Aims: Study of benign nephrosclerosis (BNS) is often mixed up with IgA nephritis (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 in 590 (8.3%) adult cases among 7,108 renal biopsies of a mean age of 56.5 years (male: female ratio = 2.5:1). The post-biopsy follow-up period ranged from 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 biopsy. Poor prognostic factors included poor or no control of arterial blood pressure by anti-hypertensive drugs, global glomerulosclerosis (GS) (> or = 41%) at biopsy, presence of collapsed glomeruli and/or segmented or semi-global GS. Tubulointerstitial damage, glomerular hypertrophy and loop dilatation were secondary to GS. Gender, duration of HT and onset of HT to biopsy were not significant factors.
Conclusion: GS in BNS is due to ischemia induced by luminal narrowing or obstruction of preglomerular vessels, and glomerular HT due to loss of autoregulation in preglomerular vessels (irregularly shaped atrophic or segmented medial smooth muscle cells, 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.