The proximal nephron is responsible for reabsorbing 80 to 99 percent of several filtered solutes, including amino acids, glucose and bicarbonate. Separate, high-affinity sodium co-transport mechanisms are used. Increasing luminal concentration of each of these solutes stimulates its active transcellular reabsorption until there is saturation. Slightly less than half of the filtered chloride is reabsorbed, partly by passive mechanisms that are linked to the reabsorption of organic solutes and bicarbonate, as well as by less well defined independent cellular and/or paracellular mechanisms that appear to be sensitive to transepithelial osmotic pressure gradients. Proximal tubule reabsorption is isosmotic and isonatric, and about 50 to 60 percent of the filtered sodium and water in reabsorbed. Disorders or proximal nephron function include conditions in which luminal, cellular and/or peritubular factors affecting reabsorption are altered. Clinical disorders caused by modification of the luminal reabsorptive determinants include conditions in which tubular flow rate is increased or luminal composition is altered, as when non-reabsorbable solutes (mannitol) are filtered or when reabsorbable solutes (glucose) are filtered in concentrations exceeding their tubular transport capacity. Other disorders occur due to loss of affinity or capacity of the cellular active transport systems for specific solutes, such as amino acids (renal aminoacidurias), glucose (renal glycosurias) and bicarbonate (proximal renal tubular acidosis), or for all solutes (Fanconi syndrome). Finally, disorders due to changes in the peritubular factors affecting reabsorption include states of altered peritubular Starling forces or pH, which modify sodium chloride or sodium bicarbonate reabsorption, respectively.