Pediatr Nephrol (2009) 24:2375–2380
DOI 10.1007/s00467-009-1246-2
ORIGINAL ARTICLE
Oxidant stress in primary nephrotic syndrome:
does it modulate the response to corticosteroids?
Ashraf Bakr & Sami Abul Hassan & Mohamed Shoker &
Mayssa Zaki & Rasha Hassan
Received: 18 April 2009 / Revised: 24 May 2009 / Accepted: 8 June 2009 / Published online: 31 July 2009
# IPNA 2009
Abstract In order to assess the oxidative stress in newly
diagnosed children with primary nephrotic syndrome
(PNS), we serially measured serum total antioxidant
capacity (TAC) and malondialdehyde (MDA) in 33 children
with PNS and ten healthy matched controls. Patients were
classified into two groups: those who had steroid-sensitive
nephrotic syndrome (SSNS; n = 26) and those who had
steroid-resistant nephrotic syndrome (SRNS; n = 7). Of the
patients with SSNS, 15 were non-relapsers and 11 were
relapsers. At the proteinuric phase, all patients had
significantly higher MDA levels and lower TAC than the
controls. These changes were more marked in patients with
SRNS than in those with SSNS. During remission and
still on corticosteroids, patients had higher TAC and
similar MDA levels as in the proteinuric phase, but the
TAC and MDA levels still significantly differed from
those of the controls. More improvement in TAC and
MDA levels occurred in patients following the weaning
of corticosteroids, but TAC was still lower in the patients
than in the controls. Moreover, TAC was higher in non-
relapsers than in relapsers. Using a receiver operating
characteristic curve, the initial response to corticosteroids
could be predicted at serum TAC level ≥0.73 mM/L
(sensitivity 89%, specificity 86%), while serum TAC
levels ≤1.14 mM/L after the weaning of corticosteroids
could predict that the patient would not relapse (sensitivity
91%, specificity 80%). In conclusion, based on our results,
PNS can be considered to be associated with oxidative
stress even during remission. This stress may modulate
A. Bakr (*) : S. Abul Hassan : M. Shoker : M. Zaki : R. Hassan
Pediatric Nephrology, Mansoura Faculty of Medicine,
Mansoura University Children’s Hospital,
Mansoura, Egypt
e-mail: ashbakr@mans.edu.eg
the response to corticosteroids. Further prospective
studies using larger numbers of patients are needed to
validate these results.
Keywords Children . Corticosteroid response .
Oxidant stress . Primary nephrotic syndrome
Introduction
The generation of reactive oxygen species (ROS) is a normal
steady state process in cells, although uncontrolled production
results in damage to cellular molecules. Malondialdehyde
(MDA), the main indicator of lipid peroxidation, causes the
cross linking and polymerization of membrane components
and also reacts with DNA nitrogenous bases [1]. Cellular
defense mechanisms against ROS include enzyme systems
that directly remove these species (superoxide dismutase,
catalase and glutathione peroxidase) and non-enzymatic
scavengers that are either endogenous molecules (albumin,
glutathione and uric acid) or derived from the diet (vitamin
C, vitamin E, carotenoids, selenium and zinc). The cumulative
effect of endogenous and food-derived antioxidants represents
the total antioxidant capacity (TAC) of the system. An
imbalance between the production and elimination of ROS
is referred to oxidative stress [2].
The study of oxidant/antioxidant balance in primary
nephrotic syndrome (PNS) in both animal [3, 4] and human
[5–7] models has gained the attention of many researchers in
recent years. However, the results of these studies have been
conflicting. Almost all of the human studies were carried out
on patients with steroid-sensitive nephrotic syndrome. More-
over, whether the studied patients were relapsers or non-
relapsers was not taken into account. The longitudinal study
reported here was carried out to assess the serial changes in
2376
serum TAC and MDA levels in newly diagnosed PNS
children. We also evaluated the prognostic value of TAC and
MDA levels in predicting the response to corticosteroids.
Subjects and methods
Subjects
This study was a prospective observational study carried
out on 33 newly diagnosed children with PNS. The patients
were consecutively recruited from the Nephrology Unit at
Mansoura University Children's Hospital during the period
from February 2005 to October 2006. They included 22
male and 11 female pediatric patients whose ages ranged
from 2 to 10 years. Ten healthy children of matched age
and sex were included in the study as a control group.
Patients were diagnosed to have PNS according to the
criteria of the International Study of Kidney Disease in
Children (ISKDC) [8]. None of the children enrolled in the
study showed evidence of acute infection or systemic
diseases, and none had received albumin, blood or non-
steroidal anti inflammatory drugs in the last 2 weeks prior
to the study.
All patients received standard oral corticosteroids induction
therapy for 1 month. If the patients achieved remission, the
corticosteroids were tapered and withdrawn over a 2-month
period.
Serum levels of TAC and MDA were measured at three
stages of the disease:
Stage I: (proteinuric stage): the period immediately
following the diagnosis of PNS in all patients,
prior to the initiation of corticosteroid treatment;
Stage II: (remission on corticosteroids): at the end of the
induction of corticosteroid therapy in patients
who achieved remission;
Stage III: (after weaning of corticosteroids): immediately
after standard corticosteroid therapy had been
stopped.
Patients were followed up until the last clinic visit
(December 2008).
The patients were retrospectively classified into two
groups according to the criteria of ISKDC [8]: steroid-
sensitive nephrotic syndrome (SSNS) and steroid-resistant
nephrotic syndrome (SRNS). The SSNS group (n = 26)
included those who responded to standard corticosteroid
induction therapy, of whom 15 were non-relapsers
(patients who did not show any relapse during the
follow-up period) and 11 were relapsers (patients who
developed one or more relapses). The SRNS group (n = 7)
comprised patients who did not respond to standard
corticosteroid induction therapy. Renal biopsy of these
Pediatr Nephrol (2009) 24:2375–2380
patients revealed focal segmental glomerularsclerosis in
three patients, minimal change nephrotic syndrome in two
patients and diffuse mesangial proliferation in two
patients.
Measurement of serum TAC Levels
Serum TAC levels were measured according to the method
described by Koracevic et al. [9] in which the determination
of antioxidative capacity is based on the reaction of
antioxidants in the sample with a defined amount of
exogenously provided hydrogen peroxide. The antioxidants
in the sample eliminate a certain amount of the provided
hydrogen peroxide, and the residual hydrogen peroxide is
determined calorimetrically by an enzymatic reaction that
involves the conversion of 3,5 dichloro-2-hydroxy benzen-
sulphonate to a colored product.
Measurement of serum MDA
The colorimetric method described by Satoh [10] and
Ohkawa et al. [11] was used to measure serum MDA levels.
Thiobarbituric acid reacts with MDA in an acidic medium
at 95°C for 30 min to form a thiobarbituric acid reactive
product. The absorbance of the resultant pink product can
be measured at 534 nm.
Statistical analysis
The SPSS software program, ver.10 (SPSS, Chicago, IL)
was used to analyze the data. Data on the clinical and
laboratory characteristics of patients at presentation are
presented as mean ± standard deviation (SD). One-way
analysis of variance (ANOVA) was used to compare these
data between patients and controls. The chi-square test was
used to assess gender distribution in the studied groups.
The serum levels of MDA and TAC are presented as the
median and range. The Mann–Whitney test was used to
compare data between two groups, and the Wilcoxon
Signed Rank test was used to compare one group at
different times. A receiver operating characteristic (ROC)
curve was drawn to differentiate between SSNS and SRNS
as well as between non-relapsers and relapsers. P values
≤0.05 were considered to be significant.
Results
Characteristics of the study cohort
The clinical and demographic data on the children enrolled
in the study are given in Table 1. The data presented in
Table 2 reveal that, relative to the controls, all of the
Pediatr Nephrol (2009) 24:2375–2380 2377

Table 1 Descriptive data of the study cohort at presentation

Parameter SSNS SRNS (n=7) Controls (n=10) P value

Non-relapsers (n=15) Relapsers (n=11)

Age (years) 4.7±2.8 4.3±2.0 6.0±.81 4.3±2.0 0.36

Gender (male/female) 10/5 9/2 3/4 6/4 0.23
Systolic BP (mmHg) 96±6.32 95±4.47 97.86±10.7 95.5±4.38 0.83
Diastolic BP (mmHg) 61.3±7.4 62.72±0.1 62.85±7.55 65.5±4.38 0.43
Protein in 24-h urine (g/m2 per day) 3.6±0.5 3.22±0.97 5.41±1.6 − <0.0001
Serum albumin (g/dL) 1.9±0.3 1.7±0.33 2±0.23 4.3±0.44 <0.0001
Serum cholesterol (mg/dL) 346.0±1.9 352.18±16.73 401.86±90.09 139.62±5.68 <0.0001
Serum creatinine (mg/dL) 0.67±0.24 0.70±0.27 0.84±0.54 0.73±0.15 0.67
Serum C3 (mg/dL) 2.13±0.75 2.41±0.89 2.11±0.87 2.14±0.54 0.78

SSNS, steroid-sensitive nephrotic syndrome; SRNS, steroid-resistant nephrotic syndrome; BP, blood pressure
Data are presented as mean ± standard deviation (SD)

patients enrolled in the study had significantly lower TAC
serum levels during the three stages of the disease. In
comparison, serum MDA levels were significantly higher in
the patient group in stage I and II only, and no significant
difference was observed in stage III.
In stage I, SRNS patients had significantly lower TAC
levels (P=0.001) and higher MDA levels (P=0.003) than
SSNS patients (Table 3).
Figure 1a demonstrates that TAC levels significantly
increased in both non-relapsers (P=0.001) and relapsers
(P=0.005) in stage II compared to stage I. A further
significant increase was observed in stage III in non-
relapsers (P=0.001) and relapsers (P=0.003). No significant
difference in TAC levels was observed between non-relapsers
and relapsers in stage I. However, non-relapsers had higher
TAC levels in stages II (P=0.004) and III (P=0.001) than
relapsers.
There were no significant differences in MDA levels
between stage I and II in both relapsers and non-relapsers,
but MDA levels were significantly lower in stage III than
stage II in both non-relapsers (P=0.001) and relapsers
(0.004). No significant differences were observed in MDA
levels between non-relapsers and relapsers in the three
stages of PNS (Fig. 1b).
Figure 2 shows that it is possible to predict the
response to corticosteroids in the proteinuric stage of
PNS by using TAC levels at the cut-off point ≥0.73 mM/L
(sensitivity 89%, specificity 86%, predictability 93%).
Alternatively, TAC levels after the weaning of cortico-
steroids at a cut-off point ≤1.14 mmol/L could be used to

Table 2 Comparison of serum total antioxidant capacity and malondialdehyde levels between the studied patients and controls at different stages of primary
nephrotic syndrome

Stage I Stage II Stage III Controls

SSNS SRNS

Non-relapsers relapsers Non-relapsers Relapsers Non-relapsers Relapsers

TAC (mM/L) 0.86 (0.72–0.91) 0.82 (0.68–0.91) 0.66 (0.59–0.81) 0.97 (0.87–1.14) 0.88 (0.72–0.96) 1.43 (0.97–1.6) 1.05 (0.87–1.16) 1.78 (0.99–2.0)
MDA (nmol/mL) 12.5 (8.72–20.5) 14.4 (9.24–23) 17.5 (14.3–29) 10.8 (4.3–22.43) 13.2 (6.6–19.2) 4.8 (2.47–7.5) 6.4 (2.5–15.5) 6.6 (4.5–7.5)
a
P1 <0.0001 <0.0001 0.001 <0.0001 <0.0001 0.007 0.001
P2b <0.0001 <0.0001 0.001 0.006 <0.0001 0.08 0.86

TAC, Total antioxidant capacity; MDA, malondialdehyde

Values are presented as median, with the range given in parenthesis
a
P1, TAC vs. controls
b
P2, MDA vs. controls
2378 Pediatr Nephrol (2009) 24:2375–2380

Table 3 Comparison of serum levels of TAC and MDA between 1.00

SSNS and SRNS patients in the proteinuric stage of primary nephrotic
syndrome

Potential prognostic SSNS SRNS P 0.75

factors (n=26) (n=7)

TAC (mM/L) 0.85 (0.68–0.91) 0.66 (0.59–0.81) 0.001

0.50
MDA (nmol/mL) 13.4 (8.72–23.0) 17.5 (14.3–29.0) 0.003

Values are presented as median, with the range given in parenthesis

0.25

0.00
0.00 0.25 0.50 0.75 1.00

Fig. 2 The receiver operating characteristic (ROC) curve to differen-

tiate between steroid-sensitive nephrotic syndrome (SSNS) and
steroid-resistant nephrotic syndrome (SRNS) in the proteinuric stage
a TAC (mM/L) of PNS using serum TAC levels
2
8 Median level of controls
predict relapses (sensitivity 91%, specificity 80%, and
1.6
predictability 88%), as presented in Fig. 3.
1.4
1.2
1
0.8
Discussion
0.6

0.4 To the best of our knowledge, this is the first study to assess
Non relapser
0.2 Relapser serial changes in oxidants and antioxidants in a cohort of
0 newly diagnosed children with PNS with different
Stage I Stage II Stage III
responses to corticosteroids.
P1= Stage I vs. stage II (non relapsers: 0.001, relapsers: 0.005) All of the newly diagnosed patients with PNS in the
P2= Stage II vs. stage III (non relapsers: 0.00, relapsers: 0.003)
P3= Stage I vs. stage III (non relapsers: 0.001, relapsers: 0.003)
proteinuric phase of the disease prior to starting corticoste-
P4=non relapsers vs. relapsers (stage I: 0.49, stage II: 0.004, stage III: 0.001) roid therapy had oxidative stress in the form of high serum
MDA with low TAC concentrations. This condition of
b MDA (nmol/mL)
oxidative stress was similar whether the patients were
16
proved later to have SRNS or SSNS (either non-relapsers or
14

12 1.00

10

8
0.75
Median level of controls
6

Non relapser
0.50
2 Relapser

0
Stage I Stage II Stage III
0.25
P1= Stage I vs. stage II (non relapsers: 0.45, relapsers: 0.37)
P2= Stage II vs. stage III (non relapsers: 0.001, relapsers: 0.004)
P3= Stage I vs. stage III (non relapsers: 0.001, relapsers: 0.003)
P4=non relapsers vs. relapsers (stage I: 0.07, stage II: 0.15, stage III: 0.06) 0.00
0.25 0.50 0.75 1.00
Fig. 1 Serial changes in serum total antioxidant capacity (TAC) (a)
and malondialdehyde (MDA) level (b) in relapsers and non-relapsers Fig. 3 The ROC curve to differentiate between non-relapsers and
at different stages of primary nephrotic syndrome (PNS) relapsers using serum TAC after the weaning of corticosteroids
Pediatr Nephrol (2009) 24:2375–2380
relapsers). Interestingly, this pattern was more evident in
SRNS than in SSNS, while it was similar in non-relapsers
and relapsers.
Low TAC concentrations have been reported in the
proteinuric phase of SSNS during the first episode [12, 13]
or at relapse [13]. In contrast, Karthikeyan et al. reported
significantly increased ferric-reducing antioxidant power in
nephrotic syndrome in the active disease state and that this
remained high during remission when compared to the
controls [14]. While many studies have documented high
serum MDA levels [15–17], Ginveri et al. [6] reported high
intra-erythrocyte concentrations of MDA and reduced
concentrations of the antioxidant glutathione in both SSNS
and SRNS. However, Gusmano et al. [18] and Kinra et al.
[19] observed an insignificant rise of serum MDA, which
they explained as being due to factors associated with the
study design, including small sample size and bias resulting
from their selection of hospital controls, as well as to the
possibility that the much higher concentrations of membrane
cholesterol found in the acute phase provided a protective
effect.
The low TAC concentration in the proteinuric phase of
PNS could be attributable to many mechanisms. Hypo-
albuminemia may be a contributory factor as albumin is the
leading preventive antioxidant of the serum due to its role
as a metal binding protein [20]. Other contributory factors
are the impaired intestinal absorption of some antioxidant
components and/or the low antioxidant content of the diet
in patients with PNS as most have a poor appetite [21].
There are some data in the literature showing that a diet
deficient in selenium and vitamin E may lead to renal injury
characterized by proteinuria [22]. The low TAC during the
acute stage may also result from the increased consumption
of certain antioxidant components, such as vitamin C,
which is significantly lower in the acute phase of nephrotic
syndrome [7]. The impaired antioxidant status enhances
lipid peroxidation. There is some evidence available
showing that during the proteinuric stage of PNS circulating
lipids bind to and become trapped by extracellular matrix
molecules where they undergo oxidation, thereby increasing
the formation of ROS [23]. Enhanced lipid peroxidation is
known to be manifested by increased serum MDA levels [1].
During remission when patients were still receiving
corticosteroids, serum TAC improved in both non-relapsers
and relapsers compared to the proteinuric stage; however,
the levels were still significantly lower than those found in
the controls. This improvement was more marked in
non-relapsers than in relapsers. In comparison, although
serum MDA levels were still significantly higher in patients
during remission than in controls, they did not significantly
differ from levels in the proteinuric stage, and there was no
significant difference between non-relapsers and relapsers.
Previous studies have reported similar changes in serum
2379
TAC [12] and MDA [13, 24] concentrations in patients with
SSNS during the remission stage. High serum MDA levels
were more common among the relapsers than in another
group of patients during remission [24], but none of these
earlier studies took the differences between non-relapsers
and relapsers into account.
The normalization of serum albumin and the improvement
in a patient’s appetite as well as intestinal absorption of
antioxidants may be responsible for the increase in TAC levels
during the remission of the disease. The use of corticosteroids
may be another explanation for the improvement of TAC
levels. In an experimental rat model, the administration of
corticosteroids increased glomerular antioxidant enzymes,
which in turn reduced the proteinuria caused by hydrogen
peroxide infusion [25].
There was a further improvement in serum TAC levels in
both non-responders and responders following weaning of
the corticosteroids, in comparison to the previous two
stages of the disease, but the levels were still lower than
those found in the controls. Interestingly, relapsers still had
lower TAC levels than non-relapsers. In contrast, the MDA
level decreased significantly in both groups and reached the
level found in the controls; no significant difference was
observed between non-relapsers and relapsers.
The persistence of oxidative stress in patients with SSNS
after long-term remission has been reported by a number of
investigators [26, 27]. These changes in the studied
parameters suggest that although there is clinical remission,
as indicated by the absence of proteinuria and the
normalization of serum albumin, ongoing oxidative stress
still remains, even during remission. This indicates that the
body can withstand a certain degree of stress, only beyond
which do proteinuria and the clinical picture of nephrotic
syndrome occur [15].
It is difficult to interpret why patients with SRNS had more
oxidative stress than SSNS patients at the time of diagnosis
and why the oxidative stress was more evident in relapsers
than in non-relapsers during the remission of the disease. It
can be speculated that the oxidant/antioxidant imbalance
partly modulates the response of newly diagnosed PNS
patients to corticosteroids. Since our study cohort was
insufficient in terms of the number of enrolled patients,
further studies with larger numbers of patients are required to
prove/disprove this hypothesis. However, our results are
encouraging in terms of suggesting the use of serum TAC
and MDA levels as potential predictors of the response of
newly diagnosed patients to corticosteroid therapy. At the time
of diagnosis, we found that the response to corticosteroids
could be predicted at serum TAC level ≥0.73 mM/L
(sensitivity 89%, specificity 86%), while serum TAC levels
≤1.14 mM/L after the weaning of corticosteroids could
predict that the patient would be a relapser (sensitivity 91%,
specificity 80%).
2380
In conclusion, newly diagnosed patients with PNS
persistently have oxidant stress even during remission of
the disease. This stress may modulate the response to
corticosteroids. Serum TAC level at the time of the
diagnosis could predict the response to corticosteroids
while serum TAC after weaning of corticosteroids could
predict whether the patient would relapse or not. Further
prospective studies using larger numbers of patients are
needed to validate these results.
References
1. Valenzuela A (1991) The biological significance of malondialde-
hyde determination in the assessment of tissue oxidative stress.
Life Sci 48:301–309
2. McCord JM (2000) The evolution of free radicals and oxidative
stress. Am J Med 108:652–659
3. Pedraza-Chaverri J, Arevalo AE, Hernandez-Pando R, Larriva-
Sahd J (1995) Effect of dietary antioxidants on puromycin
aminonucleoside nephrotic syndrome. Int J Biochem Cell Biol
27:683–691
4. Ohtake T, Kimura M, Nishimura M, Hishida A (1997) Roles of
reactive oxygen species and antioxidant enzymes in murine
daunomycin-induced nephropathy. J Lab Clin Med 129:81–88
5. Clemens MR, Burza-Zanetti Z (1989) Lipid abnormalities and
peroxidation of erythrocytes in nephrotic syndrome. Nephron
53:325–329
6. Ginevri F, Ghiggeri GM, Candiano G, Oleggini R, Bertelli R
(1989) Peroxidative damage of erythrocyte membrane in children
with nephrotic syndrome. Pediatr Nephrol 3:25–32
7. Warwick G, Waller H, Ferns G (2000) Antioxidant vitamin
concentrations and LDL oxidation in nephrotic syndrome. Ann
Clin Biochem 37:488–491
8. International Study of Kidney Disease in Children (1981) The
primary nephrotic syndrome in children. Identification of patients
with minimal change nephrotic syndrome for initial response to
prednisone. J Pediatr 98:561–564
9. Koracevic D, Koracevic G, Djordjevic V, Andrejevic S, Cosic V
(2001) Method for the measurement of antioxidant activity in
human fluids. J Clin Pathol 54:356–361
10. Satoh K (1978) Serum lipid peroxide in cerebrovascular disorders
determined by a new colorimetric method. Clin Chim Acta 90:37–43
11. Ohkawa H, Ohishi N, Yagi K (1979) Assay for lipid peroxides in
animal tissues by thiobarbituric acid reaction. Anal Biochem
95:351–358
12. Zachwieja J, Bobkowski W, Dobrowolska-zachwieja A, Zaniew
M, Maciejewski J (2003) Decreased antioxidant activity in
hypercholesterolemic children with nephrotic syndrome. Med
Sci Monit 9:235–239
Pediatr Nephrol (2009) 24:2375–2380
13. Ece A, Atamer Y, Gurkan F, Davutoglu M, Kocyigit Y, Tutanc M
(2005) Paraoxonase, total antioxidant response, and peroxide
levels in children with steroid-sensitive nephrotic syndrome.
Pediatr Nephrol 20:1279–1284
14. Karthikeyan K, Sinha I, Prabhu K, Bhaskaranand N, Rao A
(2008) Plasma protein thiols and total antioxidant power in
pediatric nephrotic syndrome. Nephron Clin Pract 110:c10–
c14
15. Mathew JL, Kabi BC, Rath B (2002) Anti-oxidant vitamins and
steroid responsive nephrotic syndrome in indian children. J
Paediatr Child Health 38:450–454
16. Balamurgan R, Bobby Z, Selvaraj N, Nalini P, Koner BC, Sen SK
(2003) Increased protein glycation in non-diabetic pediatric
nephrotic syndrome: possible role of lipid peroxidation. Clin
Chim Acta 337:127–132
17. Ece A, Atamer Y, Gurkan F, Balici M, Kocyigit Y (2004) Antioxidant
status in relation to lipoproteins, leptin and pro-inflammatory
cytokines in children with steroid sensitive nephrotic syndrome. J
Nephrol 9:336–373
18. Gusmano R, Ginevri F, Ghiggeri GM, Perfumo F, Oleggini R,
Candiano G, Bertelli R, Piccardo MT (1988) Intraerytrocytary
markers of peroxidative alteration in children with nephrotic
syndrome. Contrib Nephrol 67:99–102
19. Kinra S, Rath B, Kabi BC (2000) Indirect quantification of lipid
peroxidation in steroid responsive nephrotic syndrome. Arch Dis
Child 82:76–78
20. Moran EC, Kamiguti AS, Cawley JC, Pettitt AR (2002)
Cytoprotective antioxidant activity of serum albumin and
autocrine catalase in chronic lymphocytic leukaemia. Br J
Haematol 116:316–328
21. Zachwieja J, Bobkowski W, Dobrowolska-Zachwieja A, Zaniew
M, Maciejewski J (2001) Dietary intake of antioxidants and
antioxidant status in nephrotic syndrome. Pol Merk Lek 58:237–
240
22. Baliga R, Baliga M, Shah SV (1992) Effect of selenium deficient
diet in experimental glomerular disease. Am J Physiol 263:56–61
23. Trevisan R, Dodesini A, Lepore G (2006) Lipids and renal
disease. J Am Soc Nephrol 17:145–147
24. Nagla T, Nagwa A, Mohamed M (2008) Oxidative modification
of low-density lipoprotein in relation to dyslipidemia and oxidant
status in children with steroid sensitive nephrotic syndrome.
Pediatr Res 63:404–409
25. Kawamura T, Yoshiok T, Bills T, Fogo A (1991) Glucocorticoid
activates glomerular antioxidant enzymes and protects glomeruli
from oxidant injuries. Kidney Int 40:291–301
26. Zachwieja J, Bobkowski W, Zaniew M, Dobrowolska-Zachwieja
A, Lewandowska-Stachowiak M, Siwinska A (2003) Apoptosis
and antioxdant defense in the nephrotic syndrome. Pediatr
Nephrol 18:1116–1121
27. Fydryk J, Jacobson E, Kurzawska O, Malecka G, Gonet B,
Urasinski T, Brodkiewicz A, Bokowska H (1998) Antioxidant
status of children with steroid sensitive nephrotic syndrome.
Pediatr Nephrol 12:751–754