We evaluated the correlation between histologic features and glomerular permselectivity based on fractional clearances of
dextrans relative to
inulin (FCsDex). The subjects consisted of 12 healthy volunteers, 18 patients with
membranous nephropathy, and 20 patients with
immunoglobulin A nephropathy. In
membranous nephropathy, FCsDex measured with large
dextrans (radii larger than 56 A) increased as the capillary lesion progressed. Histologic examination showed that glomerular capillary alteration was the factor most closely linked to changes in FCsDex in
membranous nephropathy.
Proteinuria (normalized to glomerular filtration rate) did not correlate with FCsDex. Increased FCsDex tended to normalize during
prednisolone treatment in
membranous nephropathy. In
immunoglobulin A nephropathy, the impairment of glomerular size selectivity depended on the degree of mesangial
sclerosis and tubulointerstitial injury. FCs of
dextrans of 59 A were correlated with the mesangial
sclerosis index (r = 0.573, p = 0.050) and the tubulointerstitial injury index (r = 0.707, p = 0.003).
Proteinuria (again normalized to glomerular filtration rate) was significantly correlated with FCs of large
dextrans in
immunoglobulin A nephropathy (r = 0.668, p = 0.008). We conclude that glomerular size-selective barriers were impaired both in
membranous nephropathy and
immunoglobulin A nephropathy. However, the mechanisms of impaired size selectivity might differ, at least in part, between these nephropathies. The predominant factors responsible for the size-selective defect seemed to be glomerular capillary wall lesions in
membranous nephropathy but mesangial
sclerosis or tubulointerstitial damages (or both) in
immunoglobulin A nephropathy.