THE RENAL RESPONSE TO CHRONIC MINERAL ACID FEEDING - A REEXAMINATION OF THE ROLE OF SYSTEMIC PH

It has been widely held that systemic acidemia represents the proximate event signaling the kidney to elicit its acidification response to chronic metabolic acidosis. However, a previous study from this laboratory has cast serious doubt on the validity of this conventional viewpoint. When a large acid load (7 mEq/kg/day) was fed chronically to dogs as HCl, H2SO4 or HNO3, net acid excretion increased similarly in all three groups of animals despite wide variability in the prevailing systemic acid-base composition. Marked or moderate hypobicarbonatemia and acidemia were observed in the HCl- or H2SO4-fed animals respectively, but strikingly, plasma [HCO3-] and pH did not change significantly from the control in the HNO3-fed animals. That study concluded that the renal response to chronic mineral acid feeding appears to be triggered, not by acidemia, but by the interplay of sodium delivery to and sodium avidity of the distal nephron as modulated by the reabsorbability of the "acid" anion. We have re-examined the above provocative conclusion in the light of the observation that the only evidence for a dissociation of the renal response from systemic acidemia in that study was derived from preprandial (8:00 a.m.) blood samples obtained som 23 h after the ingestion of the daily acid load (administered at 9:00 a.m.). We investigated the diurnal variation of plasma acid-base composition in two groups of dogs fed chronically a large acid load (7 mEq/kg/day) as either HCl HNO3. Both groups exhibited significant diurnal oscillations of plasma acid-base composition. Most importantly, HNO3-fed animals that were normohydric in the preprandial period developed substantial acidemia (peak .DELTA. [H+] + 10 nEq/liter, P < 0.01) and hypobicarbonatemia (peak .DELTA. [HCO3-] -6.9 mEq/liter, P < 0.01) following ingestion of the daily acid load; more than 16 hours were required for the plasma acid-base composition to return to the preprandial, normal baseline. The data demonstrate that the renal acidification response during HNO3 feeding, just like that during HCl feeding, is indeed associated with systemic acidemia. Acid feeding data, therefore, cannot exclude a role of systemic pH in mediating the renal response to a chronic acid load.