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Clinical Characteristics and Outcome of Post-

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Article in The Indian Journal of Pediatrics · April 2015

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Indian J Pediatr
DOI 10.1007/s12098-015-1752-0

ORIGINAL ARTICLE

Clinical Characteristics and Outcome of Post-Infectious

Glomerulonephritis in Children in Southern India: A
Prospective Study
Kuralvanan Gunasekaran 1 & Sriram Krishnamurthy 1 & Subramanian Mahadevan 1 &
B. N. Harish 2 & Ajith Prabhu Kumar 3

Received: 8 October 2014 / Accepted: 18 March 2015

# Dr. K C Chaudhuri Foundation 2015

Abstract PIGN in 7 (9.7 %) cases. Complications included AKI in 15

Objectives To evaluate the clinical characteristics, complica-
tions and outcome of post-infectious glomerulonephritis
(PIGN).
Methods This prospective observational study was conducted
from January 2013 through July 2014 at a tertiary care hospi-
tal in south India. Post-streptococcal glomerulonephritis
(PSGN) was diagnosed in the presence of: a) Hematuria and
proteinuria b) Clinico-serological evidence of recent strepto-
coccal infection [recent pyodermas or pharyngitis; positive
antistreptolysin-O (ASO) titres, anti-DNAse B titres or throat
swab positivity for Group A streptococcus], and c) Low serum
C3 levels, with normalization on 8 wk follow up. PIGN in-
cluded PSGN and other infectious etiologies. AKI was classi-
fied as per Acute Kidney Injury Network (AKIN) criteria.
Clinical features, biochemical and serological investigations
in the study subjects were recorded.
Results Among 83 children with acute nephritic syndrome
(ANS) recruited, 72 (86.7 %) had PIGN. PSGN was the most
common etiology [65(90.3 %)] among the PIGN cases. Pyo-
dermas, upper respiratory infections and varicella preceded
hematuria in 58 (80.6 %), 4 (5.6 %) and 2 (2.8 %) cases
respectively. Pneumonia, mumps and liver abscess caused
* Sriram Krishnamurthy
drsriramk@yahoo.com
1
Department of Pediatrics, Jawaharlal Institute of Postgraduate
Medical Education and Research (JIPMER), Pondicherry 605006,
India
2
Department of Microbiology, Jawaharlal Institute of Postgraduate
Medical Education and Research (JIPMER), Pondicherry, India
3
Department of Community Medicine, Jawaharlal Institute of
Postgraduate Medical Education and Research (JIPMER),
Pondicherry, India
(20.8 %), hypertensive emergency in 14 (19.4 %), cardiac
failure in 8 (11.1 %), encephalopathy in 3 (4.2 %) cases and
retinopathy in 1 (1.4 %) case. Among the AKI patients,
3(20 %) were in AKI stage 3, while 1 child required hemodi-
alysis. Twenty three cases (31.9 %) had evidence of residual
renal injury at discharge. Renal biopsy showed diffuse prolif-
erative glomerulonephritis in 4 and crescentic glomerulone-
phritis in one case of PIGN. At 6 mo follow up, one patient
continued to have microalbuminuria.
Conclusions PIGN (including PSGN) remains a significant
contributor to morbidity in children with ANS. The study is
notable for high incidence of hypertensive emergency and
AKI, that often required intensive care management.
Keywords Post infectious glomerulonephritis . Post
streptococcal glomerulonephritis . Acute nephritic syndrome
Introduction
Post-infectious glomerulonephritis (PIGN) is a glomerular
disease resulting from immunological events triggered by bac-
terial, viral or protozoal infections. The prototype of PIGN is
post-streptococcal glomerulonephritis (PSGN), which con-
tinues to be an important non-suppurative complication of
Group A streptococcal infection [1]. Throughout the world
most of the burden of PSGN is borne by developing nations.
Pyoderma-associated PSGN continues to exist in tropical
countries, where pyoderma-associated streptococcal infec-
tions are endemic [1]. Other reported causes of PIGN in de-
veloping countries, include pneumonia [2], liver abscess [3],
varicella [4] and dengue [5]. Although mortality from PIGN is
quite low, the disease contributes significantly to morbidities
and requirement for hospitalizations [1]. Only few studies on

clinico-etiological profile of PIGN have been reported from
India in recent years. Hence, the present study was conducted.
Material and Methods
This prospective observational study was conducted at a ter-
tiary care hospital in south India from January 2013 through
July 2014 after obtaining approval from Institute Ethics Com-
mittee (Approval No.IEC/ SC/ 2012 /5 /166). The primary
objective was to study the proportion of PSGN among chil-
dren presenting with acute nephritic syndrome (ANS). The
secondary objectives were to evaluate the proportion of acute
kidney injury (AKI), hypertension, congestive heart failure,
encephalopathy; and incidence of residual renal injury in
PIGN.
All consecutive children aged 1–13 y presenting with acute
nephritic syndrome who presented to the department of pedi-
atrics were included in the study. Children with chronic kid-
ney disease (clinical, radiological, biochemical or histopatho-
logical evidence of kidney disease for more than 3 mo), uri-
nary tract infection, renal stones and recurrent hematuria (two
or more episodes) were excluded.
Acute nephritic syndrome was defined as acute onset of
hematuria (gross or microscopic; with RBC casts on urinaly-
sis) and proteinuria; in the presence of edema, hypertension or
oliguria [6]. Acute post-streptococcal glomerulonephritis
(PSGN) was diagnosed in the presence of the following
criteria [6]: a) Features of acute nephritic syndrome, and b)
Evidence of clinico-serological evidence of recent streptococ-
cal infection (e.g., recent pyodermas or pharyngitis; with pos-
itive antistreptolysin-O titres, anti-DNAse B titres or throat
swab positive for Group A streptococcus), and c) Low serum
complement 3 (C3) levels, with normalization of C3 levels on
an 8 wk follow up. Histopathological evidence (if available)
consistent with PSGN was considered as an additional corrob-
orative evidence for the diagnosis. Exclusion of clinical and/or
histopathological evidence of other etiologies e.g., IgA ne-
phropathy, lupus nephritis, Henoch-Schönlein nephritis was
considered as essential for the diagnosis of PSGN. Post-infec-
tious glomerulonephritis (PIGN) was defined as features of
acute nephritic syndrome and evidence of an infectious etiol-
ogy e.g., PSGN, pneumonia, liver abscess, varicella. Rapidly
progressive glomerulonephritis (RPGN) was defined as rapid
decline in renal function (50 % decline in glomerular filtration
rate) within few days to weeks, with extensive crescent for-
mation (involving more than 50 % of glomeruli) in children
presenting with acute nephritic syndrome [6]. Hematuria was
defined as 5 red blood cells/ high power field on a centrifuged
urinary specimen [7]. Hypertension was defined as systolic
and/or diastolic blood pressure values exceeding the 95th
centile for age, sex and height [8]. Sub-nephrotic range
proteinuria was defined as urinary protein: urinary creatinine
Indian J Pediatr
ratio between 0.2 and 2. Nephrotic range proteinuria was
defined as urinary protein: urinary creatinine ratio >2. Acute
kidney injury was defined as an abrupt (within 48 h) reduction
in kidney function leading to an absolute increase in serum
creatinine≥0.3 mg/dl or a percentage increase in serum creat-
inine of more than or equal to 1.5-fold from the baseline [9].
Residual renal injury at discharge was defined as abnormal
creatinine for age (>0.2–0.4 mg/dl for infants; >0.3–0.7 mg/dl
for 1–12 y; >0.5–1.0 mg/dl for >12 y), hypertension,
microalbuminuria or urinary protein: urinary creatinine ratio
(UP:UC) >0.2 [10].
Treatment of patients with PSGN was as per the guidelines
for management of these children [6, 11]. Children with
PSGN received oral penicillin (phenoxymethylpenicillin tab-
let 250 mg TID) for 10 d [6, 11]. Renal biopsy in children with
acute nephritic syndrome was performed as per the criteria
mentioned in the literature [6, 11]. Serum C3 levels were mea-
sured by ELISA method. Anti Streptolysin O (ASO) and anti-
DNAse B were measured by latex agglutination and ELISA
respectively. ASO titre >200 units/ml [12] or anti- DNAse B
>170 IU/ml were considered as evidence for recent strepto-
coccal infection [13, 14]. Samples for C3, anti-DNAse B and
ASO were collected within 12 h of hospitalization. Throat
swabs were cultured for Group A streptococcus.
Patients with PIGN who were discharged were advised to
follow up for any evidence of residual renal injury at 1 mo, 2
mo, 3 mo, and 6 mo after discharge. During these visits, serum
creatinine, estimated glomerular filtration rate (eGFR) (as
measured by Schwartz formula), blood pressure and urinalysis
for microalbumin: creatinine ratio were recorded.
The incidence of PIGN in ANS was estimated to be 85 %
based on clinical records. Assuming 10 % variation with 95 %
confidence, the sample size for estimating the incidence of
PIGN in ANS was 49 subjects. However, finally, 83 subjects
with acute nephritic syndrome were recruited. Continuous da-
ta were expressed as mean and standard deviation or median
and interquartile range as appropriate. Predictors of AKI in
children with PIGN were studied by univariate analysis.
Results
Figure 1 depicts the inflow of subjects into the study. Out of 83
children recruited with ANS, 72 (86.7 %) were PIGN. Out of
these 72 children, 65 (90.3 %) showed clinico- serological
evidence of PSGN. Other causes of ANS included lupus ne-
phritis, Henoch-Schönlein purpura, IgA nephropathy,
mesangioproliferative and membranoproliferative glomerulo-
nephritis (Fig. 1).
PSGN cases (n=65) were encountered throughout the year.
However, 47.7 % of cases were encountered between August
and November. Age of the patients ranged from 2.3 to 12 y.
Pyodermas, upper respiratory infections and varicella
Indian J Pediatr

Fig. 1 Flowchart depicting Acute nephritic syndrome

inflow of subjects into the study.
*
2 PSGN cases occurred (N=83)
following varicella (Both
developed pyoderma and were
anti-DNAse B positive).
$
Etiology of acute nephritic
syndrome could not be
ascertained.
MesPGN Mesangioproliferative
glomerulonephritis; MPGN Post infectious glomerulonephritis Other causes
Membranoproliferative [72(86.7%)] a. Lupus nephritis [2(2.4%)]
glomerulonephritis; HSP b. MesPGN [2(2.4%)]
Henoch-Schönlein purpura c. IgA nephropathy [1(1.2%)]
d. HSP nephritis [1(1.2%)]
e. Micro- PAN [1(1.2%)]
f. MPGN [1(1.2%)]
g. Unknown [2(2.4%)]$

Post streptococcal Other causes of PIGN

glomerulonephritis* [65(90.3%)] a. Liver abscess [1(1.4%)]
b. Pneumonia [4(5.6%)]
c. Mumps [2(2.8%)]

Symptomatic management Renal replacement therapy required

[64(98.5%)] [1(1.5%)]

preceded hematuria in 58 (80.6 %), 4 (5.6 %) and 2 (2.8 %) of Discussion

PIGN cases respectively. Pneumonia, mumps and liver ab-
scess caused PIGN in 4 (5.6 %), 2 (2.8 %) and 1 (1.4 %) cases
respectively. Complications included AKI in 15 (20.8 %), hy-
pertensive emergency in 14 (19.4 %), cardiac failure in 8
(11.1 %), encephalopathy in 3 (4.2 %) and retinopathy in 1
(1.4 %) of PIGN cases. Among the AKI patients, 3 (20 %)
were in AKI stage 3 as per AKIN classification, while 1 child
required hemodialysis (Table 1).
Nephrotic range proteinuria was found in 33.3 and 32.3 %
of PIGN and PSGN cases respectively. The eGFR improved
on follow up. ASO was positive in only 3 subjects with
PSGN. Anti- DNAse B was positive in 61 cases of PSGN
with median (IQR) value being 326.1 (185.4–400.1) units/L.
One patient had throat swab positive for Group A streptococ-
cus (Table 2). Twenty three cases of PIGN (31.9 %) had evi-
dence of residual renal injury at discharge while one case
continued to have evidence of microalbuminuria at 6 mo fol-
low up (Table 3).
Renal biopsy was performed in 5 cases of PIGN (due to
clinical suspicion of RPGN) and showed diffuse proliferative
glomerulonephritis in 4 cases (three cases having 25–50 %
crescents; 1 case with<25 % crescents), while 1 case showed
crescentic glomerulonephritis (>50 % crescents). Gross
hematuria was found to be associated with AKI on uni-
variate analysis [OR (95 % CI) being 4.92 (0.99–
24.29)] (p 0.036).
Eighty three children presenting with the acute nephritic syn-
drome were prospectively recruited. Out of these, 86.7 % were
diagnosed as PIGN. An overwhelming majority of these
PIGN cases were post- streptococcal in etiology. Although
PIGN dominated the clinical profile of this prospective obser-
vational study on children with acute nephritic syndrome, it is
prudent to recognize that etiologies other than PIGN were
encountered (e.g., lupus nephritis, IgA nephropathy, HSP ne-
phritis etc.) in 13.3 % cases. It is therefore imperative that a
search for etiologies other than PIGN be made in children
presenting with acute nephritic syndrome. Similarly, although
PSGN dominated the clinical profile of cases diagnosed as
PIGN, other non-post streptococcal etiologies such as pneu-
monia, liver abscess and mumps constituted 9.7 % of such
cases, emphasizing the need to recognize acute nephritic syn-
drome as a potential complication of these tropical infections.
The mean age of subjects presenting with PSGN was 6.8 y
with 78.5 % of subjects being above 5-y-old. These observa-
tions are in accordance with other reports mentioning the me-
dian age at presentation for PSGN in childhood between 6 and
8 y [1]. The rarity of PSGN in very young children has been
attributed to immature immune response [1, 15]. Majority of
PSGN followed pyodermas (89.2 %), a presentation classical-
ly described in developing countries. Serious complications
such as hypertensive emergency, congestive heart failure,
 Indian J Pediatr

Table 1 Demographic and

clinical profile of Post-infectious Characteristics PIGN** (n=72) PSGN (n=65)
glomerulonephritis (PIGN) and
Post-streptococcal glomerulone- Age (years) 6.7±2.7 6.8±2.8
phritis (PSGN) in children <5 y 20 (27.8) 19 (29.2)
>5 y 53 (72.2) 46 (70.8)
Males 40 (55.6) 35 (53.9)
Etiology
Pyoderma-associated* 58 (80.6) 58 (89.2)
Pharyngitis-associated 4 (5.6) 4 (6.2)
Pneumonia 4 (5.6) -
Mumps 2 (2.8) -
Liver abscess 1 (1.4) -
Gross hematuria 47 (65.3) 40 (61.5)
Hypertension 66 (91.7) 60 (92.3)
Hypertensive emergency 14 (19. 4) 14 (21.5)
Oliguria 50 (69.4) 44 (67.7)
Edema 64 (88.9) 58 (89.2)
Congestive heart failure 8 (11.1) 8 (12.3)
Encephalopathy (altered sensorium and/or seizures) 3 (4.2) 3 (4.6)
Hypertensive retinopathy 1 (1.4) 1 (1.5)
Acute Kidney Injury (AKI) incidence 20.8 % 23.1 %
AKI (as per AKIN classification) (n=15)
Stage 1 7 (46.7) 7 (46.7)
Stage 2 5 (33.3) 5 (33.3)
Stage 3 3 (20.0) 3 (20.0)
AKI (as per pRIFLE criteria) (n=15)
Risk 4 (26.7) 4 (26.7)
Injury 8 (53.3) 8 (53.3)
Failure 2 (13.3) 2 (13.3)
Loss 1 (6.7) 1 (6.7)
End stage - -
Requirement for dialysis 1 (1.4) 1 (1.5)
Length of hospital stay (days) 5.3±2.7 5.2±2.7
Outcome at discharge$
Complete resolution of symptoms 49 (68.1) 46 (70.8)
Partial resolution of symptoms 23 (31.9) 19 (29.2)

Values depicted as mean (standard deviation) and n (%)

*
2 varicella cases developed pyodermas
**
PIGN included patients with PSGN
$
Complete resolution defined as normal creatinine levels for age: Infants — 0.2–0.4 mg/dl; 1–12 y
— 0.3–0.7 mg/dl; >12 y — 0.5–1.0 mg/dl and absence of hypertension and proteinuria
IQR Interquartile range; PIGN Post-infectious glomerulonephritis; PSGN Post-streptococcal glomerulonephritis

encephalopathy and retinopathy were observed in 21.5, 12.3,
4.6 and 1.5 % cases of PSGN respectively, emphasizing the
need for regular monitoring of these children in order to limit
morbidities. Cerebral complications of hypertension have
been reported to occur in 30–35 % of children with PSGN
in some series [1, 16, 17]. The number of children presenting
with congestive heart failure was also quite high (12.3 %).
Though some authors have reported a high incidence of
hypertension in children with PSGN, the proportion
with hypertensive emergency has not been specified
[16, 17]. In the index study, 21.5 % of children with
PSGN developed hypertensive emergency and required
sodium nitroprusside intravenous infusion in an inten-
sive care setting. Although persistence of hypertension
and nephrotic range proteinuria during follow up were
predictors of AKI in study conducted in adults [18],
gross hematuria was found as a predictor of AKI in
the index study.
Indian J Pediatr

Table 2 Laboratory parameters

of subjects with Post-infectious Characteristics PIGN (n=72) PSGN (n=65)
glomerulonephritis (PIGN) and
Post-streptococcal glomerulone- Serum creatinine (mg/dl)
phritis (PSGN) Initial (at admission) 0.75(0.7–0.9) 0.7(0.7–0.9)
Maximum creatinine reached 0.8(0.7–1.0) 0.8(0.7–1.0)
At discharge 0.7(0.6–0.8) 0.7(0.65–0.85)
At 6 mo follow up 0.7(0.6–0.7) 0.7(0.6–0.8)
Blood urea (mg/dl) 44(29–70) 45(30–68)
UP:UC**(g/g)
0.2 22(30.6) 19(29.2)
0.2–2 (Subnephrotic range proteinuria) 26(36.1) 25(38.5)
>2 (Nephrotic range proteinuria) 24(33.3) 21(32.3)
ASO positivity (>200 units/ml) 3(4.2) 3(4.6)
Serum anti-DNAse B (units/ml)$ - 326.1(185.4–400.1)
Serum albumin (g/dl) 3.6(3.3–3.9) 3.6(3.3–3.9)
Serum complement 3 (g/L) (at admission)* 0.18(0.17–0.35) 0.180(0.17–0.35)
eGFR (ml/min/1.73 m2)
At admission 63.5(46.3–73.4) 64.1(45.3–72.8)
At 12 wk follow up 76.5(65–98.1) 74.6(64.5–84.8)

Values depicted as median (Interquartile range) and n (%)

*
C3 levels normalized on an 8 wk follow up in all patients of PSGN
**
UP: UC Urinary protein: urinary creatinine ratio; IQR Interquartile range; eGFR Estimated glomerular filtra-
tion rate
$
Positive in 61 cases

It is known that glomerular filtration rate is often decreased
during acute phase of PSGN. The estimated glomerular filtra-
tion rate (eGFR) in the index study was low (mean 64.1 ml/
min/1.73 m2) at admission which subsequently improved
(mean 74.6 ml/min/1.73 m2) at 12 wk follow up. In the index
study, the incidences of AKI in PIGN and PSGN were 20.8 %
and 23.1 % respectively. The authors further classified acute
kidney injury (AKI) as per the Acute Kidney Injury Network
(AKIN) classification as well as the pRIFLE criteria. Accord-
ing to the AKIN classification 20 % of PSGN were in stage 3
AKI, whereas according to the pRIFLE criteria, 20 % were in
either failure or loss stage. Upto 31.9 % of all cases of PIGN
had evidence of residual renal injury at discharge. There are no
prior studies delineating the incidence and classification of
AKI in a prospective cohort of PSGN or PIGN as per AKIN
classification or pRIFLE criteria.
There is a paucity of studies on clinical features of children
presenting with ANS including PSGN in recent years. Most of
the previous studies are quite old [19]. Table 4 enlists the
salient features of earlier studies in comparison with the index
study. In the index study, among the 72 cases of PIGN (in-
cluding 65 cases PSGN), no deaths were recorded. One

Table 3 Follow up laboratory

parameters in PIGN cases Characteristics At 1 mo (N=60) At 6 mo (N=52)

Blood pressure
<95th centile 59(98.3) 51(98.0)
>95th centile 1(1.7) 1(2)
Urine protein: creatinine (UP:UC) (g/g)
<0.2 58(96.7) 51(98.1)
0.2–2 (Subnephrotic range proteinuria) 2(3.3) 1(1.9)
>2 (Nephrotic range proteinuria) Nil Nil
Abnormal creatinine levels for age* 9(15) 4(7.7)
Microalbuminuria# 5(8.3) 1(1.9)

All values depicted as [n(%)]

*
Normal creatinine levels for age: Infants — 0.2–0.4 mg/dl; 1–12 y — 0.3–0.7 mg/dl; >12 y — 0.5–1.0 mg/dl
#
Microalbuminuria defined as 30–299 mg/g of creatinine
Table 4 Clinical and laboratory features of earlier studies on PSGN in comparison with the present study

Rajajee et al. [16] Becquet et al. [19] Sarkissian et al. [7] Wong et al. [17] Present study

Place of study Madras, India French Polynesia Armenia New Zealand (Maori and Pondicherry, India
Pacific island ethnic groups)
Year of study 1981–1983 2006–2007 1992–1996 2008 2014
Type of study Prospective Retrospective Prospective Retrospective Prospective
Sample size 135 50 474 27 65 cases of PSGN
Mean age (years) Range 2–12 with peak at 4 6.7 7.5 9.4 6.8
Male : Female ratio Slight male preponderance 1.17:1 1.86:1 1.45:1 1.16:1
Hypertension 82 % 64 % 72 % NA 92.3 %
Encephalopathy 4.4 % 4% 3% NA 4.6 %
Congestive heart failure 5.9 % 14 % 10 % NA 12.3 %
Proteinuria on follow up 2 % at 6 mo Proteinuria resolution 3 % after 1 y 29.6 % at median follow 1.9 % at 6 mo
in all cases at mean up of 3.2 y
follow up of 3.9 mo
Pyoderma related Majority followed scabies 20 % 13 % NA 89.2 %
or impetigo
Pharyngitis related NA 30 % 51 % NA 6.2 %
Hypocomplementemia (low C3) NA 90 % 95 % 61.5 % 100 %* among 65 PSGN
Acute renal failure 13.3 % 43.7 % 29 % 26 % 23.1 %
Nephrotic range proteinuria 1.48 % 25 % 1% 18 % 32.3 %

NA Data not available

*
Hypocomplementemia (low C3) with normalization at 8 wk was chosen as a diagnostic criterion in the present study
Indian J Pediatr
Indian J Pediatr
patient was complicated by crescentic glomerulonephritis.
The proportion of PSGN cases with elevated ASO titers was
extremely low (4.6 %). In pyoderma-associated PSGN, ASO
titers are usually low in contrast to pharyngitis-associated
PSGN [19]. The patients were diagnosed as PSGN based on
anti-DNAse B titers (positive in 93.8 %) or ASO positivity,
normalization of C3 level on at 8 wk follow up and clinical
evidence of streptococcal infection. The sudden decrease of
serum C3 concentration in PSGN with the return to normal
levels within six weeks of onset has been considered as of
foremost diagnostic importance when renal biopsy is not done
[1]. The authors did not screen the contacts serologically or
microbiologically for Group A streptococcal infection. The
contacts did not have clinical signs and symptoms of pyoder-
ma, pharyngitis or systemic infections.
The present study has many merits. Firstly, there is a pau-
city of published studies on the clinical spectrum of PIGN, in
general and PSGN in particular, in recent years. Secondly,
serious and potentially life threatening complications were
encountered in a considerable proportion of the enrolled sub-
jects, emphasizing the importance of timely therapeutic inter-
ventions in order to prevent morbidity or mortality arising
from PIGN. Thirdly, data in the current study were collected
in a prospective manner unlike many previously conducted
studies on the subjects [7, 17]. Fourthly, this is the first study
to have analyzed the incidence and staging of AKI as per the
AKIN and pRIFLE criteria, in a prospective cohort of subjects
with PIGN. Analysis of incidence of AKI and staging of AKI
as per these consensus criteria allows for rational interpreta-
tion of data and standardization of patient care in these patient
populations.
The present study has some limitations too. The study was
conducted at tertiary level referral hospital and the profile of
enrolled subjects may not be representative of the disease
profile encountered at the community level. Secondly, it is
known that children with PIGN as well as AKI may have long
term residual renal injury [1, 20]. Long term follow up of the
patients could not be done due to logistic reasons.
Conclusions
The present prospective observational study on 83 children
recruited with clinical features of ANS found an 86.7 % inci-
dence of PIGN, which was predominantly of post- streptococ-
cal etiology (90.3 %). A considerable proportion (9.7 %) of
children had infections of non- post streptococcal etiology.
These included pneumonia, liver abscess and mumps.
The study is notable for high incidence of hypertensive
emergency (21.5 %) and AKI (23.1 %) in PSGN, complica-
tions that often required management in an intensive care set-
ting. Although no deaths were encountered in children with
PIGN, this study serves as a timely reminder that PSGN
continues to remain an important pediatric disease and con-
tributes significantly to morbidity and inpatient care, in chil-
dren in southern India.
Contributions KG, SK and SM were involved in management of the
patients. KG collected the data, reviewed the literature and drafted the
manuscript. SK conceptualized the study, reviewed the literature and
critically reviewed the manuscript. SM critically revised the manuscript.
BNH supervised the laboratory tests. APK performed the statistical anal-
ysis. All authors contributed to writing the paper and approved the final
version of the manuscript. SK shall act as guarantor of the paper.
Conflict of Interest None.
Source of Funding The study was supported by an intramural grant
from the authors’ institution for estimation of serum anti-DNAse B and
C3 levels, which is gratefully acknowledged.
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