[Histopathology of the biopsied kidney and its related glomerular deterioration]

This paper presents the incidence of glomerulonephritis (-pathy: GN) from a large number of more than 10,000 serial renal biopsies examined in one laboratory using the same criteria over the past 25 yrs. in Japan. Each incidence is as follows: IgA nephropathy (IgAN), 33%; thin glomerular basement membrane disease (TBMD), 17.8; athletic pausal urinary abnormality (APUA), 8.2; primary membranous glomerulonephritis (memb GN), 6.5; while all others were less than 5% each. Out of 3,300 IgAN cases, 51% consisted of a minimal change IgAN (MCIgAN), while the IgAN cases with moderate to severe glomerular damage comprised 20% of all cases. In addition, the survival curves of the IgAN cases coincided with those of FGS and benign nephrosclerosis (BNS) with a similar extent of glomerular damages. On the other hand, glomerular damage mostly occurred due to intra- and intercapillary cell infiltration; poststreptococcal GN (AGN), lupus N, Cat. III a IV a and IV b, and MCIgAN all had a favorable outcome (follow-up mean: 12.4 +/- 6.7 yrs). More than 50% of the dialized patients came from both IgAN, focal type with hypertension, and IgAN with more than moderate glomerular damage regardless hypertension. The incidences of AGN, MPGN, HBvN have all decreased at the present time, while renal amyloidosis and crescentic glomerulonephritis (Cres. GN) have increased in number and this is reflected by the increased number of renal biopsies in elderly men. Glomerular deterioration is thus considered to be caused more by non-immunologic and hemodynamic injuries than by immune-derived, repeated inflammation, in human chronic glomerulonephritis(-pathy).