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Year : 2023  |  Volume : 66  |  Issue : 1  |  Page : 216-218
Are renal microvascular lesions the novel histological predictors in IgA nephropathy

Department of Nephrology and Kidney Transplantation, Virinchi Hospitals, Hyderabad, Telangana, India

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Date of Submission16-Jun-2021
Date of Acceptance08-Nov-2021
Date of Web Publication18-Jan-2023

How to cite this article:
Etta PK, Madhavi T. Are renal microvascular lesions the novel histological predictors in IgA nephropathy. Indian J Pathol Microbiol 2023;66:216-8

How to cite this URL:
Etta PK, Madhavi T. Are renal microvascular lesions the novel histological predictors in IgA nephropathy. Indian J Pathol Microbiol [serial online] 2023 [cited 2023 Mar 20];66:216-8. Available from:

Dear Editor,

IgA nephropathy (IgAN) is the most common cause of primary glomerulonephritis with a variable clinical course, and shows diverse pathological findings ranging from minimal glomerular lesions, segmental glomerulosclerosis (S), mesangial (M) and endocapillary (E) hypercellularity, diffuse proliferative and crescentic (C) glomerulonephritis and advanced glomerulosclerosis with marked tubular atrophy/interstitial fibrosis (T). Lee et al. (1982),[1] Haas (1997),[2] Manno et al. (2007),[3] and the Oxford classification (2009; updated in 2016) have evaluated and classified several glomerular and tubulointerstitial lesions with prognostic significance.[4],[5] The Oxford classification initially identified four histologic variables (MEST), which were shown to be independently associated with renal outcome in biopsy specimens with a minimum of eight glomeruli.[4] Later, the presence of crescents was found to be an independent risk factor for the combined renal outcome in larger studies.[6] This has prompted the inclusion of cellular or fibrocellular crescents (C) score in addition to the four components of the original MEST score i.e., MEST-C score in updated Oxford classification [Table 1].[5] Oxford classification has been evaluated and a number of validation studies have supported it in predicting clinical outcome in multiple population cohorts. In majority, including studies from India, the most consistent histological predictor is the extent of tubular atrophy/interstitial fibrosis (T).[7],[8],[9],[10],[11],[12] Later, various risk prediction tools employing clinical and histological components from MEST-C score were developed and validated.[13],[14],[15] However, the clinical implications of renal microvascular lesions in IgAN has not been investigated well.
Table 1: Current MEST-C scoring of IgAN (updated Oxford classification)

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Recently, we have observed significant microvascular lesions in the form of hypertensive vasculopathy and thrombotic microangiopathy (TMA) in six patients (five males; one female) with non-crescentic IgAN and all of them ended up with end-stage kidney disease (ESKD) within 24 months of presentation. All of them were presented with rapidly progressive renal failure. Though hypertension was seen in all of them, only one of them presented with malignant hypertension at the time of biopsy. Age varied from 24 to 38 years (mean 30.5 years). Serum creatinine ranged from 1.9 to 4.2 mg/dl (mean 2.8 mg/dl). Proteinuria ranged from 1.4 to 3.9 g/day (mean 2.4 g/day). Nephrotic range proteinuria was seen in two patients. Two of them had significant chronicity (T2) in the biopsy. MEST scoring was not done for one case due to lesser number of viable glomeruli in biopsy sample. Serum complement levels were normal in all. There was no systemic or laboratory evidence of TMA in any of these patients, however, alternate complement pathway was not analyzed. All of them were treated with supportive measures such as RAAS blockers. Four patients were treated with immunosuppression (steroids alone in three; steroids + mycophenolate mofetil in one). Time to reach ESKD ranged from 4 to 36 months (mean 17 months). Two of the six underwent kidney transplantation with live related donors. We have observed a relatively rapid progression of kidney disease in the IgAN patients with microvascular lesions compared to those without.

Microvascular lesions in IgAN are diverse [Table 2] and often accompany the presence of hypertension. TMA has been variably described in association with IgAN (as high as 53% of biopsies).[16] TMA in IgAN may not always be associated with malignant hypertension and portends a poor renal outcome.[16],[17] Other vascular lesions such as fibrinoid necrosis is seen in ~ 10% of IgAN biopsies and these necrotizing lesions seem to be responsive to immunosuppression. It remains poorly understood whether microvascular lesions play an important role in the progression of IgAN. Preliminary data from West supports the hypothesis that microvascular lesions may correlate with hypertension, greater proteinuria and renal dysfunction and overall poorer renal outcomes and serve as important histological prognostic indicators in IgAN.[16],[17],[18],[19] Further long-term prospective multicenter studies will be necessary to assess the significance of microvascular lesions on the renal outcome. In future, these lesions could be considered for inclusion in formal scoring systems of IgAN. This may further improve our current understanding of this diverse disease and help in clinical decision-making.
Table 2: Microvascular lesions in IgA nephropathy

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Conflicts of interest

There are no conflicts of interest.

   References Top

Lee SM, Rao VM, Franklin WA, Schiffer MS, Aronson AJ, Spargo BH, et al. IgA nephropathy: Morphologic predictors of progressive renal disease. Hum Pathol 1982;13:314-22.  Back to cited text no. 1
Haas M. Histologic subclassification of IgA nephropathy: A clinicopathologic study of 244 cases. Am J Kidney Dis 1997;29:829-42.  Back to cited text no. 2
Manno C, Strippoli GFM, D'Altri C, Torres D, Rossini M, Schena FP. A novel simpler histological classification for renal survival in IgA nephropathy: A retrospective study. Am J Kidney Dis 2007;49:763-75.  Back to cited text no. 3
Roberts IS, Cook HT, Troyanov S, Alpers CE, Amore A, Barratt J, et al. The Oxford classification of IgA nephropathy: Pathology definitions, correlations, and reproducibility. Kidney Int 2009;76:546-56.  Back to cited text no. 4
Trimarchi H, Barratt J, Cattran DC, Cook HT, Coppo R, Haas M, et al. Oxford classification of IgA nephropathy 2016: An update from the IgA Nephropathy Classification Working Group. Kidney Int 2017;91:1014-21.  Back to cited text no. 5
Haas M, Verhave JC, Liu ZH, Alpers CE, Barratt J, Becker JU, et al. A multicenter study of the predictive value of crescents in IgA nephropathy. J Am Soc Nephrol 2017;28:691-701.  Back to cited text no. 6
Alamartine E, Sauron C, Laurent B, Sury A, Seffert A, Mariat C. The use of the Oxford classification of IgA nephropathy to predict renal survival. Clin J Am Soc Nephrol 2011;6:2384-8.  Back to cited text no. 7
Shi SF, Wang SX, Jiang L, Lv JC, Liu LJ, Chen YQ, et al. Pathologic predictors of renal outcome and therapeutic efficacy in IgA nephropathy: Validation of the oxford classification. Clin J Am Soc Nephrol 2011;6:2175-84.  Back to cited text no. 8
Lv J, Shi S, Xu D, Zhang H, Troyanov S, Cattran DC, et al. Evaluation of the Oxford classification of IgA nephropathy: A systematic review and meta-analysis. Am J Kidney Dis 2013;62:891-9.  Back to cited text no. 9
Coppo R, Troyanov S, Bellur S, Cattran D, Cook HT, Feehally J, et al. Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments. Kidney Int 2014;86:828-36.  Back to cited text no. 10
Bagchi S, Singh G, Yadav R, Kalaivani M, Mahajan S, Bhowmik D, 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.  Back to cited text no. 11
Gowrishankar S, Gupta Y, Vankalakunti M, Gowda KK, Kurien AA, Jansi Prema KS, et al. Correlation of Oxford MEST-C scores with clinical variables for IgA nephropathy in South India. Kidney Int Rep 2019;4:1485-90.  Back to cited text no. 12
Tanaka S, Ninomiya T, Katafuchi R, Masutani K, Tsuchimoto A, Noguchi H, et al. Development and validation of a prediction rule using the Oxford classification in IgA nephropathy. Clin J Am Soc Nephrol 2013;8:2082-90.  Back to cited text no. 13
Okonogi H, Kawamura T, Joh K, Koike K, Miyazaki Y, Ogura M, et al. A grading system that predicts the risk of dialysis induction in IgA nephropathy patients based on the combination of the clinical and histological severity. Clin Exp Nephrol 2019;23:16-25.  Back to cited text no. 14
Barbour SJ, Coppo R, Zhang H, Liu ZH, Suzuki Y, Matsuzaki K, et al. Evaluating a new international risk prediction tool in IgA nephropathy. JAMA Intern Med 2019;179:942-52.  Back to cited text no. 15
El Karoui K, Hill GS, Karras A, Jacquot C, Moulonguet L, Kourilsky O, et al. A clinicopathologic study of thrombotic microangiopathy in IgA nephropathy. J Am Soc Nephrol 2012;23:137-48.  Back to cited text no. 16
Chang A, Kowalewska J, Smith KD, Nicosia RF, Alpers CE. A clinicopathologic study of thrombotic microangiopathy in the setting of IgA nephropathy. Clin Nephrol 2006;66:397-404.  Back to cited text no. 17
Zhang Y, Sun L, Zhou S, Xu Q, Xu Q, Liu D, et al. Intrarenal arterial lesions are associated with higher blood pressure, reduced renal function and poorer renal outcomes in patients with IgA nephropathy. Kidney Blood Press Res 2018;43:639-50.  Back to cited text no. 18
Cai Q, Shi S, Wang S, Ren Y, Hou W, Liu L, et al. Microangiopathic lesions in IgA nephropathy: A cohort study. Am J Kidney Dis 2019;74:629-39.  Back to cited text no. 19

Correspondence Address:
Praveen Kumar Etta
Department of Nephrology and Kidney Transplantation, Virinchi Hospitals, Hyderabad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpm.ijpm_613_21

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