Quantitation of glomerular angiotensin II receptors in IgA nephropathy

Mesangial cells have receptors for angiotensin II (AII) and contract in its presence. All is known also to increase the uptake of macromolecules by the mesangium. As a first step towards the investigation of a possible role for local disturbances of the renin-angiotensin system (RAS) in immune mediated mesangial proliferative glomerulonephritis, glomerular All receptors have been quantitated retrospectively in biopsy tissue from 20 patients with IgA nephropathy for comparison with 16 biopsies that showed only minor abnormalities by light microscopy and negative immunofluorescence. An autoradiographic technique using 125I labelled [Sar1, Ile8] All facilitated the quantitation of All receptors in frozen tissue sections. Following exposure to the treated sections, x-ray film was analyzed by computerized micro-densitometry. The data obtained were optical densities of areas corresponding to the presence of glomeruli verified by reference to adjacent sections stained with periodic acid-Schiff (PAS). There was no significant difference between patients 0.67 +/- 0.16 (mean +/- SD) and controls 0.61 +/- 0.15. Among patients there was no statistically significant correlation of glomerular All receptor density with either the degree of mesangial proliferation or the extent of hyperplasia of the juxtaglomerular apparatus (JGA). There was no apparent relationship with hypertension. The absence of an increase in glomerular All receptors despite proliferation of the glomerular mesangium may represent a local down regulation in patients with IgA nephropathy.