Structural changes in the renal vasculature in streptozotocin-induced diabetic rats without hypertension

JOO TURONI CLAUDIO; REYNOSO HECTOR; MARAÑON RODRIGO; COVIELLO ALFREDO; PERAL DE BRUNO MARIA

Nephron Physiology

Karger publisher

Lugar: Basel, Switzerland ; Año: 2005 vol. 99 p. 50 - 57

1660-2137

Background/aim: We evaluated in diabetic-streptozotocin rats (STZR) the structural changes of glomeruli, preglomerular vessels, tuft and renal parenchyma in order to determine the degree of renal injury and the presence of remodeling in afferent arterioles (AA) developed by diabetes without over-imposed hypertension. Methods: Renal mass index (RMI) and histological score (glomerular number, density, tubular lesions and degree of arteriosclerosis) were estimated. In AA the ratio of wall thickness/lumen was obtained by stereological methods. Results: In comparison with euglucemic normotensive control rats (CR), STZR developed diabetes without hypertension, RMI increased and matched changes in glomeruli (decrease of capillary number and enlargement of mesangium and basement capillary membrane). Both glomerular number and density as well as AA number were diminished. However an increase in the number of glomeruli with glomerulosclerosis (GS) was observed (STZR:11.66±5.93, n=9 vs CR:2.5±0.36, n=4, p< 0.05). Degenerative changes in both proximal (glycogenic and hyaline degeneration) and distal tubules (hyaline casts) were observed. At variance with preglomerular vessels, the efferent arterioles only presented initial arteriosclerosis. Finally, the stereological study of AA showed a significantly lower arteriolar lumen area and arteriolar wall thickness in STZR resulting in a remodeling without modification of wall/lumen ratio. Conclusion: Diabetes uncomplicated by hypertension, is associated with 1) reduction in glomerular number without GS 2) degeneration in parenchyma and renal tubules 3) a specific patron of remodeling in preglomerular vessels different of that induced by hypertension. Although this work demonstrated that these changes are not triggered by hypertension, further investigations are required in order to determine which mediators are involved in diabetic-vascular renal dysfunction.