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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
RENAL DATA FROM ASIA–AFRICA  
Year : 2018  |  Volume : 29  |  Issue : 3  |  Page : 680-688
Primary IgA nephropathy in the Kashmiri population


Department of Nephrology, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

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Date of Submission06-Apr-2016
Date of Decision28-Jul-2016
Date of Acceptance31-Jul-2016
Date of Web Publication28-Jun-2018
 

   Abstract 

IgA nephropathy (IgAN) remains one of the most common glomerular lesions, which has a striking geographic distribution and is the most common form of primary glomerular disease in Asia. However, the exact prevalence or clinicopathological spectrum of IgAN in India is not well documented. This retrospective study analyzed the presentation in 126 patients of primary IgAN out of 298 native kidney biopsies (42.28%) performed over a period of three years (2013–2015). The patients were followed up for three months. This is the second highest prevalence recorded in the world after Japan. Among the clinical features of our cohort, the mean age was 31 years, with a male-to-female ratio of 2:1, with the highest incidence observed in the third decade of life in both sexes. The majority of our patients (47%) presented with renal failure with a mean serum creatinine value of 3.1 mg/dL and with burnt out morphology on histo-pathology; 72.2% of patients were hypertensive at presentation. On histopathology, Haas class V (35.5%) had the highest frequency followed by class IV (25.8%). The Oxford MEST score was not applicable in 36 patients because of advanced sclerosis (>50%). In the remaining ninety patients, majority had tubular atrophy and interstitial fibrosis of varying degrees. At three months of follow-up, the patients who had presented with renal failure (47.6%), settled in chronic kidney disease stage III (25.4%) followed by stage IV (18.6%) and stage V (11.8%). Our study in Kashmir suggests that IgAN is more common in the younger age group, with a significant number of patients presenting with advanced renal failure and, on morphology, showing a burnt out disease, with many developing end-stage renal disease. Studies evaluating the underlying factors can have immense importance in dealing with the disease.

How to cite this article:
Chowdry AM, Najar MS, Mir MM, Azad H, Rashid RA, Ashraf BM, Ahmed BK, Maqsood WM, Ahmed WI. Primary IgA nephropathy in the Kashmiri population. Saudi J Kidney Dis Transpl 2018;29:680-8

How to cite this URL:
Chowdry AM, Najar MS, Mir MM, Azad H, Rashid RA, Ashraf BM, Ahmed BK, Maqsood WM, Ahmed WI. Primary IgA nephropathy in the Kashmiri population. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2019 Jul 23];29:680-8. Available from: http://www.sjkdt.org/text.asp?2018/29/3/680/235167

   Introduction Top


IgA nephropathy (IgAN) was described by Berger and Hinglais in 1968 and its distribution varies in different regions around the world.[1] It is the most common form of primary glomerular disease in Asia, accounting for up to 30%–40% of all biopsies performed for the diagnosis of glomerular disease, and it accounts for 20% of all biopsies in Europe and 10% of all biopsies in North America.[1] The bulk of the disease burden is borne by Asians and Caucasians, as compared to African-Americans from the USA and people from South Africa.[2],[3] A Japanese study of biopsy specimens obtained from kidney donors immediately before transplantation showed that 16% of donors had covert mesangial deposition of IgA.[4] IgAN has been reported to be rare in African-Americans[3],[5] and is quite common in native Americans of the Zuni and Navajo tribes.[6] The prevalence of IgA in the general population has been estimated to be between 25 and 50 cases per 100,000.[1] Population-based studies in Germany and France[7],[8],[9],[10] calculated an incidence of two cases per 10,000, but autopsy studies in Singapore[11] suggested that 2%–4.8% of the population had IgA deposition in their glomeruli. In addition, Polynesians from New Zealand[12] have a low frequency of the condition, whereas native Americans from New Mexico[13] and Australian aborigines[14] have a high frequency. In European countries, a high incidence has been reported in the literature from France,[10] Germany,[7] and Italy[15] and varies from 15 to 40 new cases per million population per year. IgAN is more frequent in the eastern part of the world (Singapore,[16] Japan,[17] China,[18] and Pakistan[19]) than in the western part of the world.

The history of IgAN in India is based on various studies on native renal biopsies. In 1987, a frequency of 4.25% was reported from Tamil Nadu.[20] A low incidence (7.24%) but marked severity characterized IgAN in a study by Bhuyan et al in 1992.[21] In 1995, Sehgal et al[22] from North India quoted a prevalence of 10.4% (11 of 106 biopsies). Many other studies from South India have reported on the prevalence and other features of IgAN.[23],[24],[25] In 2006, the largest series of histopathological renal biopsy data of 27 years (1986–2002) was analyzed by Narasimhan in South India, who detected IgAN in 8.6% of 5415 native kidney biopsies.[26] Studies by Vanikar et al[27] from western part of India documented IgAN in 16.2%, with pure mesangiopathy being the most common lesion and Chandrika[28] from South India found IgA in 14.26% of their kidney biopsies, which is much lower than the prevalence of 50% in Japan.[18]

The natural history of IgAN shows that no clinical pattern is pathognomonic of the disease. The clinical spectrum varies from asymptomatic microhematuria to rapidly progressive glomerulonephritis (GN). The vast majority of patients are characterized by recurrent episodes of gross hematuria, which usually occurs concomitantly with mucosal infections of the upper respiratory tract or other infections, or by asymptomatic microscopic hematuria with or without proteinuria.[1] Some patients have abdominal or flank pain.[29] In a minority of patients (<5%), malignant hypertension[30] may be an associated presenting feature. In most severe cases (<10%), acute GN results in acute renal insufficiency and failure.[31],[32] One study has reported that acute kidney injury (AKI) may be the presentation in up to 27% of patients older than 65 years.[33] European[34] and Chinese[35] studies have suggested that renal insufficiency may occur in 20%–30% of patients within two decades of the original presentation.[34]

The present study was conducted to examine the incidence and presentation of IgAN in our population to know whether it is different in our part of the world.


   Materials and Methods Top


This retrospective study was conducted at the Department of Nephrology, Sher-I-Kashmir Institute of Medical Sciences, a tertiary care center of Jammu and Kashmir, India, to review all the cases of different types of IgAN diagnosed on histopathology over a period of three years (January 2013–December 2015). It was approved by the ethical committee of the institute.

Basic demographic profile of all patients including age, sex, clinical presentation, relevant investigations, and the histopathological type of GN was noted. The histopathological sections were stained for hematoxylin and eosin, periodic acid–Schiff silver methamine, and any other particular stain depending on the requirement. Particular note was made of glomerular architecture; mesangial hypercellularity; crescents; focal, segmental, and global glomerular sclerosis (indicating disease has been going on for some time); tubulointers-titial inflammation; interstitial fibrosis; and tubular atrophy. Diffuse immunofluorescence was performed in all cases, but electron microscopy was not performed due to nonavailability. Histological parameters were studied according to the 2009 consensus meeting[36] for histological grading and also according to the guidelines of the Haas classification.[37]

Oxford-Mest score

Mesangial hypercellularity score <0.5 = 0, or score >0.5 = 1

Endocapillary hypercellularity: absent = 0, or present = 1

Segmental glomerulosclerosis: absent = 0, or present = 1

Tubular atrophy/interstitial fibrosis: cortical area <25% = 0, 26–50% = 1, or >50% = 2

HAAS classification

Class I: Minimal or no mesangial hypercellularity without glomerulosclerosis.

Class II: Focal and segmental glomeruloscle-rosis without active cellular proliferation.

Class III: Focal proliferative GN.

Class IV: Diffuse proliferative GN.

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

Exclusion criteria

IgAN cases due to secondary causes such as Henoch–Schonlein purpura, IgA with rheuma-tologic, autoimmune disease, gastrointestinal, hepatic, skin, lung diseases, and infections (hepatitis B, HIV, and brucellosis) were excluded from the study.


   Results Top


Among the clinical features of our cohort, the mean age was 31 years, with a male-to-female ratio of 2:1, and the highest incidence was observed in the third decade of life in both sexes [Table 1]. IgAN comprised 126 (42%) of the 298 native kidney biopsies performed during the study period. Clinical presentations are summarized in [Table 1]. The majority of our patients (47.6%) presented with renal failure with a mean serum creatinine value of 3.1 mg/dL and 72.2% of patients were hypertensive at presentation. The clinical presentations of IgAN in our study are shown in [Figure 1]. The histopathological subclasses are shown in [Figure 2], with Haas class V (35.5%) having the highest frequency followed by class IV (25.8%). The Oxford classification of histopathology in IgAN is shown in [Table 2]. The MEST score was not applicable in 36 patients because of advanced sclerosis of >50%. In the remaining 90 patients, majority had tubular atrophy and interstitial fibrosis of varying degrees. At three months of follow-up [Table 3], of the 47.6% of patients who has presented with renal failure, 25,4% were in CKD stage III, 18 were in stage IV and 11.8% were in CKD stage V.
Figure 1: Distribution of clinical syndromes in IgA nephropathy among the study patients.
Values in parenthesis are absolute numbers.
AUA: Asymptomatic urinary abnormality.


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Figure 2: The distribution of subclasses of IgA according to the Haas classification.

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Table 1: Baseline demographic characteristics of patients.

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Table 2: Distribution of histopathological changes in renal biopsies of patients with IgA nephropathy, according to Oxford classification 2009.

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Table 3: Distribution of patients according to the stage of chronic kidney disease after 3 months of follow-up.

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   Discussion Top


This study demonstrates that IgAN is very common in this part of the world with a prevalence of 42%, highest ever recorded in India and second only to Japan (47.2%). In previous reports from different parts of India, prevalence is high but not more than 20%. The frequency of IgAN reported in the international literature varies widely from as low as 2% to as high as 52%.[38] The striking geographic variation has been associated with the presence of particular gene alleles that protect from IgAN.[39] It was found that IgAN accounted for 40% of all diagnoses in a recent large retrospective review of 600 biopsies from China,[40] and Koyama et al noted a prevalence of IgAN of 47.2% in Japan.[41] A single center in Nepal found IgAN in 9.8% cases only,[42] and among recent studies from Pakistan, the highest prevalences of IgAN noted were 12.65%[38] and 20.83%.[19] IgAN has been reported in 10% of all biopsies in America. These lower rates in the US may be influenced by a conservative approach by nephrologists in that country, who are reluctant to perform renal biopsies in asymptomatic patients with only mild urinary abnormalities on urinalysis. High prevalence rates have been observed in Singapore (52%),[16] Japan (47.2%),[4] Australia, Hong Kong, Finland, and Southern Europe, whereas low prevalence rates are the rule in the United Kingdom, North America, and Canada. The frequency reported from North America, the United Kingdom, and North-Western Europe varied from 5% to 10%.[43],[44],[45],[46],[47] In Europe, the highest was in Italy (35.9%)[48] followed by France (30.1%)[8].

The typical patterns of clinical presentation described in the natural history are hematuria, proteinuria, and hypertension, and rarely renal failure. In our study, majority (47%) of the patients presented with renal failure followed by asymptomatic urinary abnormalities (21%) and macroscopic hematuria (17%). Higher occurrence of renal failure has been traced long ago in the history of IgAN in Asian countries. In 1992, Bhuyan et al[21] described IgAN presenting with renal failure in 34% of patients, a recent study in South India showed that 38% of patients presented with renal failure and in Pakistan, 24% of patients presented with renal failure in one study.[19] This high occurrence of renal failure in Asians has been attributed to the genetic susceptibility of Asians to IgAN and its complications.[49],[50] Renal failure is uncommon (<5% of all cases) in the presentation of IgAN in regions other than Asia, but one study in Spain has reported that AKI may be the presentation in up to 27% of patients older than 65 years.[33] In our study, most of the patients were young, in their second and third decades of life, and presented with advanced renal failure. In our study, this high incidence of renal failure was neither explained by acute severe immune and inflammatory injury with necrotizing GN and crescent formation nor by heavy glomerular hematuria leading to tubular occlusion by red blood cells. In fact, our patients showed a burnt out disease with a pattern of advanced sclerosis at the time of first presentation which may or may not be accompanied by proliferative lesions.

The natural course of IgAN is not completely understood and the outcome is generally unpredictable. However, according to Mark Haas, IgAN can be classified into three groups with different prognosis: an excellent prognosis group (subclasses I and II) corresponding to glomerular lesions without proliferative glomerulonephritis, an intermediate prognosis group (subclass III) corresponding to focal proliferative GN, and a poor prognosis group (subclasses IV and V) corresponding to diffuse proliferative GN and advanced chronic GN.[7] The largest fraction of cases in our study belonged to the poor prognosis group classes IV and V, corresponding to advanced sclerosis. All these patients had impaired renal function. Majority of our patients were hypertensive and histologically had progressed to a higher subclass of IV or V.

Majority of our patients presented with advanced renal impairment which could be due to the fact that most of the patients attending our hospital are of low socioeconomic status and our center is a tertiary care referral center and thus, patients possibly present late in the course of the disease process. The survival rate in India is not known since longterm follow-up is difficult for reasons such as financial constraints, ignorance, and illiteracy.

Biopsy practice pattern is another important factor affecting the frequency of IgAN as has been pointed out in a study from the UK, in which the frequency varied from 7.1% (1972–1978) to 21.1% (1979–1986).[47] The high prevalence of IgAN in our population is partly explained by a low threshold for the biopsy practice patterns. In our center, isolated hema-turia found during routine screening obliges the patient to submit to a renal biopsy, but in North America, significant clinical indicators of the underlying renal disease such as proteinuria >1 g/day or systemic features of disease are the dominant indicators for renal biopsy.

Although we did not study the impact of socioeconomic status in detail on the prevalence of IgAN, most (72%) of our patients belonged to the rural areas with low gross domestic product per capita. A study from Scotland found a significant two-fold increase in the diagnosis of IgAN in patients residing in the most deprived areas compared with the least. The variation was not explained by the demographics of the underlying population in this study. In a study from South Africa, the authors reported a very low prevalence in the local population (0.7%) as compared with the Indian residents.[3] This supports the conclusion from Yoshinos study that race and ethnicity are important factors affecting the distribution of IgAN.[51]

We acknowledge the important limitation in the present study that it was a hospital-based study and it does not give an exact burden and pattern of glomerular diseases in the whole Kashmir valley as only those cases were included in the study, which were biopsied at our tertiary care center. Retrospective nature and short follow-up of patients were other limitations of this study.

In these patients, renal transplant is the only option, but in a developing country like India, financial constraints are enormous. Renal dis-orders are neglected and as a consequence, patients present late with advanced disease process. Thus, in developing countries like India, with limited resources and an estimated end-stage renal disease (ESRD) of 150–200 pmp,[52] a decisive plan of action should be charted and implemented.


   Conclusion Top


IgAN in this part of world is more common in the younger age group and bulk of the patients (47%) present with renal failure and on morphology show a burnt out disease. As kidney disease is emerging as a major health problem globally and ESRD is showing an alarming growth rate, efforts are needed for early diagnosis and proper management of these patients.

Conflict of interest: None declared.

 
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Correspondence Address:
Dr. Abdul Majeed Chowdry
Department of Nephrology, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir
India
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DOI: 10.4103/1319-2442.235167

PMID: 29970746

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