Iran J Pediatr

Jun 2010; Vol 20 (No 2), Pp:199-205

Original Article

AnEstimationofSteroidResponsivenessofIdiopathic
NephroticSyndromeinIranianChildren
AbbasMadani1,2,MD;DarioushFahimi1,MD;RambodTaghaodi2,MD;
FatemehMahjoob2,3,MD;NiloofarHajizadeh*1,2,MD,andBehdadNavabi1,MD
1. DepartmentofPediatrics,TehranUniversityofMedicalSciences,Tehran,IRIran
2. Children'sMedicalCenter,PediatricsCenterofExcellence,Tehran,IRIran
3. DepartmentofPathology,TehranUniversityofMedicalSciences,Tehran,IRIran
Received:Apr20,2009;FinalRevision:Sep24,2009;Accepted:Mar12,2010

Abstract
Objective: Idiopathic Nephrotic syndrome (INS) is the most common form of nephrotic
syndrome(NS)inchildrenwiththepotentialofprogressiontoendstagerenaldisease(ESRD).
INS is steroidresponsive in most children, but not all patients respond to it. The aim of this
studywastodeterminetherateofsteroidresponsivenessinchildrenwithINSthatreferredto
Children'sMedicalCentersince1995to2007.
Methods:Inasacrosssectionalstudy,themedicalrecordsofallchildrenwithINSaged1to15
years who were referred to our referral hospital was reviewed. All patients with onset of
diseaselessthan1yearofage,spontaneousremission,secondaryformsofNSassociatedwith
systemicdiseases,andfollowupdurationoflessthan12monthswereexcludedfromthestudy.
Patientswerecategorizedinto6groups:Group1neededbiopsypriortoanytreatment,group2
nonrelapsingNS,group3infrequentlyrelapsingNS,Group4frequentlyrelapsingNS,group5
steroiddependentNSandgroup6steroidresistantNS.
Findings:Atotalof238patientswereenrolledinthestudy.Kidneybiopsywasperformedin
79cases.Minimalchangelesion(MCL)wasthemostcommon(36.7%)pathologicaldiagnosis.
Steroidresponsivenesswasfoundin81.5%ofallcasesincluding:96%ofMCL(consistingof
biopsyprovencasesandpresumedones),32%offocalandsegmentalglomerulosclerosis,73%
of diffuse mesangial proliferation and 58% of membranoproliferative glomerulonephritis
patients.Duringminimalfollowupperiodof12months,therewere194patientsinremission,
32patientswithactiveNS,and12patientsinESRD.
Conclusion: Our study results showed that 81.5% of all patients, 96.2% of MCL and 32% of
FSGSpatientsinitiallyrespondedtosteroidtherapy.
IranianJournalofPediatrics,Volume20(Number2),June2010,Pages:199205

KeyWords:IdiopathicNephroticSndrome;SteroidResponsiveness;Glomerulonephritis;FSGS
* Corresponding Author;
Address: Division of Nephrology, Children's Medical Center, Pediatrics Center of Excellence, No 62, Dr Gharib St, Tehran, Iran
E-mail: hajizadn@tums.ac.ir
2010byPediatricsCenterofExcellence,ChildrensMedicalCenter,TehranUniversityofMedicalSciences, Allrightsreserved.

200

SteroidResponsivenessofIdiopathicNephroticSyndrome;AMadani,etal

Introduction
Idiopathicnephroticsyndrome(INS)isthemost
common form of NS in children with the
potential of progression to end stage renal
disease (ESRD)[1]. It is more common in boys
than in girls with a ratio of 1.6:1 and occurs in
children at a median age of 4 years[2]. The
mortality rate of nephrotic syndrome (NS) was
40%before1940,primarilyduetoinfection;but
this has been significantly reduced with the
introductionofsteroidtreatmentandantibiotics.
Steroids have long been used as the first line of
treatment in NS, however, other immune
suppressives may be indicated when
prednisolone fails to induce or sustains
remission[3].
The overall incidence of childhood INS has
been generally stable over the past three
decades (two to seven cases per 100,000
children)[3].However, the histologicalpattern of
childhood INS is changing, and the incidence of
FSGS seems to be increasing[4,5]. Histopatho
logical findings in NS may reflect in patterns of
responsiveness[1].ThemostcommonformofNS
in children is minimal change lesion (MCL)[6,7].
The vast majority of patients with MCL (>90%)
respond to steroid therapy. Other types of INS
like focal and segmental glomerulosclerosis
(FSGS), diffuse mesangial proliferation (DMP),
membranoproliferative
glomerulonephritis
(MPGN) and membranous glomerulonephritis
(MGN)arelesssteroidresponsive.Morethan90
percent of patients who respond to steroid
therapy have MCL[6]. MCL can accurately be
diagnosed based on presenting clinical findings
inchildrenyoungerthan6yearsofage,absence
of hypertension, absence of hematuria, normal
complementlevels,andnormalrenalfunction[1].
Corticosteroids play a key role in the
treatment of INS. Although a high proportion of
patients experience relapses, many of them
continue their steroid responsiveness. The
International Study for Kidney Diseases in
Children (ISKDC) first introduced an empirical
treatment protocol for INS which later faced
some minor changes. The ISKDC recommends
that the initial episode be treated with
prednisoloneatadailydosageof60mg/mfor4
wk, followed by 40 mg/m for 3 days out of a

week(intermittenttherapy)foranother4wk[8,9].
Roughly 95% of patients with MCL and 20%
withFSGSachievedremissionwiththisprotocol
[2,3]. Approximately 90% of patients who will
respond to steroids (urine trace or negative for
proteinfor3consecutivedays)dosowithinfour
weeksafterstartingsteroids[10].
Majority of children with INS experience
relapses (proteinuria >40mg/m2/hr or urine
protein test tape 3+ or more for 3 consecutive
days after achieving remission) which could be
categorized as infrequent relapsing NS (IFRNS):
lessthan3relapsesduring1yearafterachieving
remission, Frequent Relapsing NS (FRNS): 3 or
more relapses during 1 year after achieving
remission, and steroid dependent NS (SDNS): 2
consecutive relapses during steroid therapy or
within2weeksafterdiscontinuationoftherapy.
On the basis of response to empiric
glucocorticoidtherapy,patientswithINScanbe
classified into GlucocorticoidResponsive and
GlucocorticoidResistant. Resistance to steroid
therapyrepresents10%ofINS[11].Gulatietalby
reviewing histopathology of 136 steroid
resistant NS (SRNS) children found that FSGS
wasthemostcommoncauseofSRNSinchildren
withonsetofNSatallagegroups[12],alsoKariin
Saudi Arabia[13] reported the same results. Del
Rio et al by reviewing the previously published
data on SRNS in literature showed a rise in the
incidence of FSGS[4]. A literature review of
steroidsensitive NS (SSNS) by Hodson et al
indicated that the mechanism of steroid
sensitivity is due to lymphocytederived
circulating factors leading to podocyte injury
withsubsequentproteinuria[14].
The current study aimed to define the true
steroid responsiveness pattern of Iranian
children with INS, since there is not much
statistical information regarding this issue in
Iranianchildren.

SubjectsandMethods
The study was conducted as a cross sectional
retrospective descriptive study. The medical
records of all children with INS aged 1 to 15

IranJPediatr;Vol20(No2);Jun2010

years who were referred to the hospital since

1995 to 2007 were reviewed. Cases were
selectedinanonrandomsimplefashion.Medical
records of patients with INS who fulfilled the
studycriteriawerethesourceofinformation.
Exclusioncriteriawereageofonsetofdisease
lessthan1year,secondaryformsofNS,lessthan
12 months followup, and initial spontaneous
remission. In each patient clincopathological
findings, responsiveness to employed treat
ments, and outcome or status at the follow up
periodofatleast12monthswasdetermined.
Renal biopsy was performed prior to
treatmentinthosewiththeonsetofthedisease
occurredat>7yearsofage,hypertension,renal
failure, macroscopic or high grade microscopic
hematuria, low C3 level, family history of Alport
syndrome, and in steroid unresponsive patients
atanytimeduringthecourseoftreatment.
Prednisolonewasadministeredatadosageof
60 mg/m2/day (maximum 80mg/day) three
timesadayfor4weeks;inthecaseofremission,
it continued at the dosage of 40mg/m2/day
every other day for another 4 weeks and then
tapered 10mg/m2 each 2 weeks in all patients
except MPGN cases. Patients with MPGN were
treatedwithprednisoloneatthedosageof2030
mg/m2/day plus dipyridamole 23 mg/kg/day
for2years.
On the basis of the steroid responsiveness
patternandthenecessityofkidneybiopsyprior
to initial treatment, patients were categorized
into 6 groups: Group 1: those needed renal
biopsy prior to initial treatment, Group 2: non
relapsing NS patients (NRNS) (no relapse in at
least 12 months after discontinuation of initial
therapy),Group3:IFRNS(lessthantworelapses
within6monthsorthreerelapsesduring1year
after achieving remission), Group 4: FRNS (two
or more relapses within 6 months or three or
more during 1 year after achieving remission),
Group5:SDNS(twoconsecutiverelapsesduring
tapering of steroid therapy or within 2 weeks
after discontinuation of therapy), and Group 6:
SRNS.
Data were analyzed using the Statistical
Package of SPSS (version 17). Descriptive
statistics were used, such as meanstandard
deviation (SD) for continuous variables and
percentage (%) to describe the proportion of

201

categorical variables such as sex and the

frequency of different histopathological
diagnosis.

Findings
Atotalof282patientsinitiallyenteredthestudy;
44caseswereexcludedduetoinadequatefollow
up (34 cases), secondary forms of NS (8 cases)
and spontaneous remission (2 cases). Finally
238patientsremainedinthestudy.
Theagerangeofpatientswas115yearswith
an average onset of 4.52 years. There were 152
(63.8%) males and 86 (36.2%) females. The
male/female ratio was 1.76 in this study. Sex
distribution of our six study groups is
summarized in Table 1. Range of follow up
period was 12144 months with a mean of 51
months.
Prior to the initial treatment, kidney biopsy
wasperformedin35patientsonthebasisofone
or two indications (family history of Alport
syndrome in 1 case, high grade microscopic
hematuria in 23 cases, onset of the disease
occurred at >7 years of age in 22 cases,
hypertension in 9 cases, decreased complement
level in 7 cases, and renal failure in 5 cases; 17
cases had more than one indication for renal
biopsy).
Prednisolone was administered in the
remainder 203 patients without initial renal
biopsy,butlaterinthecourseoftreatment44of
thesepatientsunderwentrenalbiopsy(Group4:
13 cases, Group 5: 13 cases, and Group 6: 18
cases). Renal biopsy is performed in totally 79
patients. Histopathological diagnoses were MCL
in 29 patients (36.7%), FSGS in 22 patients
(27.8%), DMP in 11 patients (13.9%), MPGN in
12 patients (15.1%), and others (MGN:
membranous
glomerulonephritis,
Alport
syndrome, FPGN: focal proliferative glomerulo
nephritis)in5patients.
Histopathological diagnoses were MCL in 29
patients (36.7%), FSGS in 22 patients (27.8%),
DMP in 11 patients (13.9%), MPGN in 12
patients (15.1%), and others membranous
glomerulonephritis(MGN),Alportsyndrome,

202

SteroidResponsivenessofIdiopathicNephroticSyndrome;AMadani,etal

Table1:Characteristicsofgroupsofpatientswithnephriticsyndromeonthebasisofthesteroidresponsiveness
No(%)

Male

Female

1*

35(14.7)

21

14

2(NRNS)
3(IFRNS)

45(18.9)
44(18.4)

32
30

13
14

Histopathologicaldiagnosison
renalbiopsy
MCL:13;FSGS:5;DMP:5;MPGN:
11;Alport:1

4(FRNS)

39(16.3)

25

14

MCL:7;FSGS:3;DMP:2;FPGN:1

5(SDNS)

47(19.7)

31

6(SRNS)

28(11.7)

15

Group

16

13

MCL:8;FSGS:3;DMP:1;FPGN:1
MCL:1;FSGS:11;DMP:3;FPGN:1;
MGN:1;MPGN:1

Statusafterthe
followupperiod
Remission:19;active
disease:12;ESRD:4
Remission:45
Remission:44
Remission:37;Active
disease:2;ESRD:0
Remission:44;Active
disease:3;ESRD:0
Remission:5;Active
disease:15;ESRD:8

*Group1:allpatientsunderwentbiopsybeforetreatment;NRNS:nonrelapsingnephroticsyndrome;IFRNS:infrequent
relapsingnephroticsyndrome;FRNS:frequentrelapsingnephroticsyndrome;SDNS:steroiddependentnephrotic
syndrome;SRNS:steroidresistantnephroticsyndrome;MCL:minimalchangelesion;FSGS:focalandsegmental
glomerulosclerosis;DMP:diffusemesangialproliferation;MPGN:membranoproliferativeglomerulonephritis;
MGN:membranousglomerulonephritis;FPGN:focalproliferativeglomerulonephritis,ESRD:endstagerenaldisease
10patientswerenotbiopsied,ofwhom3patientsexperiencedESRDandotherswereinactivedisease.

focalproliferativeglomerulonephritis(FPGN)in
5patients.
Steroid responsiveness was totally found in
194patients(81.5%)ofwhom175cases(73.5%
of all) were in Groups 25, and 19 (7.9% of all)
cases in Group 1 (out of 23 patients in Group 1
whoreceivedsteroids).Group6patients(11.7%
of total) were not responsive to steroids (Table
1).Thesteroidresponsivenessofthe79patients
with histopathological diagnosis on the basis of
renalbiopsyissummarizedinTable2.
The most prevalent relapsing patterns of
presumed MCL patients were 410 relapses
withameanfollowupperiodof60monthsin37
(24.8%) patients, 2 relapses with mean follow
up period of 51 months in 26(17.4 %) patients,
one relapse with mean follow up period of 35
months in 21 (14%) patients, and 3 relapses
with meanfollow up period of 54 months in 17
(11.4%)patients.

If we consider total number of MCL cases as

178 cases including biopsy proven ones (29
cases) and presumed ones (149 cases) (all
patients of Group 2 and Group 3 plus non
biopsiedcasesofGroup4andGroup5),steroid
responsiveness of MCL was 96.2% in this study
(171caseswereresponsivetosteroidsandonly
7casesdidnotrespond).

Discussion
Theaimofourstudywastoidentifythesteroid
responsiveness pattern in Iranian children with
INSduring12years.Ourstudyfindingsshowed
that majority of children with NS (81.5%)
respond to steroid therapy. This finding is
similar to other studies in other countries in

Table2:Steroidresponsivenesscharacteristicsofbiopsiedpatients
Histopathological
diagnosis
MCL
FSGS
DMP
MPGN
Others(MGN,Alport
syndrome,FPGN)

No
29
22
11
12
5

Initialsteroid
responsiveness
22
7
8
7
0(steroidin3
patientswithFPGN)

Statusafterthefollowupperiod
Remission:22;activedisease:6;ESRD:1
Remission:6;activedisease:12;ESRD:4
Remission:8;activedisease:1;ESRD:2
Remission:7;activedisease:4;ESRD:1
Remission:0;activedisease:4;ESRD:1

IranJPediatr;Vol20(No2);Jun2010

203

Middle East and around Iran, but is less (94%)

thanthatinISKDCreport[11].
Table 3 shows comparison of our findings
withthose of other studies. However, there are
few studies that reported a smaller rate of
steroidresponsivenessinINS(66%bySafaeiet
al[15]and22.5%byEke[16]).
Jung Sue Kim et al in 2005 found that the
frequency of SRNS in children is higher than
reported earlier. During the initial steroid
therapy, 71% were steroidsensitive, 15%
steroidresistant and 14% achieved partial
response. The follow up study showed that at
least45%ofthechildrenwithnewonsetNSdid
notshowthetypicalsteroidresponsivepattern.
Two factors were associated with developing
steroid resistance after initial response: shorter
interval to the first relapse (2.2 vs 5.4 months)
andthefirstrelapseoccurringduringtheinitial
steroidtreatment[17].
InElSheikhetalstudy,94.5%ofthepatients
underwent kidney biopsy amongst which MCL
was the commonest (28.84%) histopathological
diagnosis[18]. In a study on the role of
histopathologyonsteroidresistance,Gulatietal
found that SRNS children constituted 15.1% of
thechildrenreferredtotheirinstitute[12].Inour
study,Kidneybiopsywasperformedin33.2%of
the cases. MCL was the most common (36.7%)
pathologicaldiagnosis.FSGSwasfoundin27.8%,
MPGN in 15.1%, DMP in 13.9%, and other
lesionsin6.3%ofthepatients.MCLwasfoundin
22.2%FSGSin44.4%,MPGNin14.8%andother
pathologies in 1.5% of steroid resistant cases.
By histopathological classification of renal

biopsies in patients nonresponsive to steroids

Zaki et al found MPGN in 55.5%, and FSGS in
33.3% of their cases[18]. In Bircan et al study,
DMPandMPGNwerefrequenthistopathological
findings[19] and Ahmadzadeh (another study
fromsouthernIran)reportedthatFSGSwasthe
mostcommon(44%)histopathologicalfindingin
nonrespondingpatients[20].
Therateofsteroidresponsivenessinchildren
withMCLinourstudyisclosetoresponsiveness
ratereportedbySrivastava[18].InSrivastavaetal
study, 76.5% of the cases were diagnosed as
MCL,andnearlyallofthem(98%)respondedto
steroids[17]. MCL was the most common proven
histopathologicaldiagnosisofstudiesconducted
by Soad El Sheikh in Saudi Arabia[18], Davutoglu
in Turkey[21], and Srivastava in India[17], but the
predominant histopathological diagnosis in
AfricancountrieswasMGNduetohighhepatitis
Bprevalence[22].
Sharples et al compared the natural history
and steroid responsiveness of NS in Asians,
Europeans,andAfroCaribbeansbyconductinga
retrospective study on 42 patients. The
incidence of NS was six fold higher in Asian
children. They estimated annual incidence of
SRNS16.9per100000inAsians,2.6per100000
in Europeans, and 3.4 per 100000 in Afro
Caribbeans[23]. This rate in Zaki study from
Kuwait has been reported 6 per 100,000
childrenbelow12yearsofage[24].InBhimmaet
al investigation steroid sensitiveness was
62%[25]. The usually expected SSNS pattern was
uncommon in blacks, and MGN accounted for
40%ofcasesofwhich86.2%wereassociated

Table3:ComparisonofourstudywithotherstudiesinMiddleEast
Study
Zakietal[24]
Bircanetal[19]
Davutogluetal[21]
Ahmadzadehetal[20]
Safaeietal[15]
Gulatietal[26]
ElSheikh[18]
Ourstudy

Country
Kuwait
Turkey
Turkey
Iran
Iran
India
Saudi
Arabia
Iran

55
114
62
231
44
127

Response
tosteroid
therapy
84
86.9
79.8
87
66
82.7

55

89.3

21

45

238

81.5%

25.1

22.2

27

Noof
patients

Infrequent
relapsers

Frequent
relapsers

Steroid
dependents

21.9
57.1
26.4
26.4
37.9

16.6
16.7

34.8
38.8
21.6

15.2
21.9
22.6

13.5
18.1

204

SteroidResponsivenessofIdiopathicNephroticSyndrome;AMadani,etal

uncommon in blacks, and MGN accounted for

40% of cases of which 86.2% were associated
withchronichepatitisBvirusantigenemia.Only
14.4% of blacks had either biopsyproven
steroidsensitiveMCLorSSNS[22].
Therateofresponsivenesstosteroidtherapy
inourstudyismorethanAfricanstudies[22,25].
There are some major differences when
comparedwithAfricancountrieswhichcouldbe
explained by NS histopathological pattern
varieties. In our study 25% patients had no
relapse, that was fewer than in other studies
especially other reports from Iran. This rate in
Safaei, Ahmadzadeh and El Sheikh studies was
23%,37%and38.8%,respectively[15,18,20].

Conclusion
Our study showed that the rate of
responsiveness to steroid therapy is 81.5%
which is close to those of several other studies.
In addition, 96.2% of MCL and 32% of FSGS
patients initially responded to steroid therapy.
Therateofnonrelapsersinthisstudywas25%,
this is smaller than that reported in other
investigationsinIran.

Acknowledgment
This research was approved by Vicechancellor
for Research of School of Medicine of Tehran
UniversityofMedicalSciences.
ConflictofInterest:None

2. Lennon R, Watson L, Webb NJA. Nephrotic

syndrome in children. Pediatr Child Health.
2009;20(1):3642.
3. Eddy AA, Symons JM. Nephrotic syndrome in
childhood.Lancet.2003;362(9384):62939.
4. Del Rio M, Kaskel F. Evaluation and
management
of
steroidunresponsive
nephrotic syndrome. Curr Opin Pediatr. 2008;
20(2):1516.
5. Ozkaya N, Cakar N, Ekim M., et al. Primary
nephrotic syndrome during childhood in
Turkey.PediatrInt.2004;46(4):4368.
6. M Mubarak, A Lanewala, JI Kazi, et al.
Histopathological spectrum of childhood
nephrotic syndrome in Pakistan. Clin Exp
Nephrol.2009;13(6):58993.
7. Uddin MGM, Rahman MH, Begum A, et al.
Childhood nephrotic syndrome: rational of
management. J Bangladesh College Physicians
Surgeons.2004;22(2):5760.
8. Ekka BK, Bagga A, Srivastava RN. Single
versus divideddose prednisolone therapy for
relapses of nephrotic syndrome. Pediatr
Nephrol.1997;11(5):5979.
9. Bagga A, Mantan M. Nephrotic syndrome in
children.IndianJMedRes.2005;122(1):1328.
10. International Study of Kidney Disease in
Children. The primary nephrotic syndrome in
children: identification of patients with
minimal change nephrotic syndrome from
initialresponsetoprednisone.JPediatr.1981;
98(4):5614.
11. Mekahli D, Liutkus A, Ranchin B, et al. Long
term outcome of idiopathic steroidresistant
nephrotic syndrome: a multicenter study.
PediatrNephrol.2009;24(8):152532.
12. GulatiS,SenguptaD,SharmaRK,etal.Steroid
Resistant Nephrotic Syndrome: Role of
Histopathology.IndianPediatrics.2006;43(1):
5560.
13. KariJA,HalawaniM,MokhtarG,etal.Pattern
of steroid resistant nephrotic syndrome in
childrenlivingintheKingdomofSaudiArabia:
a single center study. Saudi J Kidney Dis
Transpl.2009;20(5):8547.
14. Hodson EM, Alexander SI. Evaluation and
management of steroidsensitive nephrotic
syndrome.CurrOpinPediatr.2008;20(2):145
50.

References
1. International Study of Kidney Disease in
Children: Nephrotic syndrome in children:
Prediction of histopathology from clinical and
laboratorycharacteristicsattimeofdiagnosis.
KidneyInt.1978;13(2):15965.

15. SafaeiA,MaleknejadS.Spectrumofchildhood
nephritic syndrome in Iran: A single center
study.IndianJNephrol.2009;19(3):8790.
16. Eke FU, Eke NN. Renal disorders in children.
PediatrNephrol.1994;8(3):3836.

IranJPediatr;Vol20(No2);Jun2010

17. Srivastava RN, Mayekar G, Anand R, et al.

Nephrotic syndrome in Indian children; Arch
DisChild.1975;50(8):62630.
18. El Sheikh S, Andigani A, Saggaf H, et al.
Clinicopathologicalstudyofprimarynephrotic
syndromeinthewesternareaofSaudiArabia.
J King Abdulaziz University Med Sci. 1994;
4(1):2534.

205

22. Bhimma R, Coovadia HM, Adhikari M.

NephroticsyndromeinSouthAfricanchildren:
changing perspectives over 20 years. Pediatr
Nephrol.1997;11(4):42934.
23. Sharples PM, Poulton J, White RH. Steroid
responsive nephrotic syndrome is more
common in Asians. Arch Dis Child. 1985;
60(11):10147.

19. Bircan Z, Yavuz Yilmaz A, Katar S, et al.

Childhood idiopathic nephrotic syndrome in
Turkey.PediatrInt.2002;44(6):60811.

24. Zaki M, Helin I, Manandhar DS, et al. Primary

nephrotic syndrome in Arab children in
Kuwait.PediatrNephrol.1989;3(2):21820.

20. AhmadzadehA,DerakhshanA,HakimzadehM,
et al. Idiopathic Nephrotic Syndrome in
Iranian
Children.
Indian
Pediatr.
2008;45(1):523.

25. OrtaSibu N, Lopez M, Moriyon JC. Renal

diseases in children in Venezuela, South
America.PediatrNephrol.2002;17(7):5669.

21. Davutoglu M, Ece A, Bilici M, et al. Steroid

responsiveness of children with idiopathic
nephroticsyndromeinsoutheasternregionof
Turkey.RenFail.2007;29(7):8559.

26. Gulati S, Kher V, Sharma RK, et al. Steroid

response pattern in Indian children with
nephrotic syndrome. Acta Paediatr. 1994;
83(5):5303.