Exercise induces profound changes in renal haemodynamics and protein excretion. The rate of ultrafiltration across the glomerular capillary is determined by the imbalance between the transcapillary hydraulic and colloid osmotic pressure gradients. Despite a major reduction in the renal plasma flow, the filtration fraction can double with maximal exercise, preserving the transfer of metabolites or substances through the glomerulus. Tubular processes and excretion rates are modified by exercise. Despite large increases in plasma lactate during strenuous exercise, renal excretion plays a limited role in lactate metabolism. Apparently, the mechanism of transcellular transport of lactate is saturated during severe exercise. Urea reabsorption is enhanced during prolonged exercise, and this process may act to limit the dehydration of an individual. As uric acid transport is also carrier-mediated, it appears that there is no saturation of the carrier system during prolonged exercise. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This excretion of excess proteins is a transient state with a half-time decay of about 1 hour. The increased clearance of plasma proteins suggests an increased glomerular permeability and a partial inhibition of tubular reabsorption. Studies suggest that exercise decreases the glomerular electrostatic barrier and facilitates transfer of macromolecules. Postexercise proteinuria appears to be age-dependent. Nephropathy is a common observation in the diabetic patient. In young and adult diabetic patients, exhaustive physical exercise does not provoke an enhanced dysfunction of the kidney to what is already found in healthy individuals. Heart and kidney transplant patients have a lesser postexercise proteinuria as compared with healthy individuals.