Effect of anti-schistosomal treatment on schistosomal-specific nephropathy.

Twenty-one patients with schistosomal-specific nephropathy (18 nephrotics and three with non-nephrotic proteinuria) were given anti-schistosomal treatment (oxamniquine and praziquantel). The schistosomal specificity of the kidney lesions was assessed by the detection of schistosomal-specific antigens (CAA and CCA) and antibodies deposited in the renal glomeruli of these patients. After anti-schistosomal treatment, the patients were followed for clinical and laboratory changes occurring within 12 months. In addition, 15 patients had a second kidney biopsy and the histopathological and the immunopathological findings were compared with those observed in the first biopsy. Based on clinical, laboratory and histopathological evaluations, none of the patients subjected to the study showed regression of the kidney lesion following antischistosomal treatment; in fact three patients showed progression in their lesions, one of them reaching end-stage renal failure. The histopathology of these three cases was focal segmental glomerulosclerosis. Our data suggest that anti-schistosomal treatment in an established disease state, will not produce remission.

Schistosomal specific nephropathy leading to end-stage renal failure.

In this study 17 patients, 11 with end-stage renal failure and six with nephrotic syndrome were selected. The selection criteria were presence of active intestinal schistosomiasis and absence of any surgical or other medical disease which could explain the renal disease. When examined by light microscopy, kidney biopsies showed membranoproliferative glomerulonephritis in nine, membranous in four, focal segmental glomerulosclerosis in two, sclerosing glomerulonephritis in one case, and no changes in another case. Direct immunofluorescence showed IgG deposits in 13 cases, IgM in 10 and different complement components (C3, C1q) in eight cases. Eluates from the kidney biopsies of the 17 schistosomal as well as six control cases were examined by ELISA against schistosoma mansoni adult worm antigen (AWA). This test showed the presence of antibodies against the AWA in 12 out of 17 of the schistosomal cases, and zero out of six of the controls. When examined by direct IFA using sheep anti-circulating anodic antigen/FITC and by indirect IFA using monoclonal antischistosomal CAA IgG3, kidney biopsies of the ELISA positive cases showed granular deposits of circulating anodic antigen (CAA). We conclude that schistosomal specific nephropathy does exist in the clinical settings and can lead to end-stage renal disease, with CAA probably being a major responsible antigen.

Characterisation of kidney lesions in early schistosomal-specific nephropathy.

In this work 42 patients with active Schistosoma mansoni infection and renal involvement were examined. Of these, 16 had asymptomatic proteinuria (group I) and 26 had the nephrotic syndrome (group II). Fifteen nonschistosomal patients with idiopathic nephrotic syndrome were included as control cases (group III). Renal biopsy specimens were obtained from all patients and controls. These were examined by light microscopy (LM), by direct immunofluorescence microscopy using antisera against human IgG, IgM, IgA, C3, C4, C1q, and fibrinogen, and by indirect immunofluorescence microscopy using monoclonal antibodies directed against the circulating schistosome antigens, circulating anodic antigen (CCA) and circulating cathodic antigen (CCA). Schistosomal-specific deposits were seen in the renal glomeruli in 24 of the 42 schistosomal patients but in none of the 15 control patients. Although schistosomal-specific deposits were seen in seven of the 16 patients presenting with asymptomatic proteinuria, no morphological changes could be seen by LM. On the other hand, schistosomal-specific deposits could be seen in the kidneys of 17 of the 26 patients presenting with the nephrotic syndrome. All but one specimen showed morphological changes when examined by LM. These were consistent with mesangioproliferative glomerulonephritis in seven, focal segmental glomerulosclerosis in five, mesangiocapillary glomerulonephritis in two, membranous glomerulonephritis in one, and focal segmental hyalinosis in one patient. The present study clearly suggests that (a) schistosomal-specific nephropathy does exist in human settings, (b) it is an immune complex disease, and (c) CAA and CCA are major responsible antigens.