Treatment of RTAs with chronic administration of alkali is warranted to prevent catabolic effect on bone and muscle.
Quick way to check the type of RTA: First look at Sr. K: if hyperkalemia it’s RTA type IV. If not, then look at urine pH: if more towards high (basic)>5.3 it’s RTA type I; if low it’s RTA type II or IV. Non-anion gap acidosis, hypokalemia, and low urine pH are all consistent with GI loss due to diarrhea.
Renal excretion of hydrogen/RTA-1: 1 meq/kg (50 - 100 mEq) of nonvolatile acid is produced each day by the metabolism of protein. This is "fixed" acid, H+ produced this way is bufferred by the HCO3 (one: one) in the ECF. If this goes on without replacement of the 50 - 100 mEq/day of HCO3, then the HCO3 would be rapidly depleted, and metabolic acidosis ensues. This is prevented by the kidney's ability to generate new bicarbonate. How does it do it? The kidney makes new HCO3- by eliminating H+ ion from the body, which adds one HCO3- to the ECF for every H+ eliminated. Renal elimination of 50 - 100 mEq/day of H+ keeps the HCO3- within its narrow range of 24 - 26 mEq/L. The kidney does this by two mechanisms:
Active secretion of H+ by an ATP-utilizing proton "pump" in the collecting tubule. One HCO3- is produced for every H+ excreted.
Hydrolysis of glutamine in the proximal tubule generates NH4+ (which is excreted in the urine) and HCO3- (which is returned to ECF). The process of ammoniagenesis rids the body of H+ ion as long as the NH4+ ions produced are excreted in the urine. This is more important quantitatively than secretion of H+ ions in generating HCO3-. The main way the kidney responds to acidosis (excess H+ ion) is by increasing the production and excretion of NH4+.