Abstract
Lupus glomerulopathies are classified into various histological patterns, which probably result from different pathophysiological origins. Podocyte injury can be demonstrated in lupus nephritis but its clinical relevance is far little appreciated and is often masked by proliferative lesions and inflammatory cell infiltrations. Two patterns of podocyte lesions may be considered, either occurring in the context of renal inflammation or reflecting podocyte dysfunction in non-proliferative and non-inflammatory glomerulopathies. This distinction remains elusive since no reliable biomarker discriminates between both entities. CMIP was recently found induced in some glomerular disease but its expression in different lupus nephritis classes has not been investigated. Twenty-four adult patients with lupus nephritis, including non-proliferative (n = 11) and proliferative (n = 13) glomerulopathies were analyzed. Clinical, biological and immunological data were compared with immunomorphological findings. We analyzed by quantitative and qualitative methods the expression of CMIP in different histological classes. We found CMIP abundance selectively increased in podocytes in class II and class V glomerulopathies, while in proliferative forms (class III and class IV), CMIP was rarely detected. CMIP was not expressed in cellular crescents, endothelial cells or mesangial cells. CMIP colocalized with some subsets of B and T cells within glomerular or interstitial mononuclear cell infiltrates but never with macrophages. Hematuria is rarely present in lupus glomerulopathies expressing CMIP. There was no correlation between classical immunological markers and CMIP expression. Thus, CMIP induction in lupus nephritis seems restricted to non-proliferative glomerulopathies and may define a specific pattern of podocyte injury.
Highlights
Systemic lupus erythematosous (SLE) is a chronic immune complex-mediated disease characterized by a disseminated inflammatory disease, which may affect multiple organs, including the kidney [1]
We aimed to study whether CMIP could be expressed in lupus nephritis, and to determine whether its expression could be correlated with a particular pattern of lupus nephritis
We provide evidence that: i) CMIP is selectively expressed in the cytoplasm compartment of podocytes in class II and class V glomerulopathies, suggesting that podocyte is presumably the main target in these lupus glomerulopathies; ii) in proliferative forms, CMIP is almost not expressed either in podocytes or in cellular crescents; iii) there is Glomeruli number Glomerulosclerosis number Mesangial hypercellularity
Summary
Systemic lupus erythematosous (SLE) is a chronic immune complex-mediated disease characterized by a disseminated inflammatory disease, which may affect multiple organs, including the kidney [1]. Histological evaluation and scoring studies of renal lesions by World Health Organisation (WHO 1982, 1995) have individualized six entities but this classification has evolved over time, because of the diversity of lesions within the same class and the difficulties to ascribe it to clinical or prognostic correlations These classifications fail to optimize the therapeutic strategy, when proliferative lesions are associated with membranous lupus nephropathy. The recent classification from the International Society of Nephrology and Renal Pathology Society (ISN/RPS) distinguishes diffuse glomerulonephritis into separate classes with either segmental (class IV-S) or global (class IV-G) lesions [4] It facilitates clinical study comparisons, this classification fails to improve prediction of disease course
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