Bicarbonate reabsorption in the dog with experimental renal disease.

Renal bicarbonate reabsorption (expressed per unit of glomerular filtration rate, GFR) has been reported to be diminished in uremic man and uremic rats. Both the increases in parathyroid hormone concentrations and in natriuretic forces have been considered to play a role in this change. The increased kaliuresis per nephron observed in chronic uremia could theoretically also contribute to inhibition of bicarbonate reabsorption. Despite the common use of normal dogs in studying bicarbonate reabsorption and of uremic dogs in studying alterations of renal function in disease, few studies of bicarbonate reabsorption in uremic dogs have been performed. In the present studies we have examined bicarbonate reabsorption in normal dogs and in dogs with experimental renal disease using a conventional bicarbonate titration technique. In unanesthetized normal dogs, the threshold for bicarbonaturia was 24.8 mEq/liter of GFR. A maximal reabsorptive rate (Tm/GFR) of 34.0 mEq/liter of GFR was obtained. In a second group of dogs, GFR was decreased to one-fifth normal. FENa was increased 16.9-fold over normal values: UKV/100 GFR and FEP were increased 5.8-fold and 10.9-fold, respectively. The threshold for bicarbonaturia in these dogs was increased to 30.5 mEq/liter of GFR and the maximal reabsorptive rate was increased to 41.2 mEq/liter of GFR. Thus, the capacity to reabsorb bicarbonate was increased despite the presence of high fractional excretion rates for sodium, potassium and phosphate. This increased reabsorptive capacity could not be accounted for by the effects of other known determinants of bicarbonate reabsorption.