Abstract
Captopril, an angiotensin II-converting enzyme inhibitor, ameliorates the renal mesangial lesions associated with subtotal nephrectomy, a process associated with increased mesangial macromolecular flux and injury. In the present study uninephrectomized rats with proteinuria and focal glomerular sclerosis had increased mesangial heat-aggregated human IgG (AHIgG) uptake. However, uninephrectomized rats treated daily with captopril, which failed to develop either glomerular lesions or proteinuria, also had significantly elevated mesangial AHIgG levels. Our results suggest that increased mesangial macromolecular flux may occur independent of altered glomerular permselectivity changes and proteinuria and appears to be related to glomerular hyperfiltration rather than glomerular hypertension. Further, glomerular mesangial sclerosis may not be the direct result of increased mesangial macromolecular flux.
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