Hong Kong Journal of Nephrology (2016) 19, 28e35
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ORIGINAL ARTICLE
The analysis of patients with primary and
secondary glomerular diseases: A
single-center experience

Yavuz Ayar a,*, Alparslan Ersoy a, Emel Isiktas a,
Gokhan Ocakoglu b, Abdulmecit Yildiz a, Aysegül Oruc a,
Dilay Demirayak a, Ismail Bayrakci a, Hakan Duger a,
Tugba Bozbudak a
a Department of Nephrology, Internal Medicine, Uludag University Medical Faculty, Bursa, Turkey
b Department of Biostatistics, Uludag University Medical Faculty, Bursa, Turkey

Available online 8 October 2016
KEYWORDS
etiology;
glomerulonephritis;
mortality;
outcomes;
renal biopsy
* Corresponding author. Uludag Univ
E-mail address: yavuzayar@hotma

http://dx.doi.org/10.1016/j.hkjn.201
1561-5413/ª 2016 Hong Kong Society
CC BY-NC-ND license (http://creativ
Abstract Background/Purpose: Glomerulonephritis is among the most important group of
diseases causing end-stage renal disease (ESRD). The prevalence of glomerulonephritis varies
depending on age, sex, geographical features, etc. In the present study, we evaluated the clin-
ical and laboratory parameters of patients who underwent renal biopsy.
Methods: In this retrospective study, demographic and clinical characteristics, specific diagno-
ses of glomerular diseases, and biopsy findings of all patients in whom native renal biopsy was
performed in our hospital between January 2009 and December 2014 were analyzed.
Results: A total of 384 patients were divided into two groups as primary glomerular diseases
(PGD) and secondary glomerular diseases (SGD). Some 37.1% of patients with PGD and 49.2%
of patients with SGD were female. The mean age was 43.8 � 14.1 years in the PGD group
and 47.3 � 16.1 years in the SGD group (p Z 0.044). Nephrotic syndrome in the PGD group
and unexplained renal dysfunction in the SGD group were observed more frequently at the
time of admission. In the SGD group, biopsy findings (crescents, sclerosis, vascular involve-
ment, etc.) were dominant and more pronounced (p < 0.001). In the PGD group, responsive-
ness to the therapy was higher than in the SGD group (p < 0.001). Mortality rates were 2.27% in
the PGD group and 18.3% in the SGD group. According to the multivariate analysis, the increase
of creatinine level after treatment (odds ratio 1.49) and presence of SGD (odds ratio 7.74)
were independent risk factors for patient death (p < 0.001).
Conclusion: The present study showed important data about the etiology, clinical findings,
follow ups, and prognosis of PGD and SGD among adults in our center. We observed that mor-
tality was higher in patients with SGD.
ersity Medicine School, Department of Nephrology, 16059 Nilüfer/Bursa, Turkey.
il.com (Y. Ayar).

6.05.001
of Nephrology. Published by Elsevier (Singapore) Pte Ltd. This is an open access article under the
ecommons.org/licenses/by-nc-nd/4.0/).

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Primary and secondary glomerular diseases 29
背景 / 目的: 腎小球腎炎是導致末期腎病 (ESRD) 的最重要疾病,其盛行率與年齡、性別、及地域

特性有關。在本研究中,我們在接受腎臟組織活檢的腎小球疾病患者間,對相關的臨床及檢驗特徵

進行了調查。

方法: 在本回溯性研究中,對象為於 2009 年 1 月至 2014 年 12 月期間,在本院接受自身腎臟組織活

檢的病人。我們對其人口學與臨床特徵、腎小球疾病診斷、及活檢結果進行了分析。

結果: 調查對象為 384 位原發性腎小球疾病 (PGD) 或次發性腎小球疾病 (SGD) 患者。在 PGD 及

SGD 組別中,女性比例分別佔 37.1% 及 49.2%,平均年齡分別為 43.8 � 14.1 歲及 47.3 � 16.1 歲

(p Z 0.044)。入院時,PGD 組以腎病症候群較常見,SGD 組則以原因不明之腎臟功能障礙較常

見。在 SGD 組間,活檢結果較多樣化 (新月形、硬化、血管病變等) 且較明顯 (p < 0.001)。治療

反應比率以 PGD 組高於 SGD 組 (p < 0.001),死亡率分別為 PGD 組的 2.27% 及 SGD 組的

18.3%。多變項分析顯示,治療後肌酸酐的增加 (OR 1.49)、及 SGD 的存在 (OR 7.74) 是病人死亡

的獨立危險因子 (p < 0.001)。
結論: 對於本中心的 PGD 與 SGD 成年患者,本研究提供了成因、臨床表現、追蹤、及預後等方面

的重要數據,並觀察到 SGD 患者的死亡率較高。
Introduction

Glomerular diseases may manifest as many clinical pre-
sentations such as nephrotic syndrome, nephritic syn-
drome, acute or chronic renal failure, rapidly progressive
glomerulonephritis (RPGN), isolated proteinuria, and he-
maturia.1 Glomerular disease may be diagnosed as primary
glomerulopathy [e.g., membranous glomerulonephritis
(MGN), minimal change disease, focal segmental glomer-
ulosclerosis (FSGS)] or as secondary glomerulopathy as a
manifestation of a systemic disease (e.g., diabetes, hy-
pertension, and amyloidosis). However, infections, genetic
diseases (e.g., Fabry disease and Alport syndrome), drugs,
malignancy, vasculitis, and other conditions should be
considered in the differential diagnosis of secondary cau-
ses.2 In addition, clinical and laboratory findings are
important for diagnosis. Today, histopathological findings
obtained by renal biopsy are valuable for diagnosing
glomerular disease and developing treatment strategies.3e5

This study aimed to evaluate biopsy findings, clinical and
laboratory characteristics, mortality, and renal survival in
patients who underwent renal biopsy with a preliminary
diagnosis of glomerular disease, retrospectively.
Materials and methods

Participants

This retrospective study was performed in consecutive pa-
tients aged� 18 years with documented biopsy findings
between January 01, 2009 and December 31, 2014. A total
of 384 patients were divided into two groups as primary
glomerular diseases (PGD) and secondary glomerular dis-
eases (SGD). PGD was described as MGN, FSGS, immuno-
globulin A (IgA) nephropathy (IgAN), minimal change
disease, and membranoproliferative glomerulonephritis. All
patients in the PGD group were evaluated with clinical
findings and laboratory tests for secondary reasons of
glomerulonephritis. Six IgAN patients (4 males, 2 females)
with crescentic glomerulonephritis were evaluated in the
PGD group. SGD included patients with RPGN due to sec-
ondary reasons, lupus nephritis, amyloidosis, and
tubulointerstitial nephritis. The patients with chronic
glomerulonephritis in whom biopsy results could not help
differentiate primary disease, single kidney, genetic dis-
eases, and malignancies were excluded from the study. In
addition, we excluded patients who had a history of long-
term diabetes and/or hypertension, were diagnosed with
diabetes and hypertension and were receiving antihyper-
tensive and antidiabetic therapy, or in whom renal biopsy
findings were compatible with hypertensive nephrosclerosis
or diabetic nephropathy. The study was in accordance with
the Second Declaration of Helsinki. An informed written
consent was taken from all patients before they entered
the study.

Demographic parameters (age, sex), indication for
renal biopsy (nephrotic syndrome, nephritic syndrome,
and unexplained renal dysfunction), laboratory test re-
sults [serum urea, creatinine, albumin, lipid profile, daily
urinary protein excretion (UPE), Ig, complement (C)
levels], pathological diagnosis, detailed description of
pathological findings, and medications after renal biopsy
were obtained from the medical data and charts of pa-
tients in our center. Nephrotic syndrome was defined as
proteinuria of > 3.5 g/d associated with edema, hypo-
albuminemia, and hyperlipidemia. Nephritic syndrome
was proteinuria< 3.5 g/d associated with hematuria, hy-
pertension, and slowly progressive renal failure. We
calculated estimated glomerular filtration rate (eGFR)
using the Modification of Diet in Renal Disease formula
[186 � plasma creatinine�1.154 � age�0.203 � 1.212 (if
black) � 0.742 (if female)].

Renal biopsy

All biopsy samples were included if a specific diagnosis was
certain. Biopsy specimens were examined by the same
nephropathologist. Light and immunofluorescence (IF) mi-
croscopies were performed in all patients. Light microscopic
examinations of sections were stained with hematoxylin and
eosin, Masson’s trichrome, periodic acid-Schiff, periodic
acid-silver methenamine, and Congo red. Homogenous am-
yloid deposits stained positive with Congo red and immu-
nohistochemical AA amyloid stain, and were sensitive to
treatment with potassium permanganate that was



Table 2 Therapy of patients in both glomerular disease
groups.

Drugs PGD group
(n Z 264)

SGD group
(n Z 120)

n (%) n (%)

Steroids 97 (36.4) 60 (50)
ACEi or ARB 22 (8.3) 61 (50.8)
Cyclosporine 50 (18.9) 1 (0.83)
Cyclophosphamide 73 (27.6) 23 (19.2)
Azathioprine 19 (7.2) 5 (4.2)
Mycophenolate mofetil 3 (1.1) 1 (0.83)
Colchicine e 67 (55.8)
Melphalan e 7 (5.8)
Dialysis e 23 (19.2)

ACEi Z angiotensin converting enzyme inhibitor;
ARB Z angiotensin receptor blockers; PGD Z primary glomer-
ular diseases; SGD Z secondary glomerular diseases.

Table 1 Distribution of etiological causes in both glomerular disease groups.

PGD group (n Z 264) SGD group (n Z 120)

Male, n (%) Female, n (%) Male, n (%) Female, n (%)

MGN 65 (60.7) 42 (39.2) AA amyloidosis 43 (64.1) 24 (35.8)
FSGS 38 (55.8) 30 (44.1) Lupus nephritis 3 (15.7) 16 (84.2)
IgAN 41 (74.5) 14 (25.4) RPGN 8 (42.1) 11 (47.9)
MCD 14 (66.6) 7 (33.3) AL amyloidosis 3 (42.8) 4 (57.1)
MPGN 9 (64.2) 5 (35.7) Acute TIN 3 (60) 2 (40)

Chronic TIN 1 (50) 1 (50)

AA Z Amyloid A; AL Z Amyloid Light chain; FSGS Z focal segmental glomerulosclerosis; IgAN Z immunoglobulin A nephropathy;
MCD Z minimal change disease; MGN Z membranous glomerulonephritis; MPGN Z membranoproliferative glomerulonephritis;
RPGN Z rapidly progressive glomerulonephritis; TIN Z tubulointerstitial nephritis.

30 Y. Ayar et al.
compatible with secondary amyloidosis. IF microscopy was
used for identification of fibrinogen, IgG, IgM, IgA, C3, C4,
and C1q staining. The etiologies of diseases are shown in
Table 1.

The causes of AA amyloidosis were familial Mediterra-
nean fever in 18 patients (23.4%), bronchiectasis in 17 pa-
tients (25.4%), rheumatoid arthritis in 14 patients (20.9%),
tuberculosis in five (7.5%) patients, and unknown etiology in
13 patients (16.9%). The causes of Amyloid Light-chain (AL)
amyloidosis were multiple myeloma in four patients and
idiopathic in three patients. The distribution of RPGN pa-
tients were granulomatosis with polyangiitis (Wegener’s) in
eight patients (42.1%), microscopic polyangiitis in five pa-
tients (26.3%), Goodpasture Syndrome in four patients
(21%), and cryoglobulinemia associated with hepatitis B in
one patient (5.3%).

Treatments

The optimal treatments for many of the PGDs and SGDs
were applied according to the clinical practice guidelines.
We empirically treated all AA amyloidosis patients with
colchicine and control of the underlying inflammatory dis-
ease. AL amyloidosis patients received with
chemotherapeutic drugs (melphalan and steroid). The dis-
tribution of drugs used in patients is shown in Table 2. Also,
responses to treatment in PGDs and SGDs groups were
evaluated. The first response to the treatment was exam-
ined no earlier than 3 months after the beginning of
treatment. Complete remission was defined as 24 hour
urinary protein< 300 mg/d and partial remission as 24 hour
urinary protein< 3 g/d with a reduction in proteinuria by at
least 50% from the baseline.6

Statistical analyses

Continuous variables are expressed as the mean � standard
deviation or median (minimumemaximum). Categorical
variables are expressed by frequency and corresponding
percentage. The Wilcoxon signed rank test was used for
comparisons within groups. The chi-square test, Mann-
Whitney test, and independent sample t test were used
to compare data between groups, if appropriate. To
compare values before and after treatment, percent
changes were computed, and the Mann-Whitney test was
applied to compare these values between groups. Inde-
pendent risk factors that affected mortality were deter-
mined using binary logistic regression analysis. Data were
analyzed using IBM SPSS Version 22 (IBM Inc., Somers, NY,
USA). In all statistical analyses, p < 0.05 was defined as
statistically significant.

Results

Data of 384 patients were included in the study and
analyzed. Some 59.1% were male and 40.9% were female.
The mean age of the patients was 44.9 � 14.8 years. MGN
(40.5%), FSGS (25.7%), and IgAN (20.8%) were more common
among patients with PGD. In the SGD group, the most
common disease was AA amyloidosis (55.8%), followed by
lupus nephritis (15.8%), and RPGN (15.8%). In the PGD
group, the mean age (42 years, range:19e83 years) was
significantly lower than the SGD group (47 years,
range:18e80 years; p Z 0.044). The male patient ratio in
the PGD group was significantly higher than in the SGD
group (62.8% vs. 50.8%, p Z 0.026). At the time of admis-
sion, serum urea and creatinine levels of patients in the
SGD group were higher than those of patients in the PGD
group, and serum albumin, IgA, and eGFR values were



Table 4 Biopsy indications and findings of patients in both glomerular disease groups.

PGD group (n Z 264) SGD group (n Z 120) p

Biopsy indication, n (%)
Nephrotic syndrome 141 (53.4) 39 (32.5) < 0.001
Nephritic syndrome 90 (34.0) 39 (32.5) 0.760
Renal dysfunction 33 (12.5) 42 (35) < 0.001
Biopsy Findings, n (range)
Total number of glomeruli 12 (5e44) 14 (7e43) 0.044
Global sclerosis 1 (0e12) 0 (0e28) < 0.001
Segmental sclerosis 0 (0e6) 0 (0e11) < 0.001
Number of crescent 0 (0e7) 0 (0e11) < 0.001
Mesangial proliferation 117 (44.3%) 20 (16.6%) < 0.001
Thickening of BM 143 (54.1%) 27 (22.5%) < 0.001
Interstitial inflammation 255 (96.6%) 120 (100%) 0.062
Interstitial fibrosis 194 (73.4%) 38 (31.6%) < 0.001
Vascular involvement 128 (48.4%) 93 (77.5%) < 0.001
Tubular atrophy 196 (74.2%) 40 (33.3%) < 0.001
IgG (0e3þ) 0 (0e3) 0 (0e3) 0.032
IgM (0e3þ) 0 (0e3) 0 (0e3) 0.005
IgA (0e3þ) 0 (0e3) 0 (0e3) 0.031
C3c (0e3þ) 0 (0e3) 0 (0e3) 0.292
C1q (0e3þ) 0 (0e3) 0 (0e3) < 0.001
Fibrin (0e3þ) 0 (0e2) 0 (0e2) 0.114

BM Z basement membrane; Ig Z immunoglobulin; PGD Z primary glomerular diseases; SGD Z secondary glomerular diseases.

Table 3 Characteristics of patients in both glomerular disease groups.

PGD group (n Z 264) SGD group (n Z 120) p

Age (y) 43.8 � 14.1 47.3 � 16.1 0.044
Sex (male/female) 166/98 61/59 0.026
Urea (mg/dL) 42 (9e181) 58 (13e214) < 0.001
Creatinine (mg/dL) 1.0 (0.3e5.4) 1.21 (0.5e11) 0.002
Albumin (g/dL) 3.2 (0.8e5.2) 2.8 (0.8e5) < 0.001
UPE (g/d) 3.95 (0.1e46) 3.83 (0.03e28) 0.605
eGFR (mL/min) 79.1 (10e267.5) 57 (4.1e212) < 0.001
Serum IgG (mg/dL) 956.5 (148e2320) 852 (138e3980) 0.459
Serum IgM (mg/dL) 112 (16e838) 110.5 (16.9e334) 0.279
Serum IgA (mg/dL) 210 (25.5e797) 154 (22.6e467) < 0.001
Serum C3 (mg/dL) 129 (17e233) 127 (16.5e260) 0.188
Serum C4 (mg/dL) 30.5 (8.19e72.9) 29.7 (5.8e59.8) 0.550

C Z complement; eGFR Z estimated glomerular filtration rate; Ig Z immunoglobulin; PGD Z primary glomerular diseases;
SGD Z secondary glomerular diseases; UPE Z urinary protein excretion.

Table 5 Responses to treatment and outcomes in both glomerulonephritis (GN) groups.

PGD group (n Z 264) SGD group (n Z 120) p

Treatment response, n (%)
Complete remission 63 (23.9) 18 (15) 0.021
Partial remission 134 (50.8) 35 (29.2) < 0.001
No remission 67 (25.4) 67 (55.8) < 0.001
Outcomes, n (%) < 0.001
Complete remission without treatment 11 (4.2) 1 (0.8)
Partial/complete remission with continued treatment 188 (71.2) 47 (39.2)
ESRDa 36 (9.5) 21 (17.5)
Uncontrolled patient 23 (8.7) 29 (24.2)
Death 6 (2.3) 22 (18.3)

PGD Z primary glomerular diseases; SGD Z secondary glomerular diseases.
a ESRD Z end-stage renal disease (the patients who received hemodialysis, peritoneal dialysis or kidney transplantation).

Primary and secondary glomerular diseases 31



32 Y. Ayar et al.
lower. There was no significant difference in UPE, serum
IgG, IgM, C3, and C4 levels among both groups (p > 0.05;
Table 3).

The indications for biopsy were nephrotic syndrome
(53.4%) in the PGD group, and unexplained renal dysfunc-
tion (35%) in the SGD group. In the SGD group, causes of
death were infectious diseases (pneumonia, sepsis, etc.) in
12 patients (54.5%), cardiovascular complications
(myocardial infarction, arrhythmias, pulmonary embolism,
etc.) in eight patients (36.4%), and cerebrovascular acci-
dents (hemorrhage, coagulopathy) in two patients (9%).
Crescent formation, vascular involvement, and segmental
and global sclerosis in renal biopsies of patients in the SGD
group were significantly more common than in those of
patients in the PGD group. Moreover, mesangial prolifera-
tion, basement membrane thickening, interstitial fibrosis,
and tubular atrophy in renal biopsies of the patients in the
PGD group were more frequent. Immunohistochemical
analysis revealed that IgA and IgG depositions in the PGD
group and IgM and C1q depositions in the SGD group were
more prominent (Table 4).

The ratios of complete and partial remission of patients
in the PGD group were significantly higher than those of
patients in the SGD group (23.9% vs. 15% and 50.8% vs.
29.2%, respectively). In the follow up, 71.2% of patients in
the PGD group continued to receive the treatment. A
significantly greater number of patients were unresponsive
to treatment in the SGD group (55.8% vs. 25.4%). Thirty-six
patients in the PGD group and 21 patients in the SGD group
Table 6 Laboratory findings before and after treatment in both

PGD group (n Z 264)

Baseline Post-treatment

Creatinine (mg/dL) 1.0 (0.3e5.4) 1.0 (0.4e10)
Albumin (g/dL) 3.2 (0.8e5.2) 3.9 (1.5e5.2)
UPE (g/d) 3.95 (0.1e46) 1.05 (0e28)
eGFR (mL/min) 79.1 (10e267.5) 82.2 (5e217.1)
Total cholesterol (mg/dL) 261.5 (104e722) 215 (68e1986
LDL cholesterol (mg/dL) 165.5 (33.5e619) 139 (34e487)
HDL cholesterol (mg/dL) 44 (5e145) 45 (12e135)
Triglycerides (mg/dL) 194 (65e919) 154.5 (36e421)

eGFRZ estimated glomerular filtration rate; HDLZ high density lipop
diseases; SGD Z secondary glomerular diseases; UPE Z urinary prote

Table 7 Percentage changes (%) in laboratory findings before a

PGD group (n Z 264)

Creatinine (mg/dL) 0 [(�64)e628]
Albumin (g/dL) 18 [(�48)e258]
UPE (g/d) �70 [(�99)e455]
eGFR (mL/min) 0 [(�89)e225]
Total cholesterol (mg/dL) �13 [(�70)e918]
LDL cholesterol (mg/dL) �15 [(�79)e4700]
HDL cholesterol (mg/dL) 5 [(�70)e500]
Triglycerides (mg/dL) �19 [(�87)e206]

eGFRZ estimated glomerular filtration rate; HDLZ high density lipop
diseases; SGD Z secondary glomerular diseases; UPE Z urinary prote
progressed to end-stage renal disease (ESRD). Twenty-two
patients in the PGD group and 12 patients in the SGD group
started hemodialysis. Also, two patients in the PGD group
were treated with peritoneal dialysis. Twelve patients in
the PGD group and nine patients in the SGD group under-
went kidney transplantation. Two patients in the PGD group
had graft loss. The number of uncontrolled patients was
greater in the SGD group (24.2% vs. 8.7%; Table 5).

In both groups, when compared with the baseline values,
mean serum creatinine, albumin, and high density lipo-
protein cholesterol levels increased after treatment, and
mean UPE, total cholesterol, low density lipoprotein
cholesterol, and triglyceride levels decreased. The mean
eGFR values of patients in the SGD group decreased, while
those of patients in the PGD group did not change signifi-
cantly (Table 6). When the percentage changes of the
above parameters were compared after treatment in both
groups, increase in serum albumin and decrease in UPE of
patients in the PGD group and increase in serum creatinine
and decrease in eGFR of patients in the SGD group were
more significant compared to those of the other group
(Table 7).

The mortality rate of the SGD group was higher than that
of the PGD group (18.3% vs. 2.27%). In the SGD group, the
mortality rate was higher in patients with amyloidosis. In
the PGD group, the causes of death were infectious dis-
eases (pneumonia and sepsis) in four patients and cardiac
diseases (myocardial infarction, arrhythmias) in two pa-
tients. The infections usually developed following intense
groups.

SGD Group (n Z 120)

p Baseline Post-treatment p

0.022 1.21 (0.5e11) 1.65 (0.48e10) 0.001
< 0.001 2.8 (0.8e5) 3.1 (0.9e5) < 0.001
< 0.001 3.83 (0.03e28) 1.89 (0e21.8) < 0.001

0.427 57 (4.1e212) 39.8 (1.3e169) 0.001
) < 0.001 253 (135e606) 200 (106e508) < 0.001

< 0.001 176.5 (64e360) 143 (55e338) < 0.001
0.005 45 (16e104) 45 (11e113) 0.001

< 0.001 252 (59e700) 213 (47e478) < 0.001

rotein; LDL Z low density lipoprotein; PGD Z primary glomerular
in excretion.

nd after treatment in both groups.

SGD Group (n Z 120) p

9.8 [(�90)e1314] 0.020
5 [(�78)e230] < 0.001
�36 [(�100)e439] < 0.001
�10 [(�95)e1435] 0.010
�16 [(�59)e90] 0.109
�16 [(�50)e80] 0.974
6 [(�87)e211] 0.172
�18 [(�76)e151] 0.262

rotein; LDL Z low density lipoprotein; PGD Z primary glomerular
in excretion.



Table 8 Mortality distributions of patients in both groups.

PGD group (n Z 264) SGD group (n Z 120)

Male (n) Female (n) Male (n) Female (n)

MGN 2 1 AA amyloidosis 12 4
FSGS 1 e Lupus nephritis 1 1
IgAN 1 e RPGN 1 1
MCD e 1 AL amyloidosis e 2
MPGN e e Acute TIN e e

Chronic TIN e e

Total 6 (2.27%) 22 (18.3%)

AA Z Amyloid A; AL Z Amyloid light chain; FSGS Z focal segmental glomerulosclerosis; IgAN Z immunoglobulin A nephropathy;
MCD Z minimal change disease; MGN Z membranous glomerulonephritis; MPGN Z membranoproliferative glomerulonephritis;
PGD Z primary glomerular diseases; RPGN Z rapidly progressive glomerulonephritis; SGD Z secondary glomerular diseases;
TIN Z tubulointerstitial nephritis.

Primary and secondary glomerular diseases 33
immunosuppressive treatment. In the SGD group, the most
common causes of death were infectious diseases (pneu-
monia, sepsis, etc.) in 12 patients (54.5%), cardiovascular
complications (myocardial infarction, arrhythmias, pulmo-
nary embolism, etc.) in eight patients (36.4%), and cere-
brovascular accidents (hemorrhage, coagulopathy) in two
patients (9%). Death occurred in 14 patients due to infec-
tion and cerebrovascular accidents after immunosuppres-
sive treatment in the SGD group (Table 8).

Multivariate analysis of the percentage changes in serum
creatinine and UPE levels, eGFR, indications of biopsies,
presence of global and segmental sclerosis, crescent for-
mation, and types of glomerulonephritis revealed that in-
crease of serum creatinine and presence of SGD increased
mortality by 1.49-fold (95% confidence interval, odds ratio:
1.24e1.79; p < 0.001) and 7.74-fold (95% CI, odds ratio:
2.98e20.12; p < 0.001), respectively.
Discussion

The most common etiology of ESRD in Turkey is diabetes
mellitus, followed by hypertension and glomerulonephritis.
The relationship of hypertension with ESRD is to be dis-
cussed with regards to the cause and effect sequence of
hypertension and renal failure.7 Recently, a multicenter
cross-sectional study examined demographic and clinical
characteristics of 1274 patients with PGD in our country.
The most frequent pathological diagnosis was MGN (28.8%),
followed by FSGS (19.3%) and IgAN (17.2%).8

In the present study, the rates of PGD and SGD were
68.7% and 31.2%, respectively. At the time of admission,
the most common clinical manifestation was nephrotic
syndrome (53.4%) in the PGD group and renal dysfunction
(35%) in the SGD group. Among PGDs, MGN and FSGS were
more frequent. The most common causes of SGDs were
amyloidosis, RPGN, and lupus nephritis because of possible
exclusion of diabetic and hypertensive patients from the
cohort. These patients usually did not undergo biopsy
since they got their diagnosis clinically. Our center is the
referral center in the south Marmara region of Turkey.
Therefore, a higher frequency of amyloidosis could be
explained by the fact that a patient with heavy proteinuria
was referred to our center. A retrospective study of 289
patients in Turkey who underwent renal biopsy between
2008 and 2012 found that 75.9% and 14.5% had PGD and
SGD, respectively (mean age 50.8 � 16.1 years; 62.3%
males).9 The distribution of PGD and SGD in this study was
similar to our findings. The main causes of PGD in patients
over 85 years of age were MGN (9.9%) and IgAN (8.5%) in a
large-scale retrospective study including 17,680 renal bi-
opsies.10 Among SGD, amyloidosis (16.9%) and RPGN
(14.1%) were the most common glomerulopathies. In other
studies, FSGS, membranoproliferative glomerulonephritis,
and IgAN in patients with PGD and lupus nephritis, multi-
ple myeloma, and vasculitis in patients with SGD have
been reported at higher rates.11e15 These studies show
that there are differences between countries in the dis-
tribution of glomerulopathies.

There are many different causes for both PGDs and
SGDs. Treatment includes nonspecific measures aimed at
controlling hypertension, proteinuria, and disease modi-
fying immunosuppression. It is very difficult to directly
compare these diseases, because the treatment for each
glomerular disease is different. It was impossible for stan-
dardization of treatments in our study due to the retro-
spective design. Therefore, we did not obtain definite
conclusions by comparing the results of treatment in pa-
tients with PGD and SGD. The ratios of complete and partial
remission of patients in the PGD group were higher than
those of patients in the SGD group. A significantly greater
number of patients were unresponsive to treatment in the
SGD group. AA amyloidosis was the most frequent in our
SGD group. Chronic inflammatory diseases are important in
the etiology of this disease. In some studies, despite
treatment, the renal survival time was 64.7 � 6.3 months,
the partial and complete remission rates were approxi-
mately 57% and 10%, respectively, and the 5-year survival
rate was 48.7%.16,17

We observed that the mortality rate of the SGD group
was higher, especially in patients with amyloidosis. The
main causes of death were infectious diseases associated
with immunosuppressive treatment. In patients with SGD,
progression to ESRD was faster than that in patients with
PGD. Mortality and progression to ESRD varies according to
the type of glomerular diseases. Some 50% of patients with
FSGS progress to ESRD within 3e8 years of diagnosis, and
the spontaneous remission rate is < 6%. The 5-year renal



34 Y. Ayar et al.
survival is reported to be 50e78%.18,19 A recent study re-
ported that 3% of patients with MGN required renal
replacement therapy with a mortality rate of approxi-
mately 10% and partial remission rates of 39%, 70%, and 83%
in the 1st, 3rd, and 5th years, respectively. The rate of
complete remission was 38% during 5 years.20 During a 30-
year follow up, 20.6% of patients with IgAN progressed to
ESRD, and the survival rate was 5.3%. Complete remission
was observed in 22.9% of patients.21,22 In other studies
conducted in Taiwan and Egypt, patients with PGD were
followed for a median of 5.9 years; the mortality rate was
3.7%, and the response to treatment reached 45%.23,24 The
life expectancies of lupus patients with renal damage and
ESRD are 23.7 years and 15.1 years, respectively.25 In
another report, during a 22-month follow up of patients
with lupus nephritis, rates of remission, relapse, and mor-
tality were 45.5%, 82%, and 16%, respectively.26 RPGN is one
of the SGD with a high mortality rate. In a retrospective
study of 34 crescentic nephritis patients who were followed
for 3.5 years, 14.7% progressed to ESRD, 23.5% achieved
remission, and the mortality rate for a 3-month period was
8.8%.27 Furthermore, high serum creatinine levels and the
presence of SGD were independent risk factors for mor-
tality in our cohort.
Conclusion

Our data are an important contribution to the epidemiology
of renal disease in our country. Glomerulonephritis is
restricted to the kidney in PGD, whereas it is secondary to a
systemic disease in SGD. This may directly affect the clin-
ical course and prognosis of the patients with PGD or SGD.
We observed that current immunosuppression strategies in
the treatment of PGD or SGD remain unsatisfactory, espe-
cially in glomerular diseases that are frequently relapsing
or are resistant to treatment. The present study did not
include patients who received biologic agents. However,
further prospective studies are needed to evaluate the
efficacy of use of biologics in treating glomerulonephritis in
the future.
Conflicts of interest

The authors have no potential conflicts of interest related
to the content of this article.
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	The analysis of patients with primary and secondary glomerular diseases: A single-center experience
	Introduction
	Materials and methods
	Participants
	Renal biopsy
	Treatments
	Statistical analyses

	Results
	Discussion
	Conclusion
	Conflicts of interest
	References