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RENAL DATA FROM ASIA - AFRICA |
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| Year : 2019 | Volume
: 30
| Issue : 2 | Page : 478-491 |
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| Epidemiologic data of biopsy-proven renal diseases: Experience from a single center in South India |
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Varun Kumar Bandi1, Ammanna Nalamati2, Bharathi Kasinaboina2, Sai Swapna Chundru2
1 Department of Nephrology, Dr. Pinnamaneni Siddhartha Institute of Medical Science and Reaserch Foundation, Gannavaram, Andhra Pradesh, India
2 Arun Kidney Center, Vijayawada, Andhra Pradesh, India
Click here for correspondence address and email
| Date of Submission | 01-Jul-2018 |
| Date of Decision | 01-Sep-2018 |
| Date of Acceptance | 14-Sep-2018 |
| Date of Web Publication | 23-Apr-2019 |
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 Abstract | | |
An analysis of the renal biopsy data is important to understand the regional prevalence of various biopsy-proven renal diseases (BPRDs). We analyzed our renal biopsy registry over a period of 15 years. We retrospectively reviewed all the renal biopsies performed at Arun Kidney Centre, Vijayawada, Andhra Pradesh, from January 2004 to March 2018. All biopsies were analyzed using immunofluorescence and light microscopy. A total of 924 renal biopsies were considered for the analysis. The mean age of the patients was 32 ± 14.77 years, with a male:female ratio of 1.5:1. Nephrotic syndrome (46.1%) was the most common indication for renal biopsy, followed by rapidly progressive renal failure (11%) and rapidly progressive glomerulonephritis (9.9%). Primary glomerulonephritis (PGN) was the most common entity (66.8%), followed by tubulointerstitial disease (17.5%), secondary glomerulonephritis (SGN) (12.1%), and vascular nephropathies (3.5%). Among cases with PGN, the most common causes were minimal change disease (22.98%), immunoglobulin A nephropathy (21.3%), and membranous nephropathy (17%), whereas the most common SGN was lupus nephritis (60.7%). Acute tubulointerstitial nephritis (61.1%) was the most common tubulointerstitial disease, whereas antineutrophil cytoplasmic antibody vasculitis (56.3%) was the most common vascular nephropathy. We also noticed significant changing trends in many nephropathies. Our study provides epidemiologic data regarding the various BPRDs and also the changing trends of the individual renal diseases.
How to cite this article:
Bandi VK, Nalamati A, Kasinaboina B, Chundru SS. Epidemiologic data of biopsy-proven renal diseases: Experience from a single center in South India. Saudi J Kidney Dis Transpl 2019;30:478-91 |
How to cite this URL:
Bandi VK, Nalamati A, Kasinaboina B, Chundru SS. Epidemiologic data of biopsy-proven renal diseases: Experience from a single center in South India. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2022 Jun 26];30:478-91. Available from: https://www.sjkdt.org/text.asp?2019/30/2/478/256855 |
| Introduction | |  |
Renal biopsy is an indispensable tool for the nephrologist in the evaluation and management of patients with varying presentations of renal disease.[1] An analysis of the renal biopsy data is important to understand the regional prevalence of various biopsy-proven renal diseases (BPRDs) and their differences with respect to geographic areas, age, gender, and clinical manifestations. The data permit to understand regional epidemiology of the individual diseases. The registry data also help in future research to identify the changing trends of the diseases and the variations in epidemiology both at the regional level and between countries.[2],[3] Furthermore, a better understanding of the regional epidemiology and its correlation with the clinical presentation guides decision-making in routine practice.
This stresses the need for a regional or national registry. However, studies on BPRD analysis in India are scarce,[4],[5],[6],[7] and such studies are further less reported from South India. The aim of our study was to outline the incidence of various BPRDs of native kidneys and determine the epidemiology of these diseases presenting at our center. We also compared our results from similar studies published previously and discuss the variations if present.
| Methodology | | |
All renal biopsies performed at our center between 2004 and March 2018 were retrospectively analyzed. Inadequate biopsies, renal allograft biopsies, and biopsies with incomplete data were excluded from the study. The following data were recorded for every patient included in the analysis: name, age, sex, clinical syndrome, and histological diagnosis. All biopsies were performed using an 18G automated biopsy gun. All the patients had normal kidney size and no structural abnormalities on renal ultrasound. The biopsy data were collected retrospectively from patient records. The biopsy specimens were analyzed by a single pathologist over the years and were prepared according to standard protocol. Light microscopy (LM) and immunofluorescence (IF) were done for all cases, whereas electron microscopy (EM) was not routinely performed. Biopsies without IF were excluded. All biopsy specimens were stained with hematoxylineosin, Masson’s trichome, periodic acid–Schiff, and Jones silver methanamine for LM, whereas antisera against human IgG, immunoglobulin (Ig) IgA, IgM, C3, C1q, and kappa and lambda light chains were used for IF.
The clinical syndromes were categorized into the following categories: nephrotic syndrome (NS), nephritic syndrome (NpS), acute kidney injury (AKI), chronic kidney disease (CKD), rapidly progressive glomerulonephritis (RPGN), rapidly progressive renal failure (RPRF), asymptomatic urinary abnormalities (AUAs), and unexplained RF. Patients with nonnephrotic proteinuria, or isolated hematuria, were categorized as AUAs. Patients with RF, who could not be categorized as AKI or CKD, such as those with acute kidney disease, were categorized as unexplained RF. Patients with RF and normal kidney size on renal ultrasound, when found to have chronic GN or chronic interstitial nephritis (CIN) on biopsy without a discernible cause, were considered as CKD. Patients with worsening RF over weeks were considered as RPGN if a clinical suspicion of crescentic glomerular disorder was considered, and considered as RPRF if the rapid worsening was presumed to be either nonglomerular or of unclear etiology.
The histopathological diagnosis was classified as follows:
- Primary glomerulonephritis (PGN): This includes minimal change disease (MCD), membranous nephropathy (MN), IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS), postinfectious glomerulonephritis (PIGN), membranoproliferative glomerulonephritis (MPGN), mesangioproliferative glomerulonephritis (MsPGN), diffuse proliferative glomerulonephritis (DPGN), crescentic glomerulonephritis, C3 glomerulopathy (CSGN), chronic glomerulonephritis (CGN), IgM nephropathy (IgMN), and C1q nephropathy (C1qN)
- Secondary glomerulonephritis (SGN): This includes lupus nephritis (LN), diabetic nephropathy (DN), amyloidosis (AM), thrombotic microangiopathy (TMA), hemolytic uremic syndrome (HUS), Henoch-Schonlein purpura (HSP), and multiple myeloma (MM)
- Tubulointerstitial nephritis (TIN) : This includes acute tubulointerstitial nephritis (ATIN), acute tubular necrosis (ATN), CIN, and acute pyelonephritis (APN)
- Vascular nephropathies: These diseases include antineutrophil cytoplasmic antibody (ANCA) vasculitis, hypertensive nephro-sclerosis (HTN), and acute cortical necrosis (ACN).
The incidence of each histological type of renal disease and the clinical syndrome was calculated. Data from the time periods between 2004 to 2010 and 2011 to 2018 were compared. Our results were then compared with data from other studies from India and across the world. Mean, median, and standard deviation were calculated for variables such as age. Percentage was obtained for the comparison of categorical data. Two-tailed t-test was used for comparing two groups. P <0.05 was considered statistically significant.
The ethical standards were maintained as per institutional policy, and no formal consent was required because it is a retrospective study.
| Results | | |
A total of 1004 renal biopsies were analyzed retrospectively from 2004 to 2018, out of which 80 were excluded (renal allograft biopsies: n = 46 and incomplete data or inadequate biopsies: n = 34). The remaining 924 patients were included in the study. Among them, 554 (60%) were male and 370 (40%) were female. The mean age of the patients was 32 ± 14.77 years (range 1.5–75 years). The most common indication for renal biopsy was NS – 426 (46.1%), followed by RPRF – 102 (11%), RPGN – 92 (9.9%), AKI – 88 (9.5%), NpS – 66 (7.1%), RF – 60 (6.5%), AUA – 58 (6.3%), and CKD – 32 (3.5%).
PGN was found in a majority of patients, i.e., 618 (66.8%), and it was the most common renal disease found in biopsy, followed by TIN in 162 (17.5%), SGN in 112 (12.1%), and vascular disease in 32 (3.5%) cases.
A further detail of the underlying histological categories in each clinical syndrome [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8] showed that most of the PGN and SGN, i.e., 422 (57.8%), presented with NS, whereas tubulointerstitial diseases mostly presented with RPRF [74 (45.7%)] or AKI [65 (40.1%)]. Four patients with NS were found to have AIN on biopsy. EM could not be performed in these patients due to logistic reasons. Patients biopsied for AUA (n = 58, 6.3%) were due to IgAN (n = 32), MsPGN (n = 6), FSGS (n = 6), MN (n = 6), MCD (n = 3), Alport’s syndrome (n = 3), and MPGN (n =2). | Figure 1: Causes of nephrotic syndrome.
DPGN: Diffuse proliferative glomerulonephritis, CGN: Chronic glomerulonephritis, MCD: Minimal change disease, MN: Membranous nephropathy, FSGS: Focal segmental glomerulosclerosis, IgAN: Immunoglobulin A nephropathy, LN: Lupus nephritis, PIGN: Postinfectious glomerulonephritis, MPGN: Membranoproliferative glomerulonephritis, MsPGN: Mesangioproliferative glomerulonephritis, DN: Diabetic nephropathy, ANCA: Antineutrophil cytoplasmic antibody, C3GN: C3 glomerulopathy, IGM: Immunoglobulin M, C1qN: C1q nephropathy.
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 | Figure 2: Causes of nephritic syndrome.
LN: Lupus nephritis, IgAN: Immunoglobulin A nephropathy, PIGN: Postinfectious glomerulonephritis, FSGS: Focal segmental glomerulosclerosis, MPGN: Membranoproliferative glomerulonephritis, MN: Membranous nephropathy, MsPGN: Mesangioproliferative glomerulonephritis, DPGN: Diffuse proliferative glomerulonephritis, MCD: Minimal change disease, HSP: Henoch–Schonlein purpura.
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 | Figure 3: Causes of rapidly progressive renal failure.
ATN: Acute tubular necrosis, TMA: Thrombotic microangiopathy, ACN: Acute cortical necrosis, CIN: Chronic tubulointerstitial nephritis, IgAN: Immunoglobulin A nephropathy, PIGN: Postinfectious glomerulonephritis, CGN: Chronic glomerulonephritis, DN: Diabetic nephropathy, HSP: Henoch–Schonlein purpura, ANCA: Antineutrophil cytoplasmic antibody.
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 | Figure 4: Causes of rapidly progressive glomerulonephritis.
PIGN: Postinfectious glomerulonephritis, Crescentic GN: Crescentic glomerulonephritis, ANCA: Antineutrophil cytoplasmic antibody, LN: Lupus nephritis, IgAN: Immunoglobulin A nephropathy, MPGN: Membranoproliferative glomerulonephritis, DPGN: Diffuse proliferative glomerulonephritis, C3GN: C3 glomerulopathy, HUS: Hemolytic uremic syndrome, TMA: Thrombotic microangiopathy, MN: Membranous nephropathy, ACN: Acute cortical necrosis, Anti-GBM: Antiglomerular basement membrane.
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 | Figure 5: Causes of asymptomatic urinary abnormalities.
IgAN: Immunoglobulin A nephropathy, MsPGN: Mesangioproliferative glomerulonephritis, FSGS: Focal segmental glomerulosclerosis, MN: Membranous nephropathy, MCD: Minimal change disease, MPGN: Membranoproliferative glomerulonephritis.
Click here to view |
 | Figure 6: Causes of acute kidney injury.
ATN: Acute tubular necrosis, IgAN: Immunoglobulin A nephropathy, PIGN: Postinfectious glomerulonephritis, DN: Diabetic nephropathy, CIN: Chronic tubulointerstitial nephritis, APN: Acute pyelonephritis, ACN: Acute cortical necrosis, CGN: Chronic glomerulonephritis, MN: Membranous nephropathy, ANCA: Antineutrophil cytoplasmic antibody, MsPGN: Mesangioproliferative glomerulonephritis.
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 | Figure 7: Causes of chronic kidney disease.
CGN: Chronic glomerulonephritis, IgAN: Immunoglobulin A nephropathy,, CIN: Chronic tubulointerstitial nephritis, FSGS: Focal segmental glomerulosclerosis, DN: Diabetic nephropathy, HTN: Hypertensive nephrosclerosis, ANCA: Antineutrophil cytoplasmic antibody,.
Click here to view |
 | Figure 8: Causes of unexplained renal failure.
IgAN: Immunoglobulin A nephropathy, FSGS: Focal segmental glomerulosclerosis, HTN: Hypertensive nephrosclerosis, ATN: Acute tubular necrosis, CGN: Chronic glomerulonephritis, C3GN: C3 glomerulopathy, LN: Lupus nephritis, DN: Diabetic nephropathy, ANCA: Antineutrophil cytoplasmic antibody, CIN: Chronic tubulointerstitial nephritis, PIGN: Postinfectious glomerulonephritis.
Click here to view |
As shown in [Figure 1], the most frequent causes of NS were MCD, MN, and FSGS.
Although only 5%–10% of patients of IgAN present as NS, in this study, we observed NS in 34.9% of patients. This probably reflects a selection bias. Among the 12 cases with amyloidosis, ten (83.3%) cases presented as NS. In the remaining two cases, amyloidosis presented with AKI and proteinuria.
Among the PGN cases, MCD (15.4%) was the leading category, followed by IgAN (14.3%), MN (11%), and FSGS (10.6%). There were three cases of hereditary glomerular diseases (Alport’s syndrome) in our analysis [Figure 9]. | Figure 9: Primary glomerulonephritis.
MCD: Minimal change disease, IgAN: Immunoglobulin A nephropathy, MN: Membranous nephropathy, PIGN: Postinfectious glomerulonephritis, CGN: Chronic glomerulonephritis, MPGN: Membranoproliferative glomerulonephritis, Crescentic GN: Crescentic glomerulonephritis, C3GN: C3 glomerulopathy, DPGN: Diffuse proliferative glomerulonephritis, IgMN: Immunoglobulin G nephropathy, C1qN: C1q nephropathy.
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Among SGN [Figure 10], lupus nephritis was the most common lesion in our series, i.e., 68 (7.4%), followed by DN (1.6%), and amyloidosis (1.3%). ATIN was the most prevalent among tubulointerstitial diseases, occurring in 99 (10.7%) cases, whereas ANCA vasculitis (1.9%, 18 cases) was the most common cause of IN vascular nephropathies [Figure 11]. | Figure 10: Secondary glomerulonephritis.
LN: Lupus nephritis, DN: Diabetic nephropathy, TMA: Thrombotic microangiopathy, HUS: Hemolytic uremic syndrome.
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 | Figure 11: Tubulointerstitial and vascular nephropathies.
ATIN: Acute tubulointerstitial nephritis, ATN: Acute tubular necrosis, CIN: Chronic tubulointerstitial nephritis, APN: Acute pyelonephritis, ANCA: Antineutrophil cytoplasmic antibody, HTN: Hypertensive nephrosclerosis, ACN: Acute cortical necrosis.
Click here to view |
LN was the most common SGN (n = 68, 60.7%). The male-to-female ratio was 1:10.5. The mean age was 23.3 ± 8.4 years. The most common clinical presentation was NS (50%), followed by NpS (35.3%), RPGN (11.7%), and RF (2.9%). Class IV was the most common histopathological subgroup (48.5%), followed by Classes III and V (17.6%), Class II (10.3%), and Class I (5.9%). Renal insufficiency (serum creatinine >1.5 mg/dL) was present in 26 (38.2%) cases.
Age and gender have an effect on the incidence of kidney diseases [Table 1]. PGN was commonly diagnosed between the second and third decades, and was more common in males. The incidence was highest in the age group between 18 and 30 years, with 64.7% (400) being males and 35.2% (218) being females. LN was more common in young females, with 56 cases (82.4%) occurring between 18 and 30 years and 89.7% (61) of those being females. DN was found to be more common in males after the age of 30 years.
[Table 2] depicts the frequency of renal diseases in the two periods between 2004 to 2011 and 2011 to 2018. The incidence of MCD, amyloidosis, DPGN, and ATN increased significantly in the second decade, whereas the incidence of FSGS, MsPGN, LN, MM, ACN, and HUS decreased significantly. There was no significant change observed in the incidence of other diseases. | Table 2: Biopsy-proven renal diseases' incidence in the two time periods.
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| Discussion | | |
We reviewed comprehensive data regarding the demographics, renal syndromes, and pattern of different biopsy-proven renal pathologies during a period of 14 years at a single stand-alone nephrology institute in a town in South India.
We present a comparison of data obtained from our study with those from studies published elsewhere from the same region and also from Western countries [Table 3]. The data show that the patterns of renal disease do not exactly correlate with the Western data and some of the Asian studies.[8],[9],[10],[11],[12],[13],[14]
In our study, the most common presentation was NS, accounting for 46.1% of all BPRDs.
Similar presentation was noted in many studies across the world.[6],[7],[10],[12],[13],[15],[16],[17],[18],[19] However, few studies from Italy and Japan have shown AUA as the major presentation.[8],[11] This could be due to more aggressive screening program of mass urinary screening. In accordance with most of the published studies, our series also showed a male predominance in all types of BPRD, except in LN.[8],[9],[10],[11],[12],[13],[15],[19],[20],[21],[22],[23],[24]
In our study, MCD was the most common cause of NS, followed by MN, FSGS, IgAN, LN, and PIGN. This is in slight discordance with other published studies from other parts of the world.[4] In other Asian countries such as Japan and Korea, MCD was the most common cause of NS followed by MN and IgAN.[8],[20] In contrast, MN and IgAN were the most common causes of NS in the Czech registry, whereas it was FSGS followed by MCD and MN in Brazil.[10],[12],[19]
In our study, PGN was the most common type of renal disease, followed by TIN and SGN. PGN was the predominant disease in other studies as well, with SGN and TIN being the second and third interchangeably.[8],[9],[10],[11],[12],[14],[15],[20],[21],[23]
In our study, MCD, IgAN, MN, and FSGS were the major causes of PGN, accounting for up to 76.7% of the cases.
MCD was the most common PGN in our study, comprising 22.9% of PGN cases, which is similar to other studies.[4],[6],[12],[20],[23] It showed a slight male preponderance (male:female 1.48:1) and was more common in the second and third decades.[22],[23]
FSGS was the fourth most common PGN in our study, accounting for 14.9% of all PGN cases. In contrast, FSGS has been reported to be the most common PGN in studies from Pakistan and Brazil.[5],[7],[12],[25] We also observed a significant decreasing trend in FSGS incidence from 2004–2010 to 2010–2018 {P <0.05). The reason for the declining trend is unknown. It was relatively more common in adults and males (male:female 1.3:1). In our study, FSGS was insignificantly more common in males (male:female 1.3:1), with peak incidence in the third decade and majority (77.6%) presenting as NS. In contrast to our study, a worldwide increase in FSGS incidence has been reported,[26],[27] with prevalence increasing over the last 20 years from <10% to 25%.[14] The increasing trend may be partly explained by broadened definition and new environmental causes.[28],[29]
MN has been taught to be the most common cause of NS in adults. However, several reports have found contrary results, with many finding MN to be the third or fourth common cause of NS in adults.[6],[8],[10],[13],[14],[15],[20],[23] In concordance with these studies, MN was the third most common PGN (16.5%) in our study. However, it was the most common cause of NS in adults, with a peak incidence in the fourth to sixth decades and a significant male predominance (male:female 2.1:1) (P <0.05). There was no significant difference in the incidence of MN between the two decades.
Even though IgAN is considered the most common glomerular disease worldwide,[8],[10],[14],[15],[20],[21],[24] its detection rate varies depending on biopsy indications and mass urinary screening programs for asymptomatic urinary abnormalities.[18],[21] However, we observed IgAN as the second most common PGN (21.4%), and there was an insignificant increase in its incidence in the last decade. In our study, NS was the most common presentation of IgAN (34.9%), followed by AUA (24.8%). Other presentations of IgAN such as RF (12.4%), NpS (9.3%), CKD (6.2%), RPGN (6.2%), AKI (4.7%), accelerated hypertension (3%), and RPRF (1.6%) were not common.
Several studies have reported a decreasing trend in the incidence of MPGN, which can be partly explained by the improvement in hygienic environments, universal precaution, and vaccinations, leading to a reduction in the infection rate.[3] Our study concurs with these observations. Another probable reason for the low incidence of MPGN in our study could be classification of the diseases with MPGN pattern into respective categories.
In our study, MPGN comprised 2.9% of all PGN, which is slightly lower than that compared to other studies conducted at Vellore (5.2%) and Hyderabad (7.5%).[7],[17]
IgMN and C1qN were the least common entities in our study, 0.5% and 0.3% of PGN, respectively. In fact, most of the studies did not mention these as distinct categories. A study done in Pakistan has reported IgMN in 2.9% cases of PGN.[5]
The most common SGN in our study was LN, which is comparable with that reported in many studies across the world.[5],[6],[7],[10],[15],[19],[20],[21] UAE, Italy, and some studies from India and Pakistan have reported a high incidence of amyloidosis, which could be partly due to the associated high prevalence of infections such as tuberculosis.[4],[5],[9],[11],[16] In our study, amyloidosis comprised 10.7% of the SGN.
Vasculitis, which presented with focal necrotizing GN, was mostly ANCA associated, 12 (66.7%), whereas the remaining was immune complex mediated. In ANCA-associated vasculitis, cANCA was positive in most of the patients (83.3%), whereas two cases showed pANCA.
TIN was found to be a relatively less frequent BPRD in many studies. However, our study showed a higher incidence of TIN (17.5%). ATIN was the most common lesion of the category, and most of the patients in the category were of older age. The most common etiology of acute and chronic tubulointerstitial diseases was drugs, especially nonsteroidal anti-inflammatory drugs and native medications.
The prevalence of obstetric AKI was less (0.4%) in our study, which could be either due to decreased referral or decreased over-all incidence with improvement in the delivery practices. There were three cases of Alport’s syndrome and no other heredo-familial nephropathies, which could be due to the lack of routine performance of EM in our study.
| Conclusion | | |
This study and similar studies from India that, in primary glomerular diseases, MCD is the most common lesion in renal biopsy among the young age group followed by MN. LN is the dominant secondary pathological lesion, occurring predominantly in young age females. The changing incidence of BPRD in the reports published over time from India is partly contributed by an increased referral due to increased awareness, together with increased workforce and infrastructure. Our study highlights the need for a central renal biopsy registry with an increased participation of many more nephrology centers of India to obtain accurate knowledge about the incidence, spectrum, and distribution of the types of renal disease.
Conflict of interest: None declared.
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Correspondence Address:
Ammanna Nalamati
Arun Kidney Center, Vijayawada, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1319-2442.256855
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
[Table 1], [Table 2], [Table 3] |
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