Both ethanol consumption and uremia are considered to be associated with wasting, malnutrition and debilitation. The present study was designed to investigate as to whether ethanol exerts a stimulatory effect on the catabolic state of renal failure. Rats underwent <sup>5</sup>/<sub>6</sub>-nephrectomy and were fed either with or without ethanol. The degree of uremia was comparable in both groups. Ethanol-fed uremic rats, however, displayed higher serum levels of urea ( + 103%) and glucose ( + 29%), as compared to uremic animals without alcohol. Subsequently, the urea N appearance was enhanced ( + 60%) in uremic rats with alcohol as compared to uremic animals without alcohol. In sham rats urea N appearance was also increased ( + 39%) following ethanol administration in comparison to sham-operated rats without alcohol, albeit to a lesser degree. Urinary N<sup>t</sup>-methylhistidine excretion, an indicator of myofibrillar protein breakdown, was enhanced throughout the experiment in uremic rats receiving ethanol. Finally, ethanol caused higher urinary excretion rates of corticosterone in uremic animals as compared to uremic rats without ethanol. There was a significant correlation between urinary corticosterone excretion and both urea N appearance and urinary N<sup>t</sup>-methylhistidine excretion. We conclude that ethanol consumption further aggravates the catabolic state of uremia and that this is mediated by an increment in glucocorticoid production.