (n=78).
 
Criteria Frequency %
Urine Volume in 24 hr.    
Anuria 03 03.8
< 250 ml 08 10.3
250 – 500 ml 07 09.0
500 – 750 ml 31 39.7
> 750 ml 29 37.2
Urinary protein    
Nil 15 19.2
One + 41 52.6
two + 11 14.1
three + 11 14.1
Urine RME*    
RBC 72 92.3%
Puss cell 16 20.5%
RBC Cast 32 41.0%
Granular Cast 14 17.9%
Hyaline Cast 04 5.1%

 
 
 
Criteria Frequency %
Urine culture    
No growth 71 91.03%
E. coli 07 8.97%
Total 78 100.0
* Percentage exceeds 100 due to multiple responses.
 
Table 6. Distribution of finding laboratory investigation. (n=78).
 
Lab investigation Frequency %
ESR > 20 mm in 1st hour 68 87.2%
Raised ASO titre 41 52.6%
Raised Urea blood 21 26.9%
Raised Serum creatinine 20 25.6%
(ASO titre > 200 IU/ml, Raised Urea blood 60 mg/dl, Serum creatinine > 1mg/dl.
 
Table 7. Distribution of the evidences of active infection. (n=78).
 
Specimen Frequency %
Throat swab examination    
No growth 63 80.8%
Streptococcus þ-hemolyticus 04 05.1%
Normal flora 11 14.1%
Skin swab examination    
No growth 71 91.0%
Streptococcus þ-hemolyticus 07 09.0%
Total 78 100.0%
 
Table 8. Distribution of Length of hospital stay. (n=78).
 
Length of hospital stay Frequency %
< 1 Week 11 14.1%
1 – 2 weeks 19 24.4%
2 – 3 weeks 31 39.7%
3 – 4 weeks 17 21.8%
Total 78 100.0%
 
Table 9. Distribution of immediate outcome of treatment discharge. (n=78).
 
Immediate Outcome Frequency %
Complete recovery on discharge 45 57.7%
Acute renal failure (ARF) 1 1.28%
Heart failure 9 11.5%
Hypertensive encephalopathy 11 14.1%
Discharge own risk bond 8 10.3%
Death 4 5.1%
Total 78 100.0%

 

5. Discussion

Even though the pathogenesis is not fully understood, existing evidence provisions that most cases of acute glomerulonephritis are due to  an  immunologic reaction to a variety of different etiologic agents. The immunologic response, sequentially, stimulates a number of biological procedures that cause glomerular inflammation and damage. Acute glomerulonephritis perhaps will be isolated to the kidney or be a factor of a systemic condition. Diseases containing the renal glomeruli are come across habitually in clinical practice and are the most common reasons of end stage renal disease globally [7]. The true incidence of the disease is difficult to ascertain because of the wide range of
clinical manifestations. Management of the disease in children is primarily dependent on supportive and symptomatic care and very little can be done to  modify the course of the disease. Physicians often face difficulty in managing children with mixed presentation and complication. The present study opted to report the Clinical profile and immediate outcome of children with admission diagnosis of AGN, in Chittagong medical college hospital. The immediate outcome of the  disease  is favorable in children than in adults. Hence prompt diagnosis in children may ease the difficulty of  physicians in treating the disease and could increase the chance of prompt recovery. Moreover, forms of presentation and extent of immediate clinical outcome is worth exploring. For these reasons, it is of considerable interest to identify the patterns of glomerular disease in

 

specific regions. Among the acute glomerulonephritis patients   9.0%   aged   less   than   3   years,   20.5% aged
between 4 – 6 years, and 39.7% aged between 7 – 9 years and another 30.8% were aged between 10 – 12 years. Majority (60%) of the patients were  female.  The pattern is identical with other researches. According to Rodriguez-Iturbe2 around 58% were from urban place of residence, 23% were from semi urban back ground and 19% were rom rural areas. Regarding socioeconomic status, 17.9% were with Middle socioeconomic  status  and only 23.1% share high socioeconomic status. Other researches also suggest that it is more prevalent among  the population where poverty  overcrowding,  poor hygiene living is prevailing. The major primary cause identified most researchers was infection  [8].  Some  of the other less common infective agents have also been identified, such as Streptococcus, schistosomiasis and malaria. Others are only speculative, being suspected  from the strikingly high prevalence of proliferative glomerulonephritis, the prototype lesion of such etiology. History of past streptococcal infection is described as an established risk factor that illustrate causal link of acute glomerulonephritis. In the current study 42.1% provided the history of skin infection, 42.1% provided the history  of infected scabies and 19.3%  reported  previous exposure to both Sore throat & skin infection. Acute glomerulonephritis presents with some complaints. Following multiple response analysis striking features found scanty urine (84.0%) puffy face  (88.5%) haematuria (80.7%) hypertension (82.5%), heart failure
(11.5%),  convulsions  (14.1%),  anuria  (3.8%), headache
(17.9%), cough (24.4%) on physical  examination  patients among the study participants pallor (57%), oedema  (69.2%),  hypertension  (82.5%),  enlarged  liver
(11.5%). Lung crepitations (14.1%). Hypertension happens in nearly 80-90% of cases of acute glomerulonephritis and cerebral complications including headache, seizures, mental status changes and visual changes occur in 30-35% of cases [9]. In this study, we found hypertension in 82.5% cases. The commonness of cerebral complications is lower compared to the observations made by other studies, whereas cardiac complications are also comparatively few [10] The high prevalence of  hypertension as presenting feature could  be due to failure to attend treatment in  the  earlier  stage of illness resulting late sequel of the disease. we found raised ASO titre in 52.6%. Also, serum creatinine level was high only in 25.6% of the cases. Similar cases have been reported in some studies [11-13].
 

6. Conclusion and Recommendations

Seventy-eight cases of different age groups were admitted during the eight months period, from June 2007 to February 2008. Highest incidence was observed during the months of October, November and December. Incidence of the disease was more among the poor socioeconomic classes. There was
male preponderance of the disease in this study. The peak  age observed was between 7-9 years. The cases were suspected to be of post-streptococcal origin as evidenced by history of skin infections or sore throat and or raised as titre although B-hemolytic streptococcus could not be isolated in most cases. Occurrence of heart failure was 11.5%. 61.4% had infected scabies and 82.5% hypertension. About complete recovery was obtained in 95% of cases. Hematuria was present in 6% during discharge. Emphasis should be given on prevention of the disease through health education, providing primary health care and early recognition and treatment of scabies infections and streptococcal pharyngitis. Timely and proper intervention is necessary and long term follow up should be done in every patient.
 

7. Limitations of the Study

The present study was conducted at a very short period of time. Recruited sample size of this study was 83, five of the patients were excluded from the analysis due to incompleteness of the data hence 78 cases were selected for analysis. For being a study in a single community with comparatively small number of sample size, the study result may not reflect the exact scenarios of the whole country.

 
  American Journal of Pediatrics
 

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[2] Rodriguez-Iturbe B, Batsford S. Pathogenesis of post- streptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney Int. 2007; 71 (11): 1094-104.
[3] Batsford SR, Mezzano S, Mihatsch M, et al. Is the nephritogenic antigen in post-streptococcal glomerulonephritis py8rogenic exotoin B (SPE B) or GAPDH? Kidney Int. 2005; 68 (3): 1120-9.
[4] Derakhshan A, Hosseini Al, Hashemi G, Fallahzadeh MH. Spectrum of inpatient renal diseases in children, a report from Southern part of Islamic Republic of Iran. Saudi J Kidney Dis Transplant. 2004; 15 (1): 12.
[5] Chadban SJ, Atkins RC. Glomerulonephritis. Lancet 2005; 365: 1797.
[6] Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal disease. Lancet Infect Dis 2005; 5: 685.
[7] Rodriguez-Iturbe B. Postinfectious glomerulonephritis. Am J Kidney Dis 2000; 35: XLVI.
[8] Sanjad S, Tolaymat A, Whitworth J, Levin S. Acute glomerulonephritis in children: a review of 153 cases. South Med J 1977; 70: 1202.
[9] Cattran DC. Evidence-Based Recommendations for The Management of Glomerulonephritis. Introduction. Kidney IntSuppl 1999 Jun; 70: S1-2. 12.

 
 

[10] Steer AC, Danchin MH, Carapetis JR. Group A streptococcal infection in children. J Paediatr Child Health 2007; 43: 203- 213.
[11] Gumus, H. Per, S. Kumandas¸, and A. Yikilmaz, “Reversible posterior leukoencephalopathy syndrome in childhood: report of nine cases and review of the literature,” Neurological Sciences, vol. 31, no. 2, pp. 125–131, 2010.
[12] T. M. Eison, B. H. Ault, D. P. Jones, R. W. Chesney, and R. J. Wyatt, “Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis,” Pediatric Nephrology, vol. 26, pp. 165–180, 2011.
[13] R. Bogdanovic, Henoch-Schönlein purpura, “Nephritis in children: risk factors, prevention and treatment,” Acta Paediatrica, vol. 98, no. 12, pp. 1882–1889, 2009.
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