Mesangial proliferative glomerulonephritis: A glomerular disease or a non‐specific morphological change?

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We read with interest the recent publication by Jiang et al.1 reporting the clinicopathological characteristics of biopsy‐proven childhood renal diseases at a centre in Guangzhou, China. Notably, the third leading cause of primary glomerular disease after IgA nephritis (27.6%) and minimal change disease (24.0%) was “mesangial proliferative glomerulonephritis” (16.9%), a diagnosis 2.7 times more frequent than focal segmental glomerulosclerosis (6.3%) and 4.6 times more frequent than endocapillary proliferative glomerulonephritis (3.7%).
However, what is “mesangial proliferative glomerulonephritis”? In recent kidney pathology textbooks, this entity is described not as a specific glomerulopathy but as a frequent pattern of glomerular alteration common to many glomerulopathies, including those associated with immune complex deposition, podocytopathies, complement alterations, metabolic diseases, and recent transplantation, among others. In primary glomerulopathies, pure mesangial proliferation (without other glomerular histological changes) is more frequently found in IgA nephropathy, class II lupus nephritis, resolving postinfectious glomerulonephritis, IgM nephropathy, and the hypercellular “variant” of minimal change disease. Other glomerulonephritides that may present with only mesangial proliferation are C3 glomerulonephritis and those associated with infective endocarditis.
Proliferation of the mesangium, i.e. the finding of an increased number of mesangial cells (four or more per mesangial area2), is a frequent non‐specific change that may be seen both in primary glomerular diseases and in association with various systemic conditions. Commonly observed in kidney allograft biopsies, such change is often found in cases without glomerulitis, chronic allograft glomerulopathy, diabetes or immune complex deposition.
In a native kidney biopsy, the study of mesangial proliferation must be complemented with immunofluorescence studies: when positive, the diagnosis is made in accordance with such positivity and when negative, the diagnosis may be made using special stains, clinical features, extraglomerular features and possibly electron microscopic features. The presence of any other alterations (e.g., extracellular deposits, tubulointerstitial or ultrastructural alterations) suggests a corresponding diagnosis.
After extensive investigations in search of a more specific diagnosis, some cases do not show other alterations and the non‐specific histological pattern of “mesangial proliferative glomerulonephritis” might appear to be “the diagnosis”. Some cases bearing this diagnosis have been reported in rheumatoid arthritis and other autoimmune diseases, without a known pathogenesis or established clinical implications.
Isolated mesangial proliferation is a frequent and non‐specific change that should prompt a search for better characterized glomerulopathies. When no other morphological, immunopathological or ultrastructural alterations are found, the non‐specific and controversial diagnosis of “mesangial proliferative glomerulonephritis” (or “glomerulopathy”) might be considered; however, this descriptive histological term does not aid in determining the aetiology or pathogenesis of a renal disease.
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