Is there a tubular maximum for the renal reabsorption of filtered Bicarbonate?
Under normal conditions, the kidneys reabsorb greater than 90% of filtered HCO 3 − in the PCT. As stated earlier, the stimuli for this process are the ambient level of angiotensin II and the usual intracellular pH in cells of the PCT.
Consequently, to inhibit this reabsorption of HCO 3 − , the effective arterial blood volume must be corrected (e.g., create a positive Na + balance in cases of reduced total body Na + content or improve cardiac output in cases of congestive heart failure) to diminish the release of angiotensin II, or the pH in the cells of the PCT must rise.
In addition, low GFR is often invoked as a perpetuator of alkalosis because low GFR prevents the high [HCO 3 − ] present during alkalosis from exceeding the maximum reabsorption (Tm) of bicarbonate.
That is, the low GFR prevents greater HCO 3 − filtration from occurring so that Tm is not reached. In that case, there is no bicarbonaturia and systemic alkalosis is maintained.
Bearing this in mind, we shall examine the conditions that were present in experimental studies that were interpreted to indicate that there is a renal threshold (Tm) for the reabsorption of HCO 3 − by the kidneys.
• Data to suggest that there is a renal threshold for the reabsorption of HCO 3 − by the kidneys: In the seminal experiments by Pitts et al. in the late 1940s, the infusion of NaHCO 3 was large enough to expand the ECF volume sufficiently to diminish circulating levels of angiotensin II and to raise the pH in cells of the PCT. Hence the two physiologic stimuli for the proximal reabsorption of HCO 3 − were removed. Rather than relate these findings to the changes in physiologic variables, the conclusion was that there is a tubular maximum for the renal reabsorption of HCO 3 − .
• Data to suggest that there is not a renal threshold for the reabsorption of HCO 3 − : The design of these experiments (e.g., Purkerson et al.) was to avoid a large expansion of the ECF volume while creating a positive balance of NaHCO 3 . Even though the HCO 3 − rose, there was little bicarbonaturia, and hence a tubular maximum for the renal reabsorption of NaHCO 3 was not observed. In support of this view, the range for the [HCO 3 − ] is from 22 to 31 mmol/L in normal subjects consuming a typical Western diet, and there is no appreciable bicarbonaturia at the upper range values for the [HCO 3 − ], despite much higher filtered loads for HCO 3 − , because the GFR is relatively constant throughout the day.
In summary, the enthusiasm for a T m for HCO 3 − reabsorption in the PCT is based on data from experimental conditions that removed the usual stimuli for the reabsorption of filtered HCO 3 − . Furthermore, an infusion of NaHCO 3 does not represent a normal physiologic occurrence.
Two other points merit emphasis. First, a steady state with metabolic alkalosis can be achieved and maintained when the blood pH rises sufficiently to overcome the stimulatory actions of angiotensin II of the reabsorption of HCO 3 − in cells of the PCT. Second, the excretion of potential HCO 3 − in the form of organic anions such as citrate is augmented by a high pH in cells of the PCT. Higher intracellular pH inhibits the action of the sodium-dicarboxylate cotransporter in the PCT, leading to excretion of citrate.
