Mesangiocapillary Glomerulonephritis

Mesangiocapillary glomerulonephritis is also called Membrano-proliferative glomerulonephritis.

·        There is both a membranous and cellular component (different from membranous glomerulonephritis!).

·        There is a proliferation of mesangial cells, as well as that of epithelial and endothelial cells.

The most important diseases that cause secondary Mesangiocapillary Glomerulonephritis are:

·        Chronic systemic immune complex diseases

o        Infections (Hepatitis B/C, Schistosomiasis)

o        Autoimmune diseases – SLE, Rheumatoid Arthritis, Cryoglobulinemia

Other causes of Meangiocapillary Glomerulonephritis

·        Neoplasia

·        alpha-1-antitrypsin deficiency

·        Sickle Cell disease

·        Sarcoidosis

·        Renal Allograft

In children and young patients, there is a persistant hypocomplementemia (low C3 levels).

·        This is diagnostic of Mesangiocapillary Glomerulonephritis.

·        ***super-important*** to remember!!!

·        A review of the alternative complement pathway.

o        Endotoxins and IgA activate C3 to become C3 convertase.

o        Properdin normally stabilizes C3 convertase so that C3 convertase cleaves C3 to C3b.

o        Diseased patients have an autoantibody called C3Nef. C3Nef antibody binds to and stabilizes C3 converstase as well. There is a further cleaving of C3 to C3b, resulting in low levels of C3 in the blood. C3Nef is not present in other glomerulonephritis diseases.

Type I Mesangiocapillary Glomerulonephritis

·        50% is due to an immune complex disease

o        Numerous peripheral, mesangial, and sub-epithelial deposits

o        IgG, C1q, C3, and C4 present (classical complement pathway)

·        C3 & C5 hypocomplementemia fluctuates.

·        There is occasional C3Nef-like activity.

Type II Mesangiocapillary Glomerulonephritis (Dense Deposit Disease – Alternative Complement Path Activation)

·        There is a thickening of the basement membrane.

·        There are no antigens present (rare to have C1q and C4 visible).

·        It is a chronic, progressive disease. 

·        The mesangial cells proliferate and extend from the mesangium to the area between the endothelial cells and the basement membrane. There, they form a new basement membrane subendothelially by producing matrix, resulting in a “tram track” appearance.

o        This is diagnostic of the disease.

o        ***super-important*** to remember!!! 

·        Immunofluorescence

o        C3 and properdin deposits (alternative complement pathway)

o        Dense intramembranous deposits; no discrete immune complexes

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