ABSTRACT
Numerous clinical factors and pathogenetic abnormalities have been cited as potential mechanisms in the propagation of glomerular injury, regardless of etiology, to glomerulosclerosis, which is one of the major histologic features of renal failure. The glomerulus is composed of a capillary network lined by endothelial cells: a central region of contractile mesangial cells with their surrounding extracellular matrix material; the visceral layer of epithelium along the outer aspect of the glomerular basement membrane; and the parietal epithelial layer of Bowman’s capsule. Systemic hypertension occurs often in both experimental and clinical glomerular disease, and may play a major role in the progression of glomerulosclerosis, even after the inciting injurious event has resolved. Renal injury of diverse origins in experimental animals leads to early compensatory increases in glomerular plasma flow rate and glomerular hydraulic pressure. The effect of chronic anemia on glomerular hemodynamics and the progression of glomerular injury has been recently examined in a number of experimental models.
