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| Year : 2023 | Volume
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| Issue : 1 | Page : 216-218 |
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| Are renal microvascular lesions the novel histological predictors in IgA nephropathy |
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Praveen Kumar Etta, Thatipamula Madhavi
Department of Nephrology and Kidney Transplantation, Virinchi Hospitals, Hyderabad, Telangana, India
Click here for correspondence address and email
| Date of Submission | 16-Jun-2021 |
| Date of Acceptance | 08-Nov-2021 |
| Date of Web Publication | 18-Jan-2023 |
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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 |
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.
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.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
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Correspondence Address:
Praveen Kumar Etta
Department of Nephrology and Kidney Transplantation, Virinchi Hospitals, Hyderabad
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijpm.ijpm_613_21
[Table 1], [Table 2] |
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