What is the role of the urinary pH and urinary anion gap (AG) in the workup of hyperchloremic acidosis?

Updated: Sep 03, 2020
  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Urinary pH tends to be increased in the presence of large amounts of ammonia in the urine.

An inability to lower the urinary pH to less than 5.5 despite systemic acidemia was formerly considered the hallmark of dRTA. Given that a lower pH implies increased excretion of acid if the concentration of urinary buffers stays constant, an inability to decrease urinary pH was interpreted as signifying decreased excretion of urinary acid. Although this is true in many cases, it is not in all cases.

The presence of large amounts of ammonia in the urine, which typically occurs with chronic metabolic acidosis, tends to increase the urinary pH. In hyperkalemic dRTA, urine pH can be maximally acidic. Decreased acid excretion is due to other concurrent defects, mainly decreased production of ammonia.

In patients with normal AG acidosis due to diarrhea, the pH can be greater than 5.5. This is because volume contraction results in decreased availability of Na+ for reabsorption in the collecting duct, lessening the negative intratubular electrochemical potential and, thus, the rate of proton secretion.

Infection with urea-splitting organisms (eg, Proteus species) can also cause elevated urinary pH and may lead to an incorrect diagnosis of RTA.

The urinary AG is calculated using the following formula: UAG = UNA+ + UK+ - UCl-.

Na+ + K+ + unmeasured cations = Cl- + unmeasured anions. In the absence of ketonuria and bicarbonaturia, there are no significant unmeasured anions in the urine. The principal unmeasured cation is NH4+ and when present in substantial concentration is evident by a negative AG. UAG is thus a measure of the urinary concentration of NH4+.

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