Membranoproliferative Glomerulonephritis Secondary to Renal Schistosomiasis: A Rare Etiological Association

Membranoproliferative glomerulonephritis (MPGN) represents a histological pattern characterized by mesangial hypercellularity and capillary wall thickening, observed in various nosological entities. While type I MPGN is often secondary to chronic infections, autoimmune diseases, or monoclonal gammopathies, etiological attribution can sometimes prove complex. Schistosomiasis (bilharzia), an endemic parasitic infection affecting hundreds of millions of people, is a recognized but rare cause of glomerulopathy. Documented renal lesions typically include amyloidosis, tubulointerstitial injuries, or less commonly, immune-complex glomerulonephritis. Among the latter, the MPGN pattern is exceptional. We report here the case of a patient presenting with impure nephrotic syndrome, whose histological exploration revealed MPGN, ultimately linking the glomerulopathy to subclinical renal schistosomiasis.

Case Report:
A 17-year-old male from Chad presented with impure nephrotic syndrome and renal impairment , along with positive HCV serology. Renal corticomedullary biopsy (29 glomeruli, 7 sclerotic) revealed severe MPGN characterized by hyperlobulated architecture, diffuse mesangial hypercellularity, double contours of basement membranes, and fibrocellular extracapillary proliferation affecting 14 glomeruli (48%). Immunohistochemistry showed diffuse granular deposits of IgG and IgM with segmental C1q component, in the absence of significant IgA deposits.

The crucial finding was the presence of active bilharzial granulomas centered around viable Schistosoma haematobium eggs (terminal spine), confirming renal infestation. This was associated with moderate chronic tubulointerstitial nephropathy with lymphoplasmacytic infiltrate. In the absence of cryoglobulinemia and after excluding other MPGN etiologies, attribution to schistosomiasis was retained, with HCV coinfection introducing an additive pathophysiological challenge.

Discussion:
This observation provides direct histological evidence of a rare association between MPGN and active renal schistosomiasis. The probable mechanism involves the formation of immune complexes containing parasitic antigens, as demonstrated in experimental models. The unusual severity of the glomerulopathy, with 48% crescents, contrasts with previous descriptions and raises the hypothesis of a potentiating effect from HCV coinfection.

From a practical standpoint, this case justifies several clinical recommendations. It argues for the systematic integration of endemic parasitic disease screening, particularly schistosomiasis, in the etiological workup of any unexplained MPGN, especially in patients from endemic areas. Histologically, it underscores the importance of meticulous examination for bilharzial eggs during systematic renal biopsy analysis in suggestive epidemiological contexts. Therapeutically, this case advocates for an integrated approach combining specific antiparasitic treatment, potential antiviral therapy in the context of HCV coinfection, and immunosuppression tailored to the severity of the glomerulonephritis.

In conclusion, this case provides anatomopathological evidence of a rare association between severe membranoproliferative glomerulonephritis and active renal schistosomiasis. The simultaneous histological demonstration of characteristic glomerular lesions and viable Schistosoma haematobium eggs in the renal parenchyma establishes a strong etiological link, expanding the spectrum of glomerulopathies induced by this parasitosis. The particularity of this observation lies in the context of HCV coinfection, which introduces complex pathophysiological questions regarding potential interactions between these two infectious agents in the genesis of the glomerulopathy. Diagnostically, this case highlights the importance of exhaustive etiological investigation in all MPGN cases, including screening for endemic parasitic diseases, even in the absence of suggestive clinical manifestations. Therapeutically, it argues for an integrated approach targeting both the parasite, the virus, and the glomerulonephritis activity, while emphasizing the need for further studies to elucidate the precise mechanisms of this pathological association.