DEVELOPMENT OF VASCULAR POLE-ASSOCIATED GLOMERULOSCLEROSIS IN THE FAWN-HOODED RAT

Fawn-hooded hypertensive (FHH) rats constitute a spontaneous model of chronic renal failure with early systemic and glomerular hypertension, proteinuria, and development of focal and segmental glomerulosclerosi s. The goal of the present study was to elucidate a step-by-step seque nce of histopathologic events leading from an initial glomerular injur y to segmental sclerosis. Segmental sclerosis in the FHH rat is consis tently associated with the glomerular vascular pole. The initial injur y involves the expansion of primary branches of the afferent arteriole . Apposition of those capillaries to Bowman's capsule, together with t he degeneration and detachment of corresponding podocytes, allows pari etal cells to attach to the naked glomerular basement membrane of this capillary, i.e., allows the formation of a tuft adhesion to Bowman's capsule. The adhesion enlarges to a broad synechia by encroaching to n eighboring capillaries, apparently based on progressive podocyte degen eration at the flanks of the adhesion. Capillaries inside the adhesion -before undergoing collapse or hyalinization-appear to stay perfused f or some time and to maintain some kind of filtration misdirected towar d the cortical interstitium. Thereby, a prominent paraglomerular space comes into existence, enlarging in parallel with the adhesion. Toward the cortical interstitium this space is delimited by a layer of sheet like fibroblast processes, which has obviously been assembled in respo nse to the formation of this space. Toward the urinary space, the para glomerular space is demarcated by the parietal epithelium and by the i nterface between the adhesion and the ''intact'' tuft remnant. Thus, t he sclerotic tuft portions all become enclosed within the paraglomerul ar space.