| Abstract|| |
IgA nephropathy (IgAN) is reported to be more common in Asians and is considered to be a very progressive disease with worse outcome. The present study encompasses a cohort of biopsy-proven IgAN in a tertiary care hospital to characterize the initial clinical presentation, Oxford classification profile and one year follow up of patients with clinical and biochemical investigations. All renal biopsies with a diagnosis of primary IgAN were included. In all biopsies with ≥8 viable glomeruli, the MEST-C scores were analyzed, according to the Oxford criteria. Demographic and clinical data included age, gender, presence of hypertension, presence of hematuria and edema. Baseline investigations include urine protein semiquantitative, spot urine protein creatinine ratio, 24-h urinary protein, serum creatinine, and serum albumin. All the details of the use of antiproteinuric drugs and immunosuppressive drugs were recorded. Total 48 renal biopsies (21.62%) were diagnosed as primary IgAN. Thirty-seven (77.08%) had renal dysfunction on initial presentation out of which 31 (64.5%) patients had subnephrotic range proteinuria (SNRP). MEST-C lesions distribution were interpreted in 39 patients. 42.85% of patients with nephrotic range proteinuria (NRP) and 55.55% of patients with SNRP had renal deterioration during follow up period while 28.57% patients with NRP and 41.66% patients with SNRP had reached end-stage renal disease (ESRD). Our study population of IgAN has a unique clinical profile with hypertension, microscopic hematuria and subnephrotic proteinuria as the predominant clinical presentation. In spite of low MEST-C score in our study cohort, the disease has an aggressive course with 47.91% of patients with renal function deterioration and about one third follow up patients approaching ESRD during the study period.
|How to cite this article:|
Jha VK, Mahapatra D, Jairam A. Clinical Profile, Histopathological Features and Outcome of IgA Nephropathy in a Tertiary Care Hospital in India. Saudi J Kidney Dis Transpl 2020;31:1091-100
|How to cite this URL:|
Jha VK, Mahapatra D, Jairam A. Clinical Profile, Histopathological Features and Outcome of IgA Nephropathy in a Tertiary Care Hospital in India. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2021 Aug 1];31:1091-100. Available from: https://www.sjkdt.org/text.asp?2020/31/5/1091/301176
| Introduction|| |
IgA nephropathy (IgAN) is the commonest lesion found to cause primary glomerulonephritis throughout most developed countries of the world. In a Chinese study, it constituted 45% of all cases of primary glomerulonephritis. Variations in disease prevalence reflect regional differences in screening for renal diseases and renal biopsy practices which may lead to the increased discovery of asymptomatic cases. Thirty to forty percent of these cases have microscopic hematuria and low-grade proteinuria who are incidentally detected on a routine examination or during evaluation for chronic kidney disease (CKD) evaluation.
The common phenotype observed in multiple cohorts of IgAN is progressive CKD and renal survival ranges according to biopsy timing and introduction of lead-time bias. Factors associated with poor prognosis include pathologic findings, hypertension, proteinuria and renal dysfunction at diagnosis., Actuarial 10 years renal survival is reported to be 57%–91%. The disease is reported to be more common in Asians and is considered to be a very progressive disease with worse outcome.,,, The prevalence in India is reported to be 7%–16% of all patients with biopsy verified glomerular disease.,,,,,, The Oxford classification and scoring identified four variables in renal outcome prediction: mesangial hyper-cellularity (M); endocapillary hypercellularity (E); segmental glomerulosclerosis (S); tubular atrophy/interstitial fibrosis (T)., The scoring of crescents (C) was also introduced as an Oxford score as a factor of predictive importance, creating the MEST-C score. The present study encompasses a large cohort of biopsy-proven IgAN in a tertiary care hospital to characterize the initial clinical presentation, Oxford classification profile and one year follow up of patients with clinical and biochemical investigations.
| Materials and Methods|| |
All renal biopsies with a diagnosis of primary IgAN based on dominant or co-dominant deposits of IgA on direct immunofluorescence IgA staining of intensity more than 1+ (on a scale of 0–3+) were included from January 2015 to January 2018. All those patients who had secondary causes of IgAN, any other coexisting disease like diabetic nephropathy, <1 year of follow up after diagnosis, inadequate kidney biopsy and missing clinical records were excluded from the study. Allograft biopsies were also excluded.
In all biopsies with ≥8 viable glomeruli, the MEST-C scores namely mesangial hyper-cellularity, endocapillary hypercellularity, segmental sclerosis, tubular atrophy/interstitial fibrosis, and crescents were analyzed, according to the Oxford criteria., A 7-panel direct immunofluorescence record was also available including anti-IgG, IgM, IgA, C3c, C1q, Kappa and Lambda light chains and the intensity and location of each of these were studied.
Demographic and clinical data included age, gender, presence of hypertension (blood pressure ≥140/90 mm Hg or on antihypertensive drugs), presence of hematuria (≥3 red blood cells per high power field) and edema. Baseline investigations include urine protein semiquantitative, spot urine protein creatinine ratio, 24-h urinary protein, serum creatinine, and serum albumin. Nephrotic range proteinuria (NRP) was defined as 24-h urinary protein ≥3 g/day. Estimated glomerular filtration rate (eGFR) was calculated using the modified four-variable MDRD formula and all the patients were grouped in chronic kidney stages as per eGFR. Renal dysfunction was defined as serum creatinine ≥1.4 mg/dL repeated twice one day apart. Renal function decline/renal deterioration was the doubling of serum creatinine or attaining end-stage renal disease (ESRD). ESRD (was defined as eGFR <15 mL/min/1.73 m2 or the patient needing dialysis support due to symptomatic uremia. All the details of the use of angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARB), any immuno-suppressive drugs (steroid, mycophenolate mofetil or both) were recorded. Steroid dose (0.5 mg/kg/day) was given and continued for six months if eGFR ≥50 mL/min/1.73 m2 and has not responded to ACEI or ARB even after three to six months of its initiation as per KDIGO guidelines 2012. Mycophenolate mofetil was added if the biopsy had pathological features either in form of endocapillary proliferation/crescents/mesangial hypercellularity without advanced chronicity (either glomerulosceroscleris ≥50% or interstitial fibrosis/tubular atrophy ≥50% or both). The study was approved by the institute ethics committee.
| Statistical Analysis|| |
First, descriptive statistics were calculated. Statistical analysis was carried out using Stata 14.0 (College Station, TX, USA: Stata Corp., 2015). All the data were summed up as mean ± standard deviation SD or frequency (%). The categorical variables were compared between the groups using the Chi-square test/Fishers exact test. The continuous variables were compared between the groups using independent t-test/Wilcox on rank-sum test.
| Results|| |
Out of total 220 native kidney biopsies done during the study period, 48 renal biopsies (21.62%) were diagnosed as primary IgAN and met our study inclusion criteria. The mean age in the study cohort was 32 years with male: female ratio 5:1 (40 male: 8 female). Only 10 (20.83%) patients presented with edema while nine (18.75%) patients had NRP. Forty-six (95.8%) patients presented with hematuria out of which only four (8.3%) patients had gross hematuria. Forty-four (91.66%) patients were newly detected hypertensive or were on antihypertensive drugs before this presentation. Thirty-seven (77.08%) patients had renal dysfunction on initial presentation out of which 31 (64.5%) patients had sub-NRP (SNRP). The prevalence of proteinuria (semi-quantitative, urine protein: creatinine ratio, 24-h urinary protein), hematuria, mean serum creatinine is depicted in [Table 1]. Using four variable MDRD formula, number of patients in different CKD stages were as follows [Table 2]: CKD Stage 1 and 2 – 11 (22.91 %) patients, CKD Stage 3 – 10 (20.83%) patients, CKD Stage 4 – 21 (43.75%) patients and CKD Stage 5 – 6 (12.5%) patients.
|Table 1: Baseline demographic data and laboratory investigations at initial presentation (total patients=48).|
Click here to view
|Table 2: Chronic kidney disease stage as per estimated glomerular filtration rate by using 4 variable MDRD formula (total number of IgA patients=48).|
Click here to view
Clinical characteristics and laboratory investigations of patients with NRP and SNRP are as shown in [Table 3]. Compared to patients with SNRP, patients with NRP had less hypertension (77.7% vs. 94.8%), less serum albumin (28 ± 6 g/L vs. 39 ± 10 g/L, P <0.001), more proteinuria (5.2 ± 1.6 g/day vs. 1.8 ± 0.7 g/day, P = 0.04), less hematuria (77.7% vs. 100 %, less serum creatinine (2.3 ± 1.6 mg/dL vs. 3.4±2.3 mg/dL) and higher eGFR (62 ± 40.5 mL/min vs. 56 ± 44.6 mL/min).
|Table 3: Clinical characteristics and laboratory investigations of patients with nephrotic range proteinuria and subnephrotic proteinuria.|
Click here to view
MEST-C lesions distribution were interpreted in 39 patients and were as follows [Table 4]:
|Table 4: Distribution of MEST-C lesions in nephrotic range proteinuria versus subnephrotic range proteinuria (n=39)*.|
Click here to view
Mesangial hypercellularity (M1) was present in two (28.5%), NRP patients versus seven (21.8%) SNRP patients, endocapillary hypercellularity in one (14.2%) NRP patients versus six (18.75%) in SNRP patients, segmental glomerulosclerosis (S1) was present in three (42.8%) NRP patients versus 11 (34.5%) in SNRP patients, tubular atrophy/interstitial fibrosis (T1/T2) in two (28.5%) NRP patients versus seven (21.8%) in SRNP patients. Only four (12.5%) SNRP patients had the presence of C1 lesions (crescents in less than one-fourth of glomeruli). Six (12.5%) patients were diagnosed to have advanced CKD (CKD stage 5 or having severe interstitial fibrosis/tubular atrophy or advanced global glomerulosclerosis or both) or they had uremic symptoms on presentation requiring dialysis support. MEST-C scores were not calculated in these patients and were reported as chronic IgAN by the renal pathologist. No patients were diagnosed to have crescentic IgAN on biopsy or acute kidney injury on follow up.
Immunofluorescence distribution in renal biopsy were as follows [Table 5]: Deposits IgA 3+ was in 45 (93.7%) patients, IgA 2+ in three (6.25) patients, C3 1+ in 44 (91.66%) patients, C32+ in four (8.33) patients, lambda 2+ in two (4.16) patients and kappa 1+ was present in one (2.08%) patient.
Forty-three patients who were not dialysis-dependent on the initial presentation at the time of renal biopsy were followed up for at least one year with a median follow up of 16.3 (12–28) months in NRP patients and 15.8 months (12–38.2) in SNRP patients. 71.4% of NRP patients and 72.2 % of SNRP patients were put on ACEi or ARB. Steroids and mycophenolate mofetil were given in four (57.14%) and three (42.85%) patients respectively in NRP patients and 16 (44.44%) and 15 (41.66%) patients respectively in SNRP [Table 6]. Three (42.85%) patients with NRP and 20 (55.55%) patients with SNRP had renal deterioration during follow up period while two (28.57%) patients with NRP and 12 (41.66%) patients with SNRP had reached ESRD. In four (57.14%) and three (42.85%) patients respectively in NRP patients and 16 (44.44%) and 15 (41.66%) patients respectively in SNRP [Table 6]. Three (42.85%) patients with NRP and 20 (55.55%) patients with SNRP had renal deterioration during follow up period while two (28.57%) patients with NRP and 12 (41.66%) patients with SNRP had reached ESRD.
| Discussion|| |
IgAN is purported to be the commonest primary glomerulonephritis worldwide with the greatest frequency in East Asians and Caucasians, its prevalence in renal biopsy series ranging from 2% to 50%.,,, In a recent study from South India comprising a total of 3345 cases, it accounted for 13.55% of the cases. In other Indian studies range has been similar, from 7% to 16 %.,,, In our study it accounted for 21.62% of total native kidney biopsies. This figure is higher as there may be selection bias as the renal biopsy threshold in our cohort is less. Our nephrology center provides services for the serving central government employees and their dependents and routine annual medical examination is mandatory for all. Persons detected to be hypertensive with proteinuria or microscopic hematuria or renal dysfunction (serum creatinine ≥1.4 mg/dL) during routine medical examination underwent renal biopsy in our center. In most other centers, in the absence of screening program, only symptomatic patients due to significant proteinuria are more likely to visit nephrologist and give consent to renal biopsy compared to those with mild proteinuria, microscopic hematuria, episodic gross hematuria, or mild renal dysfunction. Few countries like Singapore and Japan which have screening strategies have reported a very high incidence of IgAN with minimal or no symptoms., Similarly, increased male: female ratio (5:1) may be due to the reason that our dependent population is male dominant. The male population percentage in other Indian studies range from 65% to 81.4% [Table 6]. The mean age in this study was 32 years, with the youngest aged 18 years and the oldest 55 years. This range is different from other studies across the world, in which the range varied from 2 to 85 years while the mean age varied from 28.8 to 35.8 years in most Indian studies.,,, Hypertension was noticed in 91.66% of our study population which is very high. This may be because many patients were detected to be hypertensive with renal dysfunction or proteinuria/microscopic hematuria on routine medical examination and were diagnosed to have IgAN on renal biopsy later on. Though hypertension is variable across the studies, ranging from as low as 6% to as high as 65% in VALIGA (Validation study of the Oxford Classification of IgAN) cohort, in most Indian studies it is present in more than 35% of cases, approaching 78.8% in one study.
Microscopic hematuria in our population (≥3 red blood cells per high power field) was present in 95.8% of patients. In most Indian studies, the quantitative data on hematuria is not available and this figure varies from 5.1% to 91% and could be explained with the methods and definition of microscopic/macroscopic hematuria. In a recent Indian study, in which microscopic hematuria was defined as ≥2 red blood cells/high power field, it was seen in 80% of cases. Gross hematuria was present in four (8.3%) cases in our study while it is not an uncommon finding in studies outside India.,,
Subnephrotic proteinuria is a more common presentation in our study as compared to NRP or nephrotic syndrome. However, in many Indian studies, NRP with edema was the predominant presenting features, the prevalence of NRP being a minimum of 23% and a maximum of 63.1%.,,, Our study about the degree of proteinuria was consistent with studies in the western population and even in the Japanese population,,, where a maximum of 16% in the Japanese population had significant proteinuria.
Renal dysfunction was noted in 77.08% of patients on initial presentation and maybe the indication for renal biopsy in our study. Five (10.41%) patients were dialysis-dependent on presentation. In another Indian study renal dysfunction was present in 78.9% patients when serum creatinine ≥1 mg/dL was taken as cut off point. IgAN patients may have a varying degree of progression and presentation due to various genetic, racial and/or environmental factors. In a large multiracial cohort of IgAN with over 600 patients in a Canadian based study, it was concluded that individuals of the Pacific-Asian region had a higher risk of progression to ESRD. Other Indian studies have also shown than a large no of Indian patients with IgAN have significant renal dysfunction at the time of biopsy; however renal dysfunction has been not well defined.,,,,
The histopathologic lesions distribution in our study cohort was different from other Indian studies., We observed a very low proportion of patients (23.7%) with mesangial hypercellularity which was less than Oxford cohort and other Indian studies, but almost similar to VALIGA cohort, other studies in Japanese and Chinese populations,, and a recent Indian study in large cohort. Endocapillary hypercellularity and crescents were less common in our study cohort and was consistent with a recent study by Gowrishankar et al. One Indian study by Mittal et al has reported a higher proportion of endocapillary proportion compared to our patient cohort (29.6% vs. 17.9%) and crescentic (C1) lesions (56.6% vs. 10.2%). Though this study, similar to our study also reported that majority of these patients presented with renal dysfunction and SNRP, tubulointerstitial lesions were more common as compared to our study cohorts (74.2% vs. 23.07%) [Table 7]. Compared to other studies from Asia,,, endocapillary hypercellularity, crescents, and segmental glomerulosclerosis were less common in our patients.
|Table 7: Comparison of clinical and pathologic characteristic of the present cohort with other Indian study populations.|
Click here to view
In a systemic meta-analysis of 16 studies, the M-, S-, T- and C- scores were strongly associated with progression to renal failure and E-lesions have been proposed as a pathological indicator for immunosuppression. In our study despite less proportion of patients with M-, S-, T- and C-scores, endpoint events/renal function deterioration were more as compared to other studies.
There was no significant difference in the MEST-C lesion characteristics of the patients presenting with NRP compared to those with SNRP [Table 4]. When clinical and laboratory investigations parameters were compared between these two groups, only serum albumin and 24-h urinary protein values were statistically significant [Table 3].
Forty-three patients (89.5%) were being followed up in our study as five patients were dialysis-dependent after the initial presentation/at the time of diagnosis. 71.4% of NRP patients and 72.22% of SNRP patients received ACEi/ARBs which were similar in other studies.,, Only four (57.14%) NRP patients and 16 (44.44%) SNRP patients received steroids as the first line immuno-suppression. This low proportion of patients who received steroid was due to the fact large no of patients had eGFR <50 mL/min/1.73 m2 who were not given steroids. As second-line immunosuppression only mycophenolate mofetil was used in our study cohort - three (42.85%) NRP patients and 15 (41.66%) SNRP patients. Only one Indian study has discussed the immunosuppression use, in which all 62 patients who were followed up received steroids as the first line immunosuppression while 14 (22.58%) patients required second-line immunosuppressive agents.
The renal worsening defined as doubling of serum creatinine or ESRD during follow up period was observed in a large proportion of patients in our study cohort (47.91%) compared to other Indian studies (17.7%–17.4%),, though the definition of renal worsening/endpoint events was different in all these studies. About one-third of our follow up patients reached ESRD (28.57% in NRP patients and 33.13% SNRP patients) which stresses the fact that IgAN in our population is a very aggressive disease despite use of ACEi and immunosuppression.
| Limitation of the Study|| |
This study is a single-center study which included predominantly male population who were serving in the organization. Most of the patients were incidentally detected to have hypertension or mild renal dysfunction or asymptomatic urinary abnormality during a mandatory routine medical examination.
| Conclusion|| |
Our study population of IgA nephropathy has a unique clinical profile with hypertension, microscopic hematuria and subnephrotic proteinuria as the predominant clinical presentation which is different from some other Indian cohorts.,,,, Mesangial proliferation, endocapillary proliferation, crescent formation, segmental sclerosis, and tubulointerstitial lesions were less common in our population. In spite of low MEST-C score, the disease has an aggressive course with 47.91% of patients with renal function deterioration and about one third follow up patients approaching ESRD during the study period. Further studies are required to characterize the disease progression and to find out the other prognostic histopathological features and new biomarkers to improve the prediction of renal prognosis in IgA nephropathy. New drug development coupled with multiethnic trials of these pharmacologic agents may help to determine whether ethnic differences in disease progression may be related to differential disease response versus pharmacokinetics.
Conflict of interest: None declared.
| References|| |
Li LS, Liu ZH. Epidemiologic data of renal diseases from a single unit in China: Analysis based on 13,519 renal biopsies. Kidney Int 2004;66:220-3.
Donadio JV, Grande JP. IgA nephropathy. N Engl J Med 2002;347:738-48.
Hall CL, Bradley R, Kerr A, Attoti R, Peat D. Clinical value of renal biopsy in patients with asymptomatic microscopic hematuria with and without low-grade proteinuria. Clin Nephrol 2004;62:267-72.
D’Amico G. Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome. Semin Nephrol 2004;24:179-6.
D’Amico G. Natural history of idiopathic IgA nephropathy: Role of clinical and histological prognostic factors. Am J Kidney Dis 2000;36: 227-37.
Koyama A, Igarashi M, Kobayashi M. Natural history and risk factors for immunoglobulin A nephropathy in Japan. Research Group on Progressive Renal Diseases. Am J Kidney Dis 1997;29:526-32.
Chou YH, Lien YC, Hu FC, et al. Clinical outcomes and predictors for ESRD and mortality in primary GN. Clin J Am Soc Nephrol 2012;7:1401-8.
Chacko B, John GT, Neelakantan N, et al. Presentation, prognosis and outcome of IgA nephropathy in Indian adults. Nephrology (Carlton) 2005;10:496-503.
Mittal N, Joshi K, Rane S, Nada R, Sakhuja V. Primary IgA nephropathy in north India: Is it different? Postgrad Med J 2012;88:15-20.
Golay V, Trivedi M, Abraham A, Roychowdhary A, Pandey R. The spectrum of glomerular diseases in a single center: A clinicopathological correlation. Indian J Nephrol 2013;23: 168-75.
] [Full text]
Gowrishnakar S, Gupta Y, Vankalakunti M, et al. IgA Nephropathy in South India: Demographic data and correlation of Oxford MEST-C scores with clinical variables. Kidney Int Rep 2019;4:1485-90.
Bagchi S, Singh G, Yadav R, et al. Clinical and histopathologic profile of patients with primary IgA nephropathy seen in a tertiary hospital in India. Ren Fail 2016;38:431-6.
Working Group of the International IgA Nephropathy Network and the Renal Pathology Society, Cattran DC, Coppo R, et al. The Oxford classification of IgA nephropathy: Rationale, clinicopathological correlations, and classification. Kidney Int 2009;76:534-45.
Working Group of the International IgA Nephropathy Network and the Renal Pathology Society, Roberts IS, Cook HT, et al. The Oxford classification of IgA nephropathy: Pathology definitions, correlations, and reproducibility. Kidney Int 2009;76:546-56.
Trimarchi H, Barratt J, Cattran DC et al. Oxford classification of IgA nephropathy 2016: An update from the IgA nephropathy classification working group. Kidney Int 2017;91:1014-21.
Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO Clinical Practice Guidelines for Glomerulonephritis. Immunoglobulin A nephropathy. Kidney Int 2012;2 Suppl 2:139-274.
Narasimhan B, Chacko B, John GT, Korula A, Kirubakaran MG, Jacob CK. Characterization of kidney lesions in Indian adults: Towards a renal biopsy registry. J Nephrol 2006;19:205- 10.
O’Shaughnessy MM, Hogan SL, Thompson BD, Coppo R, Fogo AB, Jennette JC. Glomerular disease frequencies by race, sex and region: Results from the International Kidney Biopsy Survey. Nephrol Dial Transplant 2018;33:661-9.
Woo KT, Edmondson RP, Wu AY, Chiang GS, Pwee HS, Lim CH. The natural history of IgA nephritis in Singapore. Clin Nephrol 1986;25:15- 21.
Kitajima T, Murakami M, Sakai O. Clinicopathological features in the Japanese patients with IgA nephropathy. Jpn J Med 1983;22:219-22.
Coppo R, Troyanov S, Bellur S, et al. Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments. Kidney Int 2014;86:828-36.
Gall JH. IgA nephropathy. Kidney Int 1995; 47:377-87.
Radford MG, Donadio JV, Bergsralh EJ, Grande JP. Predicting renal outcomes in IgA nephropathy. J Am Soc Nephrol 1997;8:199- 207.
Kim JK, Kim JH, Lee SC, et al. Clinical features and outcomes of IgA nephropathy with nephrotic syndrome. Clin J Am Soc Nephrol 2012;7:427-36.
Le W, Liang S, Hu Y, et al. Long-term renal survival and related risk factors in patients with IgA nephropathy: Results from a cohort of 1155 cases in a Chinese adult population. Nephrol Dial Transplant 2012;27:1479-85.
Lv J, Zhang H, Zhou Y, Li G, Zou W, Wang H. Natural history of immunoglobulin A nephropathy and predictive factors of prognosis: A long-term follow up of 204 cases in China. Nephrology (Carlton) 2008;13:242- 6.
Barbour SJ, Cattran DC, Kim SJet al. Individuals of Pacific Asian origin with IgA nephropathy have an increased risk of progression to end-stage renal disease. Kidney Int 2013;84:1017-24.
Chandrika BK. IgA nephropathy in Kerala, India: A retrospective study. Indian J Pathol Microbiol 2009;52:14-6.
] [Full text]
Lv J, Shi S, Xu D, et al. Evaluation of the Oxford classification of IgA nephropathy: A systemic review and meta-analysis. Am J Kidney Dis 2013;62:891-9.
Zeng CH, Le W, Ni Z, et al. A multicenter application and evaluation of the oxford classification of IgA nephropathy in adult Chinese patients. Am J Kidney Dis 2012; 60:812-20.
Katafuchi R, Ninomiya T, Nagata M, Mitsuiki K, Hirakata H. Validation study of oxford classification of IgA nephropathy: The significance of extracapillary proliferation. Clin J Am Soc Nephrol 2011;6:2806-13.
Yoon CY, Chang TI, Kang EW, Lim BJ, Kie JH, Kee YK, et al. Clinical usefulness of the Oxford classification in determining immuno suppressive treatment in IgA nephropathy. Ann Med. 2017;49:217-229.
Vijoy Kumar Jha
Department of Nephrology, Command Hospital Air Force, Bengaluru, Karnataka
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]