Search

This is a study of quantitative glomerular morphology in 14 normal and 6 long-term diabetic female baboons between 3 and 25 years of age. In the normal female baboon, peripheral glomerular capillary basement membrane thickness increased until around 10 years of age, reached a plateau between 10 and 20 years of age, and possibly decreased at 25 years of age. Mean value for young (3 to 7 years of age) and older (10 to 25 years of age) controls were 266 nm and 329 nm respectively. Fractional volumes of mesangial matrix (8.9%) and mesangial cells (6.8%) were not affected by age. Glomerular basement membrane thickness and the volume of mesangial matrix increased progressively in female baboons with poorly controlled pancreatectomy-induced diabetes, while the volume of mesangial cells remained unchanged. After 106 to 145 months of diabetes, glomerular basement membrane thickness and the volume of mesangial matrix were 558 nm and 18.7% respectively. These values were significantly greater than those of the age-matched controlled (p = less than 0.05). By light and electron microscopy, the normal baboon glomerular morphology, morphometric measurements and changes with age were similar to those in man. The renal changes in diabetic baboons were also similar in morphology and rate of development to those of mild to moderate diffuse diabetic glomerulosclerosis in humans, indicating that the baboon is an ideal model for the long-term study of diabetic glomerulosclerosis. The presence of considerable interanimal variability in the degree of glomerulosclerosis attained after prolonged diabetes suggested that glomerulosclerosis progressed at different rates in these models. The reason for this was not apparent.

Cation exchange chromatography was performed on hemolysates prepared from human and baboon (Papio anubis) blood. In humans with diabetes mellitus and in baboons with pancreatectomy induced diabetes mellitus there were significant increases in Hbs A1, A1c, and A1a +A1b. The quantity of Hb A1 and Hb A1c in nondiabetic baboons was approximately one-half the quantity of Hb A1 and Hb A1c in nondiabetic humans. These differences may be explained by the differences in survival time between human and baboon red cells.