The obese Zucker rat model of nonimmune-mediated, spontaneous focal glomerulosclerosis is ideally suited to study the influence of diet on the initiation and progression of glomerular injury. Young (6 wk) and old (33 wk) lean and obese female Zucker rats were fed a carbohydrate-restricted diet intermittently for 27 wk. Carbohydrate restriction resulted in lower body weight (460 ± 16 versus 310 ± 7 g, p<0.025), kidney weight (1.26 ± 0.04 versus 1.07 ± 0.05 g, p<0.025), and glomerular area (6930 ± 290 versus 5780 ± 230 μm2, p<0.025) in young obese Zucker rats compared to ad libitum-fed rats. Although urine-albumin secretion was substantially reduced by carbohydrate restriction in young obese Zucker rats (41.1 ± 12.3 versus 6.9 ± 2.9 mg/24 h, p<0.01), glomerular injury was not significantly altered. In old obese rats, carbohydrate restriction did not significantly reduce albuminuria or prevent the progression of glomerular injury. Thus, intermittent carbohydrate restriction failed to alter significantly either the initiation of glomerular injury in young, or the progression of nephron damage in old, obese Zucker rats.