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| Year : 2015 | Volume
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| Issue : 3 | Page : 604-607 |
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| Renal vascular lesions in lupus nephritis: A need for further characterization of vasculopathy |
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Hamid Nasri1, Muhammed Mubarak2
1 Department of Nephrology, Division of Nephropathology, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Histopathology, Sindh Institute of Urology and Transplantation (SIUT), Karachi, Pakistan
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| Date of Web Publication | 20-May-2015 |
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How to cite this article:
Nasri H, Mubarak M. Renal vascular lesions in lupus nephritis: A need for further characterization of vasculopathy. Saudi J Kidney Dis Transpl 2015;26:604-7 |
How to cite this URL:
Nasri H, Mubarak M. Renal vascular lesions in lupus nephritis: A need for further characterization of vasculopathy. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2021 Jan 16];26:604-7. Available from: https://www.sjkdt.org/text.asp?2015/26/3/604/157414 |
To the Editor,
Renal vascular lesions are of paramount importance in the pathogenesis and progression of many primary and secondary medical renal diseases. In fact, many renal diseases result from a primary lesion of the vascular component, but, in the vast majority of cases, the vascular component is involved secondarily in the disease process affecting primarily either the glomeruli or the tubulointerstitial components. Some diseases affect multiple tissue components in the kidney, either simulta-neously or sequentially. Lupus nephritis (LN) and IgA nephropathy (IgAN) are prime examples of such diseases. A variety of lesions of diverse etiology can be seen affecting the vasculature of the kidney and adding to the parenchymal damage in the above diseases. [1],[2],[3],[4] An accurate diagnosis and classification of the vascular lesions is of vital importance for the optimal management of these diseases. Most work has been carried out in elucidating the nature of vasculopathies in LN. A number of investigators have studied the patterns of vascular lesions on renal biopsies in patients with LN, including Wu et al, [5] whose group recently studied the patterns of vascular lesions in one of the largest studies to date in patients with LN. Among 341 patients at a single center in China, they found either single or multiple renal vascular lesions in 279 patients (81.8%), which included 253 patients (74.2%) with vascular immune complex deposits, 82 patients (24.0%) with atherosclerosis, 60 patients (17.6%) with thrombotic micro-angiopathy (TMA), 13 patients (3.8%) with non-inflammatory necrotizing vasculopathy and two patients (0.6%) with true renal vasculitis [1] [Figure 1]. The authors concluded that vascular lesions are common in patients with LN and closely correlate with clinical disease activity and outcome. They have recommended inclusion of the renal vascular lesions into the 2003 International Society of Nephrology/ Renal Pathology Society (ISN/RPS) system for classifying LN to further strengthen the predictive value of the classification for renal outcome. This study underscores the need for careful interpretation of the renal biopsies in patients with LN to look for vascular lesions. However, we, as many other investigators, are of the view and take this opportunity to emphasize the fact that vasculopathy in LN is of multi-factorial origin, and this aspect needs to be investigated in further detail. | Figure 1: Common types of renal vascular lesions in lupus nephritis. (A) Vascular immune complex deposition. On immunofluorescence microscopy, deposits of C3 were detected in the walls of extraglomerular arterioles. The glomerulus shows trace and segmental positivity (IF, original magnification ×400). (B) Atherosclerosis. Intimal fibrous proliferation of a large lobar artery is seen (Masson's trichrome, original magnification ×400). (C) Non-inflammatory necrotizing vasculopathy. Smudgy eosinophilic material is deposited in the arteriolar wall. There is no inflammatory infiltration in the vessel wall (hematoxylin and eosin, original magnification ×400). (D) True renal vasculitis. Fibrinoid necrosis of the vessel wall associated with mixed inflammatory cell infiltration in the intima and media of a lobar artery (hematoxylin and eosin, original magnification ×400).
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Vascular lesions in LN may be due to three different etiologies. [1],[2],[3],[4],[5],[6],[7] Lupus vasculopathy, specific to lupus, associated with immune-complex deposits unaccompanied by inflammatory cell infiltration of the vessel wall is the most common pattern. [1],[2],[3] The prognostic significance of this condition is not clear and current evidence is not sufficient to justify their inclusion in the Oxford classification at this time. [1],[8],[9],[10] Secondly, there may be a true vasculitis in LN due to a rare association of LN and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. [1],[2],[3],[4] Thus, in this scenario, there are two different diseases occurring concurrently; their rare co-existence does not justify inclusion of this combination in the classification of LN. Finally, the main etiologic factor for the vascular lesions in systemic lupus erythematosus (SLE) is considered to be antiphospholipid syndrome-associated nephropathy (APS-nephropathy, APSN), which is also known as vaso-occlusive nephropathy. [11],[12],[13],[14],[15],[16],[17],[18],[19],[20] This syndrome may present as an acute vasculopathy, termed thrombotic microangiopathy, or chronic vascular lesions such as arteriosclerosis, fibrous intimal hyperplasia, fibrous occlusions of vessels, recanalized thrombi and focal cortical atrophy (FCA) [12],[13],[14],[15],[16],[17],[18],[19],[20] [Figure 2]. In this condition also, there are two different disease processes affecting the vessels. [12],[13],[16] Hence, the suggestion by Wu et al to include the vascular lesions in the ISN/RPS 2003 LN classification, without first classifying the vasculopathies from the etio-pathogenesis point of view, seems too early and superficial. [5] It is well known that the morphologic lesions of APSN aggravate kidney parenchymal damage in LN. [1],[6],[7],[14],[15] Thus, it seems prudent to propose a distinct classification for APSN to draw more attention to this disease and to avoid under-recognition of this vascular nephropathy. [21] This classification may be used together with the ISN/RPS 2003 LN classification in the same report. Indeed, much attention has been directed recently toward renal morphologic lesions of APSN and renal pathologists should be mindful of the morphologic characteristics of APSN when they sign out kidney biopsies of SLE patients, especially those with positive anti-phospholipid antibodies. [1],[14],[15],[20],[21] It has become evident that most of the vascular lesions previously thought of as lupus vasculopathy are now known to be due to APSN. [14],[15] Thus, the patients should be better categorized as LN and APSN, LN and ANCA vasculitis and LN with lupus vasculopathy. Combining the different vascular disorders into a general category of vasculopathy is not a scientifically sound practice. | Figure 2: Renal parenchymal and vascular lesions in anti-phospholipid antibody syndrome-associated nephropathy (APSN). (A) Well-demarcated, wedge-shaped area of sub-capsular tubular atrophy and thyroidization of tubules. This parenchymal change, known as focal cortical atrophy (FCA), is characteristically seen in APSN. (Hematoxylin and eosin, original magnification ×200.) (B) This shows typical pseudocystic or ballooned glomeruli in areas of FCA. One normal glomerulus is also seen in the surrounding normal parenchyma. (Hematoxylin and eosin, original magnification ×200.) (C) Typical vascular changes florid arteriolosclerosis with obliteration of the lumen of many arterioles in a case of APSN. (Hematoxylin and eosin, original magnification ×200.) (D) Thrombotic microangiopathy. Fibrin thrombi are present in arterioles at the hilum of the glomerulus and in many glomerular capillaries (Hematoxylin and eosin, original magnification ×400)
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In conclusion, vascular lesions are common in LN and are of multi-factorial origin. An attempt should be made to accurately characterize the etio-pathogenesis and classification of these lesions, and these should not be lumped together under one category of lupus vasculopathy. Further studies are needed to fully understand the prognostic implications of these different vasculopathies.
Conflict of Interest
The authors declared no competing interests.
 References | |  |
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Correspondence Address:
Dr. Muhammed Mubarak
Department of Histopathology, Sindh Institute of Urology and Transplantation (SIUT), Karachi
Pakistan
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DOI: 10.4103/1319-2442.157414 PMID: 26022040 
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