Aims: Study of benign nephrosclerosis (BNS) is often mixed up with IgA neph
ritis (IgAN) associated with hypertension or thin basement membrane disease
(TBMD). Here we examined the clinicopathological features, incidences and
prognosis of decompensated BNS. Materials and methods: BNS was identified i
n 590 (8.3%) adult cases among 7108 renal biopsies of a mean age of 56.5 ye
ars (male: female ratio = 2.5:1), The post-biopsy follow-up period ranged f
rom 3 to 22 years (10.1 +/- 4.6 years). Results: Patients with progressive
BNS were more likely to develop end-stage renal disease within 5 years of b
iopsy. Poor prognostic factors included poor or no control of arterial bloo
d pressure by anti-hypertensive drugs, global glomerulosclerosis (GS) (grea
ter than or equal to 41%) at biopsy, presence of collapsed glomeruli and/or
segmented or semi-global GS. Tubulointerstitial damage, glomerular hypertr
ophy and loop dilatation were secondary to GS. Gender, duration of HT and o
nset of HT to biopsy were not significant factors. Conclusion: GS in BNS is
due to ischemia induced by luminal narrowing or obstruction of preglomerul
ar vessels, and glomerular HT due to loss of autoregulation in preglomerula
r vessels (irregularly shaped atrophic or segmented medial smooth muscle ce
lls, with expansion of extracellular matrix with or without fibrous intimal
thickening). GS resulted in luminal dilatation. Both pathological changes
affecting the glomerulus may occur in the same kidney and different nephron
units.