| Summary: | Background: A fundamental feature of most parasitic infections is their chronicity. Although renal disease is not one of the common presenting features, many parasitic infections are associated with glomerular lesions. Glomerular lesions are observed with visceral leishmaniasis (kala-azar) caused by Leishmania donovani. Leishmanial parasites affect children under 2 yaer in more than 88 countries. Thus study of glomerulopathy Associated with Visceral leishmaniasis is very important. Methods: In this retrospective study we review the glomerulopathies observed in visceral leishmaniasis and the pathogenic mechanisms thought to be involved in the individual infections, and discuss the general mechanisms that can be extracted from these observations. Results: Prospective studies have shown that 60% of patients with kala-azar have mild proteinuria with benign changes in the urinary sediment (microscopic hematuria and leukocyturia). The pathological picture is a glomerulonephritis ranging from purely mesangioproliferative to membraneoproliferative. Amyloidosis can be a complication of kala-azar. Using immunofluorescence, IgG, IgM, IgA, and C3 are seen in the mesangium with some extensions along the capillary loop. Conclusion: Kala-azar is usually associated with hyperimmunoglobulinemia with high IgG levels, circulating immune complexes, and high titers of rheumatoid factor and cryoglobulin. Together with the presence of immunoglobulins in the glomeruli, this suggests the pivotal role of polyclonal B-cell activation and “classical” B-cell activation in the pathogenesis of leishmanial nephritis.
|
|---|
