IgM nephropathy | |
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Other names | immunoglobulin M nephropathy (IgMN) |
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Antibody type IgM scheme. Blue - heavy chains, Yellow — light chains, Dark yellow/blue — variable regions (ends are binding sites), Light yellow/blue — constant regions, Green — disulfide bridges, Black — J chain | |
Specialty | Nephrology |
IgM nephropathy or immunoglobulin M nephropathy (IgMN) is a kind of idiopathic glomerulonephritis that is marked by IgM diffuse deposits in the glomerular mesangium.[1] IgM nephropathy was initially documented in 1978 by two separate teams of researchers.[2]
Young adults or children with IgM nephropathy typically exhibit proteinuria or hematuria. In people with IgMN, proteinuria can vary from nephrotic syndrome to asymptomatic proteinuria.[3]
The cause of IgM nephropathy is unknown.[citation needed] Several systemic illnesses, including paraproteinemia, diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus (SLE), and Alport's syndrome, can cause IgM deposits in the glomeruli.[4][5]
It is yet unknown how IgM nephropathy develops, however it has been proposed that aberrant T-cell activity or a disruption in mesangial cell immunoaggregate clearance may be involved.[6][7] Several investigations have found that patients with IgM nephropathy have higher blood IgM or IgM immunocomplex concentrations, which would provide support to the previously indicated idea.[8][9]
Light microscopy (LM) on a renal sample reveals variable degrees of mesangial cell proliferation or mesangial sclerosis from minute alterations.[3][10] A small number of instances with crescentic glomerulonephritis (GN) have been documented.[11] Immunofluorescence (IF) analysis of kidney biopsy specimens shows that IgM deposits in the mesangium have a granular or diffuse appearance.[12] While there may be traces of other immunoglobulins besides IgM, significant IgM deposition is typically indicative.[3][10] Certain investigations have also revealed the existence of complement fragments, such as C3 or C1q.[3]