Patients with prerenal AKI may exhibit other signs of volume depletion, such as tachycardia, orthostatic hypotension, and dry mucous membranes. In addition, prerenal AKI can be distinguished from other causes by the intense reabsorption of solutes that results from the normal renal response to decreased perfusion. Specifically the fractional excretion of sodium (FENa, see Plate 3-6 for formula) should be low (<1%); the serum blood urea nitrogen (BUN):creatinine ratio may be elevated (i.e., >20 : 1), reflecting increased reabsorption of urea; and the urine should be concentrated (> 500 mOsm/kg H₂O). Note that FENa values may be invalid among patients who have recently taken diuretics; in this case, the fractional excretion of urea has been proposed as an alternative means of assessing tubular reabsorption because it is generally less than 35% in the prerenal state. Finally, because the renal parenchyma is not damaged, the urine sediment should not contain red blood cells, white blood cells, or other markers of renal inflammation. Hyaline casts, however, may be seen; these occur because low tubular fow rates increase aggregation of Tamm-Horsfall mucoproteins, which are secreted by the distal tubular epithelium.