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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 52  |  Issue : 1  |  Page : 14-16
IgA nephropathy in Kerala, India: A retrospective study

Department of Pathology, SUT Academy of Medical Sciences, Trivandrum, Kerala, India

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This study was conducted to assess the prevalence of IgA nephropathy in Kerala. No published data are available in literature from this part of India. This study included 1592 renal biopsies received from all parts of Kerala over a 2-year period. The age of the subjects ranged from 5 to 78 years old with a peak incidence in the third decade of life. The male:female ratio was 1.2:1. A total of 60% of the cases had presented with hematuria. Direct immunoflourescence was performed using specific antibodies for IgA, IgG, IgM, C3 and C1q. Light microscopic studies with special stains namely PAS, silver and trichrome were also done. A total of 227 cases (14.26% of all renal biopsies) were diagnosed as IgA excluding 12 cases of Henoch-Schonlein Purpura (12.74% in the first year and 15.52% in the second year). The prevalence of IgA nephropathy appears to be increasing in Kerala

Keywords: IgA nephropathy, prevalence, Kerala, India

How to cite this article:
Chandrika B K. IgA nephropathy in Kerala, India: A retrospective study. Indian J Pathol Microbiol 2009;52:14-6

How to cite this URL:
Chandrika B K. IgA nephropathy in Kerala, India: A retrospective study. Indian J Pathol Microbiol [serial online] 2009 [cited 2023 Jan 30];52:14-6. Available from:

   Introduction Top

IgA nephropathy is a very common form of primary glomerulonephritis (GN) and occurs globally. The frequency varied from 2 to 52% of all renal diseases in various studies from different parts of the world. The prevalence of IgA nephropathy has not been widely studied in the Indian population especially in South India. The objective of this study was to asses the frequency of IgA nephropathy in Kerala, a South-western state of India.

   Materials and Methods Top

A total of 1592 renal biopsies, received over a period of 2 years were included in this study. Cases of systemic lupus erythematosis (SLE) and Henoch Schonlein purpura were excluded from this study by serological and clinical findings. Separate cores of tissues were studied for immunoflourescence (IF) and light microscopy. Electron Microscopy (EM) was not performed due to the lack of this facility at our institution. For light microscopy, the specimens were fixed in 10% buffered formalin. Sections were cut at a thickness of three microns, stained with hematoxylin and eosin (H & E), periodic acid Schiff (PAS), Masson's trichrome (MT) and Gomori's Methenamine Silver (GMS). The lesions were classified according to Hass Classification [1],[2] as follows:

Class I: minimal or no mesangial hypercellularity without glomerulosclerosis

Class II: focal and segmental glomerulosclerosis without active cellular proliferation

Class III: focal proliferative of GN

Class IV: diffuse proliferative of GN

Class V: ≥ 40% globally sclerotic glomeruli and/or ≥ 40% tubular atrophy or loss

For IF, fresh tissue in transport media was frozen and cryostat sections were cut at 5µ and incubated with antibodies specific for IgA, IgG, IgM, C3 and C1q. The intensity of flourescence was graded as 0 to 4. The clinical presentations as well as age and gender incidence were also analyzed. A total of 12 cases of Henoch Schonlein purpura were diagnosed by the clinical and IF findings and were excluded from this study.

   Results Top

The youngest patient in this series was 5 years old and the oldest was 78 years old. Age and gender incidence are shown in [Table 1]. The highest incidence was found in the third decade of life in both males and females. The male to female ratio was 1.5:1.

Out of a total of 1592 renal biopsies, 227 cases were diagnosed as IgA nephropathy (14.26%). Of these, 85 out of 677 were in the first year (12.74%) and 142 out of 915 in the second year (15.52%) suggesting an increase in incidence. The histological types are shown in [Table 2]. Class II (40.5%) had the highest frequency [Figure 1] and class V (28.6%) came next. A total of 3 cases of mesangio-proliferative glomerulonepgritis (MPGN) had predominent mesangial and less capillary wall staining with IgA. A total of 28 cases of crecentic GN with segmental necrosis were noted, which also showed a mesangial predominance of IgA.

IF findings are shown in [Table 3]. A total of 46.25% of the biopsies showed IgA and C3. [Figure 2] Four cases with full-house IF and 3 cases with C1q had IgA predominance and were clinically and serologically negative for SLE.

Clinical presentations are given in [Table 4]. A total of 36.7% of the cases presented with nephrotic syndrome (NS). A total of 30.4% had nephrotic nephritic syndrome (NNiS) and 18.9% had nephritic syndrome (NS), indicating that hematuria would be a common finding in IgA nephropathy. No cases of microscopic hematuria without nephritic syndrome were noted. A total of 5.7% of the cases presented with chronic renal failure (CRF), 4.8% presented with acute renal failure (ARF) and 3.5% presented with hypertension (HT). A total of 28.6% of the cases in this series had end-stage disease.

   Discussion Top

IgA nephropathy is recognized as a major cause of end stage kidney disease worldwide.

Its incidence has not been widely studied in India. Only a few centers in the country have the facility of immunoflourescence microscopy.

The male preponderance (male to female ratio of 1.5:1) shown in our study is also borne in international literature. But in this context, it has to be remembered that more men undergo renal biopsies than women. [3] In one study, the male:female ratio was 58:22. [4]

The world-wide frequency of IgA nephropathy varies widely from 2% to 52% of all renal biopsies. [5] There is a definite geographic variation. Available evidence suggests an increasing incidence in India. In 1987, a frequency of 4.2% was reported from Tamil Nadu, a South Indian state adjoining Kerala. [6] In 1992, a frequency of 7.24% was reported from New Delhi in North India, [7] and in 1995, 10.37% was reported from the North Indian Union Territory of Chandigarh. [8] In our study, it was 12.74% in the first year and 15.52% in the second, the highest frequency so far reported in the country. Frequency reported from North America, the United Kingdom and Northwestern Europe varied from 5% to 10%. [9],[10],[11],[12],[13] In Europe, the highest was in Italy (35.9%)[14] and France (30.1%) [15] came next. Among Asian countries, it ranged from 25% to 52%. The highest of them was reported from Singapore (52%) [16] and Japan (47.2%) [17] came second.

In a study from South Africa, the authors reported a very low prevalence in the black population (0.7%) as compared with Indian residents (13.3%). [18] This supports the conclusion from Yoshino's study that race and ethnicity are important factors affecting the distribution of IgAN. [19]

Biopsy policy is another important factor affecting the frequency of IgA nephropathy as has been pointed out in a study from the UK in which the frequency varied from 7.1% (1972-78) to 21.1% (1979-86). [20] The biopsy policy varied depending on the nephrologists and the availability of immunoflourescence facility.

In our study, mesangial proliferation (class II) was the most common class of IgA nephropathy. Class V was the second most common. However, reports from different parts of the world indicate differences in the pattern of disease class. Subclass I and II were predominant in a report from Macedonia, while in a recent review, Tumlin, et al . [21] reported that proliferative and crescentic forms (Class IV) were responsible for up to 30% of reported IgA nephropathy. [21]

   Conclusions Top

In this study on 1592 consecutive renal biopsies over a 2-year period, the largest number of lesions of IgA nephropathy belonged to Class II (40.5%); Class V (28.6%) came second. These lesions occurred most frequently in the third decade of life in both men and women.

The frequency of IgA nephropathy in Kerala over 2 years was seen to be 14.3% of all renal biopsies. There was an increase from 12.74% in the first year to 15.52% in the second year. This frequency is higher than in other published Indian studies. Is it because of differing trends in the biopsy policy of nephrologists in various parts of the country or is it really increasing? The increase in the two consecutive years from 12.74% to 15.52% suggests the latter possibility.

   References Top

1.Hass M. Histological sub classification of IgA nephropathy: A clinicopathological study of 244 cases. Am J Kidney Dis 1997;29:829-42.  Back to cited text no. 1    
2.Lee HS, Lee MS, Lee SM, Lee SY, Lee ES, Lee EY, et al . Histological grading of IgA nephropathy predicting renal outcome: Revisiting HS Lee's glomerular grading system. Nephrol Dial Transplant 2005;20:342-8.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Panichi V, Pasquariello A, Innocenti M, Meola M, Mantuano E, Beati S, et al . The Pisa experience of renal biopsies, 1977-2005. J Nephrol 2007;20:329-35.  Back to cited text no. 3  [PUBMED]  
4.Milovanceva-Popovska M, Grcevska L, Dzikova S, Ristovska V, Nikolov V, Polenakovic M. IgA nephropathy: 23 years of follow-up. Prilozi 2006;27:13-27.  Back to cited text no. 4  [PUBMED]  
5.Muzaffar S, Azad NS, Kayani NS, Pervaz A. Ahmed SH, Hasanet. The frequency of IgA Nephropathy at a single center in Pakisthan. JPMA 2003:53:301-5.  Back to cited text no. 5    
6.Date A, Raghvan R, John TJ, Richard J, Kirubakaran MG, Shastry JC. Renal disease in adult Indians: A clinicopathological study of 2827 patients. Q J Med 1987;64:729-37.  Back to cited text no. 6    
7.Bhuyan UN, Dash SC, Srivasthava RN, Tiwari SC, Malhotra KK. IgA associated glomerulonephritis. J Assoc Physicians India 1992;40:310-3.  Back to cited text no. 7    
8.Sehgal S, Datta BN, Sakhuja V, Chugh KS. Primary IgA nephropathy: A preliminary report. Indian J Pathol Microbiol 1995;38:233-7.  Back to cited text no. 8    
9.Hood SA, Velosa JA, Holley KE, Donadio JV Jr. IgA-IgG nephropathy; Predictive indices of progressive disease. Clin Nephrol 1981;16:55-62.  Back to cited text no. 9  [PUBMED]  
10.McCoy RC, Abramowsky CR, Tisher CC. IgA Nephropathy. Am J Pathol 1974;76:123-44.   Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Katz A, Underdown BJ, Minta JD. Glomerulonephritis with mesangial deposit of IgA unassociated with systemic disease. Can Med Assoc J 1976;114:209-15.  Back to cited text no. 11    
12.Sissons JG, Woodrow DF, Curtis JR, Evans DJ, Gower PE, Sloper JC, et al . Isolated glomerulonephritis with mesangial IgA deposits. Br Med J 1975;3:611-4.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Ballardie FW, O'Donoghue DJ, Feehally J. Increasing frequency of adult IgA nephropathy in the UK? Lancet 1987;2:1205.  Back to cited text no. 13    
14.Schena FP. Survey of the Italian Registry of Renal Biopsies: Frequency of the renal diseases for 7 consecutive years: The Italian Group of Renal Immunopathology. Nephrol Dial Transplant 1997;12:418-26.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Simon P, Ang KS, Bavay P, Cloup C, Mignard JP, Ramee MP. Immunoglobulin A glomerulonephritis: Epidemiology in a population of 250 000 inhabitants. Presse Med 1984;13:257-60.   Back to cited text no. 15    
16.Woo KT, Edmonson RP, Wu AY, Chiang GS, Pwee HS, Lim CH. The natural history of IgA nephritis in Singapore. Clin Nephrol 1986;25:15-21.  Back to cited text no. 16    
17.Koyama A, Igarashi M, Kobayashi M. Natural history and risk factors of immunoglobulin A nephropathy in Japan. Am J Kidney Dis 1997;29:526-32.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.Seedat YK, Nathoo BC, Parag KB, Naiker IP, Ramsaroop R. IgA nephropathy in Blacks and Indians of Natal. Nephron 1988;50:37-41.  Back to cited text no. 18    
19.Yoshino NH, Eloisa FF, Glenn MC, Jean LO. Race/ethnicity and disease severity of IgA nephropathy. BMC Nephrol 2004;5:10.  Back to cited text no. 19    
20.Ballardie FW, O'Donoghue DJ, Feehally J. Increasing frequency of adult IgA nephropathy in UK? Lancet 1987;2:1205.  Back to cited text no. 20    
21.Tumlin JA, Madaio MP, Hennigar R. Idiopathic IgA nephropathy: Pathogenesis, histopathology and therapeutic options. Clin J Am Soc Nephrol 2007;2:1054-61.   Back to cited text no. 21  [PUBMED]  [FULLTEXT]

Correspondence Address:
B Kumari Chandrika
PJRRA 65, Shanti, Pothujanam Road, Kumarapuram, Trivandrum 695 011
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.44954

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  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4]

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