Membranous Glomerulonephritis Membranous glomerulonephritis (MGN) is a disease characterized by subepithelial immune deposits and formation of perpendicular projections of material similar to the glomerular basement membrane (GBM) in the external part of this one (between podocyte cytoplasm and GBM): “ spikes ”.

Glomerulonephritis is a medical term for a family of diseases involving damage to the glomeruli (the tiny filters in the kidney), usually caused by the body’s immune system. There are many types of glomerulonephritis including: Focal and segmental glomerulosclerosis (FSGS) IgA glomerulonephritis; IgM glomerulonephritis

Renal histology confirmed membranous glomerulonephritis, without any sign of amyloid deposition (Figure 1). Serum electrophoresis detected a biclonal IgA lambda at 3.2 g/l and 0.8 g/l, with IgG levels of 3.40 g/l (normal range 6.0–16.0 g/l), IgA 9.20 g/l (0.8–4.0 g/l) and IgM 0.40 g/l (0.5–2.0 g/l). Within membranous glomerulonephritis, especially in cases caused by viral hepatitis, serum C3 levels are low. Similar to other causes of nephrotic syndrome (e.g., focal segmental glomerulosclerosis or minimal change disease), membranous nephropathy is known to predispose affected individuals to develop blood clots such as pulmonary emboli.

Membranoproliferative Glomerulonephritis This term refers to a pattern of glomerular lesion with many etiologies, in which, as its name implies, there is proliferation (endocapillary and / or mesangial) and thickening of the capillary walls (" membrano ") by subendothelial immune and / or complement deposits, or some other type of subendothelial alteration (between the endothelium and the basement membrane). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalinised glomeruli are atrophic (smaller), lacking capillaries, hence these glomeruli are non-functional. Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, activating complement and damaging the glomeruli. MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults. Membranous glomerulonephritis can appear secondary to a variety of infectious or pharmacological insults as well as in conjunction with systemic diseases It should be pointed out that the pathogenesis of secondary disease is thought to be initiated by the deposition of Preformed Immune Complexes within the glomerular barrier and not 'in situ' formation (See: Basic Glomerular Pathogenesis ) Membranous nephropathy (MN) is an immune complex disease caused by subepithelial deposits.

Last Update: av R Tofik — histopathology (proliferative or non-proliferative, diffuse or focal etc.).

Kidney Histology: Histology of normal human kidney with collecting tubules and Photo of membranous nephropathy. Diabetic Nephropathy, kidney disease.

Serum electrophoresis detected a biclonal IgA lambda at 3.2 g/l and 0.8 g/l, with IgG levels of 3.40 g/l (normal range 6.0–16.0 g/l), IgA 9.20 g/l (0.8–4.0 g/l) and IgM 0.40 g/l (0.5–2.0 g/l). Within membranous glomerulonephritis, especially in cases caused by viral hepatitis, serum C3 levels are low. Similar to other causes of nephrotic syndrome (e.g., focal segmental glomerulosclerosis or minimal change disease), membranous nephropathy is known to predispose affected individuals to develop blood clots such as pulmonary emboli. Membranous nephropathy in particular is known to increase this risk more than other causes of nephrotic syndrome though the reason for this is not yet clear.

18 Jan 2013 In secondary forms of membranous glomerulonephritis, such IgG4 Schwartz MM, Silva FG(eds) Heptinstall's Pathology of the Kidney 6th edn.

Histologiskt utmärker den sig genom avlagringar mellan kapillärväggarnas epitelskikt och basmembran och förtjockning av membranet. Membranoproliferative Glomerulonephritis This term refers to a pattern of glomerular lesion with many etiologies, in which, as its name implies, there is proliferation (endocapillary and / or mesangial) and thickening of the capillary walls (" membrano ") by subendothelial immune and / or complement deposits, or some other type of subendothelial alteration (between the endothelium and the basement membrane). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalinised glomeruli are atrophic (smaller), lacking capillaries, hence these glomeruli are non-functional. Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, activating complement and damaging the glomeruli. MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults.
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Curr Opin Nephrol Hypertens. 2006 May. 15(3):258-63. .

Totally hyalinised glomeruli are atrophic (smaller), lacking capillaries, hence these glomeruli are non-functional. Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, activating complement and damaging the glomeruli. MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults.
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complex disease caused by subepithelial deposits. Primary MN is a common cause of nephrotic syn-. drome.