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Diagnosis:
Membranoproliferative Glomerulonephritis (type I)
Subsequently, systemic lupus erythematosus was diagnosed: Diffuse lupus nefritis, class IV-G (A)

Membranoproliferative glomerulonephritis (MPGN) is characterized by thickening of the capillary walls accompanied by cellular, predominantly mesangial, proliferation in all or almost all the glomeruli. The increase in cellularity and mesangial matrix produces accentuation of the lobular aspect of the glomerular tuft (lobular GN). The thickening of the capillary walls is due to subendothelial deposits and mesangial interposition with formation of material similar to the glomerular basement membrane (GBM) in the internal aspect of the wall, or subendothelial space: double contourn, as seen in Figures 4, 5 and 6.

MPGN can be idiopathic or can be secondary to systemic diseases or infections: hepatitis C, hepatitis B, subacute bacterial endocarditis, syphilis, cryoglobulinemia, systemic lupus erythematosus (SLE), and others. The morphologic aspect does not allow an approach to the etiology in these cases, but, as in the present case, a "full house" pattern on immunofluorescence suggests lupus nephritis.

Glomerular changes in lupus nephritis are highly variable, and it is frequent find a MPGN-like pattern, usually focal and without homogeneous involvement of all the glomeruli, however sometimes we can see a more homogeneous diffuse involvement as seen in the present case. In both MPGN and lupus nephritis there may be hypocomplementemia.

The diagnosis of SLE requires correlation of clinical and laboratory findings, only a renal biopsy does not permit to make the diagnosis. Although the immunofluorescence with "full house" Igs and complement deposition suggests this possibility, SLE diagnosis requires other criteria. The reviewed criteria for diagnosis are 11 and must appear 4 or more criteria to diagnose SLE. The criteria include, among others, skin lesions, oral ulcers, renal disease, neurological affectation, hematologic disorders, and immunological alterations detected by laboratory: anti-Sm antibodies, anti-DNA, anti-Ro, and others.

Then in our case, without SLE criteria at renal biopsy, was not possible to diagnose the systemic disease. Several months after the patient presented anemia, lymphopenia, skin lesion in face compatible with discoid lupus, ANAs 1:1680; ENAs, Anti-Ro, and ANCAs: negative. This clinical features together with the presence of proliferative diffuse GN (lupus nephritis) and polyarthralgia allowed diagnose SLE.

In conclusion, MPGN is a morphologic pattern of glomerular lesion and it can be caused by diverse mechanisms.

See the chapters Membranoproliferative Glomerulonephritis and Lupus Nephritis of our Tutorial.

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Bibliography

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