Alterations in renal tubular sodium and water reabsorption in chronic renal disease in man

Abstract

Alterations in renal tubular sodium and water reabsorption in chronic renal disease in man. Clearance studies were performed on subjects with GFR from 4 to 127 ml/min under conditions of maximal hydration and hypotonic mannitol loading. Nonelectrolyte solute excretion per GFR (U NES V/GFR) was calculated as [UO sm -2(U Na + U K )] V/GFR. Fractional sodium excretion (C Na /GFR) per level of U NES V/GFR in the low GFR group (GFR H 2 O /GFR + C Na /GFR) was also higher initially in the low GFR group at every level of U NES V/GFR and increased at a more rapid rate in response to a solute load. Thus azotemic subjects have a decreased fractional reabsorption of sodium in the proximal tubule independent of fractional solute load. Nevertheless, an increase in solute load provokes a greater inhibition of fractional proximal tubular sodium reabsorption in these subjects than in normals. Fractional distal tubular sodium reabsorption (C H 2 O /GFR) in the low GFR group appeared to be lower at every level of fractional distal sodium load. The higher C Na /GFR in the low GFR group appears to be consequent to decreased fractional sodium reabsorption in the proximal tubule and an alteration in the capacity of the distal tubule to reabsorb sodium.