Low birth weight humans and rats exposed to a low protein diet in utero have reduced bone mineral content. Renal calcium loss during the period of rapid skeletal growth is associated with bone loss. As young low protein rats display altered renal function, we tested the hypothesis that renal calcium excretion is perturbed in this model. Pregnant Wistar rats were fed isocalorific diets containing either 18% (Control) or 9% (low) protein throughout gestation. Using standard renal clearance techniques, Western blotting for renal calcium transport proteins and assays for Na⁺:K⁺ATPase activity and serum calcitropic hormones, we characterised calcium handling in 4 week old male offspring. Histomorphometric analysis of femurs revealed a reduction in trabecular bone mass in low protein rats. Renal calcium (Control 10.4±2.1 vs low protein 27.6±4.5 nmol min^-1 100g bwt^-1 P<0.01) and sodium excretion were increased, but glomerular filtration rate was reduced in low protein animals. Total plasma calcium was reduced in low protein rats (P<0.01), but ionised calcium, serum calcitropic hormone concentrations and total body calcium did not differ. There was no significant change in plasma membrane Ca²⁺-ATPase pump, epithelial calcium channel or calbindin-D_28K expression in low protein rat kidneys. However, Na⁺:K⁺ATPase activity was 36% lower (P<0.05) in low protein rats. These data suggest that the hypercalciuria of low protein rats arises through a reduction in passive calcium reabsorption in the proximal tubule rather than active distal tubule uptake. This may contribute to the reduction in bone mass observed in this model.