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Abstract

Recent progress of renal physiology toward molecular biology is illustrated by a study of urea transport in the kidney. The earliest clearance data suggested that urea excretion was dependent on glomerular filtration modified by passive back diffusion. Micropuncture experiments in animals have now revealed a more complex situation. Active urea transport occurs in the collecting ducts, and is clearly seen during low protein intake. High urea concentrations in the renal medulla, essential to the countercurrent concentrating mechanism, may thus be maintained by continual active reabsorption of up to 80% of the filtered load of urea by the collecting ducts. Urea transport is further characterized into three components: solvent drag, dependent on transtubular water flux, cell concentration of urea and the cell-wall reflection coefficient; passive diffusion, dependent on the concentration gradient across the membrane and the permeability coefficient (proximal convolution > collecting duct > distal convolution); and active transport, dependent on cell metabolism by as yet unknown mechanisms. In the proximal convolution, urea reabsorption depends on the two former components (one-third and two-thirds respectively), without the third. In the collecting ducts, however, active transport of urea (induced by a low-protein diet) is the driving force.