Glomerular lipidosis is a rare and very characteristic histological feature presenting the diffuse, global, and extensive glomerular accumulation of lipids, often referred to as foamy-appearing glomeruli with or without histiocytic infiltration. It develops under various conditions, including genetic and/or acquired disorders such as lipoprotein glomerulopathy (LPG), lecithin-cholesterol acyltransferase (LCAT) deficiency, familial type 3 hyperlipidemia, Fabry’s disease, hemophagocytic syndrome (HPS)/macrophage activation syndrome (MAS), thrombotic microangiopathy (TMA) and so on.
The etiology may be directly related to lipid metabolism, but it may also be associated with immunological abnormalities not directly related to lipid metabolism, and the treatments are quite different depending on its etiology, so differentiation of the pathology is important. Immunostaining for CD68 differentiates the diseases into 2 general categories; i.e., histiocytic and nonhistiocytic glomerular lipidosis. In addition, glomerular lipidosis due to HPS/MAS and TMA may be seen as secondary kidney lesions associated with systemic disease, but there are also types that are localized to the kidneys and are referred to as renal or glomerular-limited HPS/MAS or TMA.The renal clinical manifestations are very diverse as well, including acute kidney injury, chronic nephritic syndrome, rapidly progressive nephritic syndrome, and nephrotic syndrome.
In this Research Topic, we invite papers related to the diagnosis, etiology, differential diagnostic methods, and treatment of diseases that present this characteristic histological finding, in the forms of Case Reports, Original Research and Review articles.
Keywords:
Glomerular Lipidosis, Lipoprotein Glomerulopathy (LPG), Lecithin-cholesterol Acyltransferase (LCAT) Deficiency, Familial Type 3 Hyperlipidemia, Fabry’s Disease, Hemophagocytic Syndrome (HPS)/Macrophage Activation Syndrome (MAS), Thrombotic Microangiopathy
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Glomerular lipidosis is a rare and very characteristic histological feature presenting the diffuse, global, and extensive glomerular accumulation of lipids, often referred to as foamy-appearing glomeruli with or without histiocytic infiltration. It develops under various conditions, including genetic and/or acquired disorders such as lipoprotein glomerulopathy (LPG), lecithin-cholesterol acyltransferase (LCAT) deficiency, familial type 3 hyperlipidemia, Fabry’s disease, hemophagocytic syndrome (HPS)/macrophage activation syndrome (MAS), thrombotic microangiopathy (TMA) and so on.
The etiology may be directly related to lipid metabolism, but it may also be associated with immunological abnormalities not directly related to lipid metabolism, and the treatments are quite different depending on its etiology, so differentiation of the pathology is important. Immunostaining for CD68 differentiates the diseases into 2 general categories; i.e., histiocytic and nonhistiocytic glomerular lipidosis. In addition, glomerular lipidosis due to HPS/MAS and TMA may be seen as secondary kidney lesions associated with systemic disease, but there are also types that are localized to the kidneys and are referred to as renal or glomerular-limited HPS/MAS or TMA.The renal clinical manifestations are very diverse as well, including acute kidney injury, chronic nephritic syndrome, rapidly progressive nephritic syndrome, and nephrotic syndrome.
In this Research Topic, we invite papers related to the diagnosis, etiology, differential diagnostic methods, and treatment of diseases that present this characteristic histological finding, in the forms of Case Reports, Original Research and Review articles.
Keywords:
Glomerular Lipidosis, Lipoprotein Glomerulopathy (LPG), Lecithin-cholesterol Acyltransferase (LCAT) Deficiency, Familial Type 3 Hyperlipidemia, Fabry’s Disease, Hemophagocytic Syndrome (HPS)/Macrophage Activation Syndrome (MAS), Thrombotic Microangiopathy
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.