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Year : 2012  |  Volume : 23  |  Issue : 5  |  Page : 1008-1016
Histomorphological classification of focal segmental glomerulosclerosis: A critical evaluation of clinical, histologic and morphometric features

1 Department of Pathology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India
3 Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India

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Date of Web Publication13-Sep-2012


Primary focal segmental glomerulosclerosis (FSGS) has recently been divided into five subtypes by the Columbia classification. However, little is known about the incidence of these subtypes in the Indian population. In addition, there are very few studies evaluating the clinico-pathologic features with morphometric parameters in these subtypes. This study was aimed at evaluating the clinical, histopathological and morphometric parameters in various subtypes of FSGS at our referral center. Sixty-five (65) cases of idiopathic FSGS, diagnosed over two years (2006-2007), were included in the study. Detailed clinical and biochemical investigations were noted. Histological sections were reviewed and cases classified according to the Columbia classification and various glomerular and tubulo-interstitial features were noted. Glomerular morphometry on digitized images was performed using image analysis software. Renal biopsies with minimal change disease were used as controls for morphometric evaluation. In this study, FSGS not otherwise specified (NOS) was the most common subtype (44.6%), followed by perihilar FSGS (24.6%), collapsing (13.8%), tip (12.3%) and cellular FSGS (4.6%). Collapsing subtype showed significantly shorter duration of symptoms and higher degree of proteinuria, mean serum urea and creatinine compared with the other subtypes. On histologic analysis, features like glomerular hyalinosis, capsular adhesion, mesangial proliferation and visceral epithelial cell prominence (VEP) were frequently seen. The cases with VEP had a shorter duration of symptoms and a higher mean serum creatinine and 24-h urine protein excretion compared with those without VEP. The morphometric study revealed a significant higher mean glomerular area in the NOS, perihilar and collapsing variants as compared with the control biopsies. The present study highlights the differences in the prevalence in the FSGS subtypes in our population compared with the western data. Also, the significant differences in the clinical, biochemical and histological parameters reaffirm the utility of the Columbia classification of FSGS in routine reporting of renal biopsies. We found VEP (without causing collapse of the tuft) to be associated with higher serum creatinine at presentation. This feature needs to be evaluated in further studies for its potential significance.

How to cite this article:
Das P, Sharma A, Gupta R, Agarwal SK, Bagga A, Dinda AK. Histomorphological classification of focal segmental glomerulosclerosis: A critical evaluation of clinical, histologic and morphometric features. Saudi J Kidney Dis Transpl 2012;23:1008-16

How to cite this URL:
Das P, Sharma A, Gupta R, Agarwal SK, Bagga A, Dinda AK. Histomorphological classification of focal segmental glomerulosclerosis: A critical evaluation of clinical, histologic and morphometric features. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2020 Jun 4];23:1008-16. Available from: http://www.sjkdt.org/text.asp?2012/23/5/1008/100883

   Introduction Top

Primary focal segmental glomerulosclerosis (FSGS) is an important etiology of nephrotic syndrome both in pediatric and in adult patients. Over the last few decades, various histologic subtypes of FSGS have been described in the literature, including cellular, collapsing and tip variants. [1],[2],[3] However, it was only recently that a consensus histologic subclassification of FSGS was proposed by the Columbia group and came to be known as the Columbia classification. [4] This classification recommends a hierarchical approach to the histologic characterization of FSGS in a renal biopsy specimen.

The utility of the Columbia classification has been the subject of several recent publications. [5],[6],[7] These studies have demonstrated differences in the clinical presentation between the various subtypes with regard to duration of symptoms, degree of proteinuria and renal dysfunction. [5],[7] Histologic changes involving the tubulo-interstitial and vascular compartments have also shown to be different in the FSGS subtypes. [5] The data of prevalence of FSGS subtypes in the Indian population is relatively scant in the available literature, with only one recent study. This study included only adult patients with FSGS, and showed FSGS not otherwise specified (NOS) to be the most frequent subtype. [8]

Although glomerular morphometry studies have been performed in biopsies with FSGS in comparison with minimal change disease, [9] no such study was found evaluating the various subtypes of FSGS as proposed in the Columbia classification.

This study, hence, was aimed at assessing the variation in the prevalence of FSGS subtypes in our population compared with the published western data. The clinical and histological features of these subtypes were also evaluated along with a glomerular morphometric study in the subtypes.

   Materials and Methods Top

A retrospective search for idiopathic FSGS diagnosed at our department was conducted over a period of two years (2006-2007). The diagnosis of idiopathic FSGS was established when there was no evidence for another primary glomerular disease or a systemic disease known to be associated with secondary segmental glomerular sclerosis, including morbid obesity, reflux, HIV infection, nephrectomy, solitary kidney, intravenous drug abuse or a family history of renal disease.

In all cases, detailed demographic, clinical and laboratory parameters were recorded. Histologic sections, stained by hematoxylineosin, periodic acid Schiff (PAS) and silver methenamine (SM) were reviewed. A minimum of five glomeruli were required for inclusion in the study. Histologic features, including capsular adhesion, visceral epithelial cell prominence, mesangial proliferation (>4 cells in a mesangial area, away from vascular pole), intraglomerular foam cells and arteriolar changes were studied. The interstitial fibrosis and tubular atrophy were recorded and graded as mild (<25% of cortical parenchyma), moderate (26-50% of cortical parenchyma) and severe (>50% of cortical parenchyma involved). Immunofluorescence findings were also reviewed in all cases. In addition, glomerular morphometry for mean glomerular area was performed using Image ProPlus software (Media Cybernetics, Bethesda, MD, USA) by tracing the outline of the glomerulus.

All the cases were classified using the Columbia classification proposed by D'Agati et al in 2004 into FSGS NOS, tip, perihilar, cellular and collapsing variants. [4] According to this classification, collapsing variant was defined by collapse of at least one capillary loop with hyperplasia and hypertrophy of overlying visceral epithelial cells, regardless of presence of other variants of FSGS. Tip variant of FSGS requires the exclusion of collapsing variant and presence of at least one glomerulus with segmental lesion involving the tip domain (identified by origin of proximal tubule) of the glomerular capillary tuft. For this variant, any perihilar sclerosis also needs to be excluded. The cellular variant requires exclusion of collapsing and tip lesions, and is defined by segmental endocapillary hypercellularity occluding lumina in at least one glomerulus. In the perihilar variant, the segmental sclerotic lesion is located at the vascular pole and mandates the exclusion of collapsing, tip or cellular lesion. In cases where none of these definitions are satisfied, the term NOS is used. FSGS NOS is, thus, a histologic diagnosis of exclusion. [4]

   Statistical Analysis Top

Appropriate statistical tests were applied to the data as follows: Student's t-test for data with normal distribution and Mann-Whitney test for non-normal data. Difference between proportions was applied for parameters with data in percentages.

   Results Top

A total of 65 patients were included, of which 46 were males and 19 were females (male: female 2.42:1). All the patients had steroid-resistant nephrotic syndrome. There were 24 biopsies from children (<18 years of age), while only two patients were more than 50 years in age. Using the Columbia classification, FSGS NOS [Figure 1]a was the most frequent lesion (29 cases, 44.6%), followed by perihilar FSGS [Figure 1]b seen in 16 cases, comprising 24.6% of all cases. Collapsing FSGS [Figure 1]c was seen in nine cases (13.9%), tip lesion [Figure 1]d in eight biopsies (12.3%) and cellular lesion [Figure 1]e in three biopsies (4.6%). Among the various age groups, FSGS NOS was the most frequent, both in children and in adults, while collapsing FSGS was noted pre-dominantly in adults (eight out of nine cases).
Figure 1. A panel of photomicrographs showing (a) glomerulus with FSGS NOS subtype (PAS x200), (b) perihilar sclerosis (PAS x200), (c) collapsing FSGS demonstrating segmental proliferation of visceral epithelial cells with collapse of the underlying tuft (silver methenamine x200), (d) tip variant with sclerosis near the tubular pole of glomerulus (PAS ×200), (e) cellular FSGS showing a glomerulus with segmental sclerosis and endocapillary hypercellularity (H&E ×200), (f) intraglomerular foam cells (H&E ×200).

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Clinical features

Duration of the disease was found to be significantly different between the various histologic variants of FSGS. The mean duration of symptoms prior to presentation was 26.2 (±10.4) months in FSGS NOS, 24.5 (± 10.1) months in perihilar, 19.6 (±9.5) months in tip variant, 12.5 (±6.3) in cellular variant and 8.3 (±2.3) months in collapsing FSGS. Cellular and collapsing variants had significantly shorter duration of symptoms prior to clinical presentation (P <0.05) compared with the other variants. Collapsing FSGS also had a higher mean degree of proteinuria (5.92 ± 3.03 g/24 h) compared with FSGS NOS (3.96 ± 1.79) and perihilar type (4.16 ± 1.53). The mean degree of proteinuria in the tip lesion was 4.41 ± 2.52 g/24 h and 5.13 ± 2 g/24 h in the cellular variant. Nephrotic range proteinuria (>1000 mg/m 2 /d) was observed in 44 patients (67.6% cases). All the three cases of cellular FSGS presented with nephrotic range proteinuria, while the same was seen in 65.5%, 62.5%, 66.6% and 75% of FSGS NOS, peri-hilar, collapsing and tip variants, respectively. There was no significant difference in the frequency of nephrotic syndrome between the various histologic variants of FSGS. Microscopic hematuria was observed in 36 patients (55.4%) in our study. The frequency of microhematuria was 100% in collapsing FSGS compared with 44.8%, 50%, 50% and 66.6% in FSGS NOS, perihilar, tip and cellular variants, respectively. This incidence of hematuria was significantly higher in collapsing variant compared with the perihilar and NOS subtypes (P <0.05). Hypertension at first clinical presentation was noted in 30 patients (46.1%), and was most frequent in cellular (three cases, 100%) and collapsing FSGS (seven cases, 77.7%). Patients with FSGS NOS, peri-hilar and tip variants had hyperten­sion in 48.3%, 43.75% and 25% cases, respec­tively.

Biochemical parameters

Derangement in renal function tests (serum urea and creatinine) was frequent in the pa­tients included in this study. The mean serum urea levels varied from 35.6 ± 27.4 mg/dL in cellular variant to 107.4 ± 44.6 mg/dL in col­lapsing FSGS. Similarly, serum creatinine le­vels were 0.96 ± 0.2 mg/dL in the cellular variant compared with 4.43 ± 3.25 mg/dL in the collapsing variant. On statistical analysis, collapsing FSGS had significantly higher se­rum urea and creatinine compared with NOS, perihilar, tip and cellular variants of FSGS. The difference was not significant among the other groups. The salient clinical and biochemical parameters are summarized in [Table 1].
Table 1: Patient characteristic at biopsy.

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Histologic analysis

Renal biopsy in all the cases was adequate with a mean of 11 glomeruli per biopsy. All the biopsy specimens included juxtamedullary cortex. On categorization according to the Columbia classification, FSGS NOS variant emerged as the most common histologic type (44.6%), followed by perihilar variant. The mean number of glomeruli was 10.62 (±5.36) in these cases, with segmental sclerosis invol­ving 5.43 (±3.05) glomeruli. Thus, FSGS le­sion was detected in an average of 54.07% of the glomeruli included. On subclassification, the percentage of glomeruli involved varied from 28.92 (±9.28) in the tip variants to 41.8 (±19.64) in collapsing, 50.92 (±19.19) in perihilar, 59.53 (±14.64) in FSGS NOS and 73.1 (±6.7) in cellular variants.

Glomerular hyalinosis was noted in 86.2% of FSGS NOS compared with 87.5% of perihilar and tip variants, 33.3% of cellular and 100% of collapsing variants of FSGS. Capsular adhe­sion was quite frequent in the cases included in the study. Adhesion was noted in 100% of the cases of FSGS NOS, cellular and collapsing variants compared with 93.75% in perihilar and 75% of the tip variants. Mesangial hypercellularity was present in 17.2% of the cases of FSGS NOS, 43.75% of perihilar, 12.5% of the tip variant and 100% of the cases with cellular variant. Intraglomerular foam cells [Figure 1]f were seen in 13.8% of FSGS NOS compared with 25% of the perihilar, 12.5% of tip and 33.3% of the cellular cases. These histologic features are summarized in [Table 2]. Prominence of visceral epithelial cells (podocytes) was seen in 100% of the cases with collapsing variant compared with 66.67% of cellular FSGS. This was significantly more frequent than 37.5% of perihilar, 37.5% of tip and 24.1% of FSGS NOS cases. The cases with visceral epithelial cell prominence (VEP) were compared with those not showing this change. The duration of symptoms was significantly shorter in cases showing VEP (28.4 ± 9.8 months) compared with the non-VEP cases (37.3 ± 12.2), with a P-value of 0.0018. The degree of 24-h proteinuria and serum creatinine at the time of biopsy were higher in cases with VEP (5.51 ± 2.51 g/24 h and 2.26 ± 1.02 mg/dL, respectively) compared with the cases without VEP (4.17 ± 3.36 g/24 h and 1.67 ± 0.72 mg/dL, respectively). [Table 3] depicts the difference between the cases with VEP and those without VEP.
Table 2: Histological characteristics of FSGS subtypes.

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Table 3: Significance of visceral epithelial cell prominence (VEP).

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Arteriolar hyalinosis of variable degree was noted in more than 75% of the cases in all categories of FSGS. Interstitial fibrosis and tubular atrophy were frequent (87.69% and 90.7%, respectively) in the biopsies included in the present study. Severe interstitial fibrosis, involving >50% of the biopsied cortical paren­chyma, was noted in 48.3% of the FSGS NOS compared with 33.3% of the cellular and 22.2% of the collapsing variants. None of the cases of perihilar and tip variants showed severe inters­titial fibrosis. Marked tubular atrophy (>50% of biopsied cortical parenchyma) was seen in 41.3% of the NOS variant compared with 25% of the cases with tip lesion and 22.2% of the collapsing variant. There was no significant difference in the degree of tubulo-interstitial changes among the various types of FSGS.

The mean glomerular area in control biopsies (minimal change disease) was 11231.31 ± 598.12 μm 2 . Compared with this, the mean glomerular area was 15917.73 ± 859.772 μm 2 in the cases with tip lesion, 17036.96 ± 3761.722 μm 2 in NOS lesion, 17083.22 ± 4061.606 μm 2 in cellular variant, 17191.12 ± 3391.814 μm 2 in the biopsies with collapsing lesion and 18954.45 ± 5944.514 μm 2 in perihilar variant. The difference in the glomerular area, com­pared with controls, was significant for NOS (P-value 0.022), perihilar (P-value 0.0014) and collapsing (0.03) variants. There was no signi­ficant difference in the mean glomerular area between controls and tip and cellular lesions. Also, no significant difference was noted bet­ween the various types of FSGS in the mean glomerular area.

   Discussion Top

FSGS is one of the leading causes of nephrotic syndrome, both in adults and in children. The diagnosis of FSGS relies exclusively on histologic demonstration of focal sclerosis in a segmental distribution within a glomerulus. The pattern of involvement gradually becomes more diffuse and global as the disease prog­resses. When all the secondary causes are excluded by history and investigations, the re­maining cases are labeled as primary FSGS. [5] During the past years, various histologic sub­types of FSGS have been described in the lite­rature in a number of reports. Cellular lesion of FSGS was described first by Schwartz and Lewis as a FSGS lesion with endocapillary and extracapillary hypercellularity with shorter duration of disease prior to diagnosis. [1] Over the years, cellular FSGS has been limited to cases with endocapillary hypercellularity. [10] With the advent of the epidemic of HIV in­fection, malignant FSGS was described in pa­tients having a rapidly progressive disease, collapse of glomerular tuft with accumulation of podocytes in the urinary space. The term "collapsing FSGS" was coined by Weiss et al in their study. [2] Another entity to be introduced in the gamut of FSGS was "tip" lesion, a variant with favorable prognosis comparable to minimal change disease. [3] The importance of perihilar location of segmental sclerosis has been debated. Perihilar lesions have been re­ported to be more frequent in adults and in secondary forms, mediated by glomerular hyper-filtration. [11],[12]

Because of the lack of conformity of defini­tions of the variants and lack of inter-observer agreement about the terminology, an interna­tional group formulated a consensus histologic subclassification of the histologic variants of FSGS, the Columbia classification. [4] This clas­sification proposes a hierarchical approach to the categorization of FSGS lesion. Collapsing FSGS requires the presence of at least one capillary loop with obliteration of lumen and hyperplasia and hypertrophy of the overlying podocytes. The presence of even one segment of a glomerulus with this morphology over­rides all other variants. [4] The diagnosis of tip variant requires the exclusion of only collap­sing lesion, as the tip lesion may show either cellular or sclerosing features. Cellular variant mandates the exclusion of collapsing and tip variants. The Columbia classification restricts the hypercellularity in a cellular lesion to the endocapillary compartment. In the perihilar variant, the segmental sclerotic lesion is loca­ted at the vascular pole and this diagnosis can be made only after exclusion of collapsing, tip and cellular variants. In the Columbia clas­sification, FSGS NOS is used when none of the other definitions apply, and hence is a diagnosis of exclusion. [4] Since the time of publication of the Columbia classification, several studies, predominantly in the western population, have described the application of this classification in their patients with FSGS. In a study by Thomas et al, FSGS NOS was the most common form (42%), followed by perihilar (26%), tip (17%), collapsing (11%) and cellular (3%) variants. [5] The data reported by the Glomerular Disease Collaborative Network and by the Columbia University Group showed a slightly different incidence of tip 37%, NOS 32%, perihilar 26% and collapsing variant 5%. [7] In a study inclu­ding the pediatric population with a high pre­valence of African Americans, NOS remains the most common variant (44%), followed by cellular (32%) and collapsing (24%) variants. Both the tip and perihilar lesions were not represented in the pediatric series. [6] There has been a lack of data of various histological variants of FSGS in Indian patients. A recent study including only adult patients from north India reported FSGS NOS as the most frequent (72.5%), followed by tip (13.5%), cellular (8%), perihilar (4%) and collapsing (2%) variants. [8] In the present study, FSGS NOS was the most frequent (44.6%), followed by perihilar FSGS (24.6%), collapsing (13.9%), tip (12.3%) and cellular (4.6%) variants. All the variants of FSGS were represented in the pediatric pa­tients in our study, with FSGS NOS forming the most common group (58.3%), followed by perihilar (20.8%), tip (12.5%) and cellular and collapsing (4.2% each) variants. Hence, the prevalence of various subtypes of FSGS in the present study is somewhat similar to the wes­tern population, with minor differences. The Columbia classification was proposed with the understanding that a morphological subclassification of a disease should carry meaningful clinical or pathogenetic implica­tions. In their study, Nada et al showed that cellular variants were biopsied the earliest, followed by collapsing and perihilar variants. [8] In the present study, however, we found that the duration of symptoms prior to biopsy diag­nosis of FSGS was the shortest in collapsing variant (8.3 ± 2.3 months), followed by cellu­lar variant (12.5 ± 6.3 months). On statistical analysis, the collapsing and cellular variants had a shorter time to diagnosis compared with NOS, perihilar and tip lesions. Earlier studies using the Columbia classification have shown that patients with collapsing and tip variant had greater amount of proteinuria than those with perihilar and NOS variants. [5] Similar re­sults were reported by Nada et al in their study. [8] A Chinese study reported a higher level of proteinuria in cellular and tip variants, with higher incidence of nephrotic syndrome in these two variants. [13] In the present study, the degree of proteinuria was highest in collapsing variant and lowest in NOS group, the diffe­rence being statistically significant. The results were similar in both the adults and the pediatric age groups. This is in conformity with the results reported by Thomas et al. [5] Nephrotic-range proteinuria was noted in more than half of the cases in all subtypes of FSGS, although there was no statistically significant diffe­rence in the frequency of nephrotic range proteinuria among the various subtypes. Simi­larly, microscopic hematuria was found in all the subtypes, with a significantly higher fre­quency in the collapsing variant compared with perihilar and NOS subtypes. The incidence of hypertension was lowest in the tip variant, while being high in both collapsing and cellular variants. The study by Thomas et al also showed the lowest incidence of hypertension in the tip variant of FSGS. [5] In the present study, mean serum creatinine at the time of biopsy was higher in the collapsing variant compared with the other histologic variants. On the other hand, the study by Thomas et al showed a sig­nificant difference in serum creatinine between the collapsing and tip variants only while ano­ther study by Deegens et al in the Dutch popu­lation showed a difference between tip and NOS variants. [5],[7] Nada et al, in their study, did not find any significant difference in the ave­rage serum creatinine between the variants. [8]

A comparison of histologic features in the biopsies of variants of FSGS by Thomas et al showed a significantly lesser degree of glomerular, tubulo-interstitial and arteriolar changes in the tip variant compared with the other histologic variants (cellular variant not included in the analysis). [5] A study in the Dutch popula­tion reported severe glomerular sclerosis and hyalinosis in perihilar FSGS, intermediate in the NOS category and least severe changes in the tip variant. [7] In the present study, extent of glomerular involvement (proportion of glomeruli showing segmental sclerosis) was signifi­cantly lower in the tip variant and highest in the cellular variant of FSGS. No significant difference was noted in the glomerular hyalinosis, capsular adhesion, mesangial hypercellularity or glomerular foam cell infiltration.

One notable feature in our study was the frequency of VEP in variants other than col­lapsing FSGS. This histological feature was correlated with the clinical parameters at pre­sentation. The cases with VEP had a signifi­cantly shorter duration of symptoms and a higher degree of 24-h proteinuria and serum creatinine at the time of biopsy. None of the previously reported series of FSGS has eva­luated this histomorphological feature in non-collapsing variants of FSGS. We hypothesize that the cases showing VEP have a distinct injury pattern different from other cases sho­wing only the segmental sclerotic lesion. The clinical significance of this observation needs to be defined in further larger studies.

Glomerular hypertrophy has been demonstrated in diseases associated with FSGS. [9] Higher mean glomerular tuft area has been shown in biopsies during the nephrotic stage of FSGS compared with the control subjects and pa­tients with minimal change disease. [14] The mean glomerular tuft area was reduced in biopsies from FSGS in remission. In the present study, the mean glomerular tuft area was higher in the NOS, perihilar and collapsing FSGS va­riants compared with the control biopsies. Be­cause the number of cases of cellular FSGS was less, no significant difference was noted in the mean glomerular area between cellular FSGS and control biopsies. Our study con­firms the presence of a component of glomerular hypertrophy in FSGS, extending to its variants as described in the Columbia classi­fication. The present study is, to the best of our know­ledge, the second clinico-pathologic analysis of the Columbia classification of focal and segmental glomerulosclerosis in an Indian co­hort. The differences in the clinical parameters among the variants suggest that there is a clin­ical relevance of the Columbia classification. Among the subtypes, collapsing and cellular variants show worse clinical and pathological features at presentation, and, hence, accurate identification of these entities is critical for appropriate patient management. Visceral epi­thelial cell prominence, without associated col­lapse of the glomerular tuft, needs to be ex­plored further for potential clinical signifi­cance in the histologic analysis of FSGS.

   Acknowledgments Top

Dr. Prasenjit Das, Dr. Alok Sharma and Dr. Ruchika Gupta wish to acknowledge CSIR, Delhi for research grant support as Senior Research Associates.

   References Top

1.Schwartz MM, Lewis EJ. Focal segmental glomerular sclerosis: The cellular lesion. Kidney Int 1985;28:968-74.  Back to cited text no. 1
2.Weiss MA, Daquioag E, Margolin EG, Pollak VE. Nephrotic syndrome, progressive irrever­sible renal failure, and glomerular ''collapse'': A new clinico-pathologic entity? Am J Kidney Dis 1986;7:20-8.  Back to cited text no. 2
3.Howie AJ, Brewer DB. The glomerular tip lesion: a previously undescribed type of seg­mental glomerular abnormality. J Pathol 1984; 142:205-20.  Back to cited text no. 3
4.D'Agati VD, Fogo AB, Bruijn JA, Jennette JC. Pathologic classification of focal segmental glomerulosclerosis: A working proposal. Am J Kidney Dis 2004;43:368-82.  Back to cited text no. 4
5.Thomas DB, Franceschini N, Hogan SL, et al. Clinical and pathologic characteristics of focal segmental glomerulosclerosis pathologic va­riants. Kidney Int 2006;69:920-6.  Back to cited text no. 5
6.Silverstein DM, Craver R. Presenting features and short-term outcome according to patho­logic variant in childhood primary focal seg­mental glomerulosclerosis. Clin J Am Soc Nephrol 2007;2:700-7.  Back to cited text no. 6
7.Deegens JK, Steenbergen EJ, Borm GF, Wetzels JF. Pathological variants of focal segmental glomerulosclerosis in an adult Dutch popula­tion-epidemiology and outcome. Nephrol Dial Transplant 2008;23:186-92.  Back to cited text no. 7
8.Nada R, Kharbanda JK, Bhatti A, Minz RW, Sakhuja V, Joshi K. Primary focal segmental glomerulosclerosis in adults: is the Indian cohort different? Nephrol Dial Transplant 2009; 24:3701-7.  Back to cited text no. 8
9.Kiprov DD, Colvin RB, McCluskey RT. Focal and segmental glomerulosclerosis and porteinuria associated with unilateral renal agenesis. Lab Invest 1982;46:275.  Back to cited text no. 9
10.D'Agati V. The many masks of focal segmen­tal glomerulosclerosis. Kidney Int 1994;46: 1223-41.  Back to cited text no. 10
11.Fogo A, Glick AD, Horn SL, Horn RG. Is focal segmental glomerulosclerosis really focal? Distribution of lesions in adults and children. Kidney Int 1995;47:1690-6.  Back to cited text no. 11
12.Verani RR. Obesity-associated focal segmental glomerulosclerosis: Pathologic features of the lesion and relationship with cardiomegaly and hyperlipidemia. Am J Kidney Dis 1992;20: 629-34.  Back to cited text no. 12
13.Shi SF, Wang SX, Zhang YK, Zhao MH, Zou WZ. [Clinico-pathologic study of different va­riants of focal segmental glomerulosclerosis]. Zhonghua Bing Li Xue Za Zhi 2007;36:11-4.  Back to cited text no. 13
14.Nishimoto K, Shiiki H, Nishino T, Uyama H, Iwano M, Dohi K. Reversible glomerular hypertrophy in adult patients with primary focal segmental glomerulosclerosis. J Am Soc Nephrol 1997;8:1668-78.  Back to cited text no. 14

Correspondence Address:
Amit K Dinda
Department of Pathology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029
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DOI: 10.4103/1319-2442.100883

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