Relationship between glomerular mesangial cell proliferation and amyloid deposition as seen by ultrastructural and morphometric analysis in experimental kala-azar of the hamster.

Light and electron microscopic studies combined with a morphometric analysis of the hamster glomerulus in experimental kala-azar showed progressive hyperplasia of mesangial cells beginning on the 10th day and reaching a peak on the 20th day after infection. Afterward, the number of mesangial cells declined and a progressive rise of amyloid deposits over the mesangial matrix was observed. This system for amyloid production is unique if we consider that probably one cell, the mesangial cell, is involved in glomerular amyloid deposition. Our data support a slight modification in the sequence of events of the biphasic theory of amyloid formation. We observed that the number of mesangial cells declines when amyloid deposition increases and that mesangial cell morphology in this stage is not that of an actively secreting cell. It is therefore hypothesized that amyloid precursor material is secreted into the matrix during the proliferative phase. In the second phase, amyloid deposits occur in the extracellular media close to functionally impaired mesangial cells.