Distal tubule bicarbonate reabsorption in intact and remnant diabetic kidneys

In the diabetic patient, hyperkalemia and hyperchloremic metabolic acidosis has been attributed to one or more of the following factors associated with diabetic nephropathy: hypoaldosteronism, altered potassium homeostasis, or a distal tubular (DT) defect in hydrogen ion secretion. To evaluate maximal in vivo DT acidification in streptozotocin (STZ) diabetes, unidirectional bicarbonate reabsorption (JHCO3) was measured in DTs after acid loading and in surviving DT after 2/3 nephrectomy (Nx).

Acid gavage induced hyperchloremic metabolic acidosis in four groups of rats: diabetic rats with hyperglycemia two (a) and (b) eight weeks after STZ injection, (c) diabetic rats with tight glucose control two weeks after STZ injection and insulin pump implantation; and (d) control nondiabetic rats. Another group of diabetic rats underwent (e) Nx one week after STZ injection; these rats were neither acid loaded nor pump implanted.

In the acidotic rats, the plasma potassium concentration, the plasma and urine acid-base parameters in the three STZ diabetic groups was not different from control rats, whereas JHCO3 fluxes were brisk without important differences between groups. In Nx rats, although the plasma potassium concentration and acid-base status were normal, surviving JHCO3 fluxes were still brisk and not different from the acid-loaded rats.

These in vivo measurements indicate there is no impairment in DT unidirectional bicarbonate reabsorption in the intact or remnant STZ diabetic kidney.