Skip to main content
Fig. 1 | BMC Nephrology

Fig. 1

From: A case report of recurrent membranoproliferative glomerulonephritis after kidney transplantation due to ventriculoatrial shunt infection

Fig. 1

Differential diagnosis of endocapillary proliferative glomerulonephritis with subendothelial electron-dense deposits and membranoproliferative GN type I or III. Histopathological distinction into IgG/IgM-dominant forms and C3-dominant forms can help in the differential diagnosis. Note that light chain restriction may become apparent even in seemingly C3-dominant forms only after protease digestion [16]. The final diagnosis into the listed entities should always consider clinical findings, serum and urine tests for monoclonal gammopathy, complement serology, and complement genetics. Note that infection-associated glomerulonephritis can present histologically histology indistinguishable from C3-GN. C3-GN can be defined by its pathogenesis as mediated through complement dysregulation. The most common causes are hereditary or due to LPD-associated or idiopathic inhibitory autoantibodies, some of them presenting as C3-nephritic factors. Cryoglobulinemia falls into either the autoimmune-, LPD- or infection-associated categories in the left arm. Transplant glomerulopathy as a form of chronic antibody-mediated rejection may or may not show mesangial and subendothelial immune complexes, usually very few in number and [9] is thus not depicted in this scheme. Also not listed are TMA and associated lesions which are distinguished from MPGN or endocapillary proliferative GN by the absence of immune-complex-like electron dense deposits. * - Idiopathic is a diagnosis of exclusion, and the proportion of cases labelled as such is expected to shrink further with careful clinical assessment and our growing body of knowledge

Back to article page