On the nature of the renal concentrating defect in malnutrition

Abstract

The concentrating and diluting ability of the kidney was studied in adult patients with protein malnutrition before and after protein repletion. During malnutrition, values for maximal urine osmolality and solute-free water reabsorption (T cH 2O) were diminished. Renal diluting capacity, measured by minimal urine osmolality and free-water clearance (C H 2O ), was normal. The renal response to the administration of exogenous antidiuretic hormone (ADH) was adequate, as was the response to nicotine and hypertonic saline solution. During protein repletion there was an improvement in maximal urine osmolality and T cH 2O values. The improvement in concentrating ability occurred pari passu with an increase in urinary nitrogen excretion. The oral administration of urea to four malnourished patients resulted in changes in maximal urine osmolality and T cH 2O similar to those observed with protein repletion. A classification of renal concentrating defects is presented and the mechanism of the renal concentrating defect in malnutrition is discussed within the framework of this classification. The primary role of decreased urea concentration in the renal medulla as the cause of the concentrating defect in malnutrition is emphasized.