To the Editor.
—The recently published study by Michelis et al1 demonstrates a defect in tubular reabsorption of uric acid in patients with cirrhosis, and the authors suggest this relates to hyperbilirubinemia. However, patients with liver disease frequently have metabolic alterations other than hyperbilirubinemia that may cause renal tubular dysfunction. Tubular transport of solutes such as uric acid may be linked with sodium transport and changes in extracellular fluid volume may alter tubular reabsorption of many solutes, including sodium and uric acid, in a relatively nonspecific manner.2 Disorders associated with a contracted extracellular fluid volume (diabetes insipidus, salt restriction, vigorous diuretic therapy) may be associated with increased proximal tubular sodium reabsorption and decreased uric acid clearance. Conversely, situations in which there is expansion of the extracellular fluid volume (saline loading, excessive circulating antidiuretic hormone, diuretic use with salt replacement) have been associated with hypouricemia and increased excretion