Renal tubular acidosis laboratory findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Laboratory Findings

• The presence of renal tubular acidosis (RTA) should be considered in any patient with an otherwise unexplained normal anion gap (hyperchloremic) metabolic acidosis.
• The first step in the diagnosis of a patient with a reduced serum bicarbonate and elevated chloride concentration is to confirm that metabolic acidosis is present by measuring the blood pH.
• The next steps in the diagnosis of possible RTA in patients who have a normal anion gap metabolic acidosis are measurement of the urine pH and estimation of urinary ammonium excretion.

Urine PH

• Patients with normal renal function and normal renal acidification mechanisms who develop metabolic acidosis usually have a urine pH of 5.3 or less.
• In most cases of distal RTA, the urine pH is persistently 5.5 or higher, reflecting the primary defect in distal acidification, and a urine pH below 5.5 generally excludes distal (but not proximal) RTA.
• However, the urine pH can be reduced below 5.5 in occasional patients (2 of 17 in one study) with distal RTA.
• In contrast to the persistently elevated urine pH in distal RTA, the urine pH is variable in proximal RTA, a disorder characterized by diminished proximal bicarbonate reabsorption.
• The urine pH will be inappropriately elevated if patients with proximal RTA are treated with alkali, increasing the serum bicarbonate concentration enough to produce a filtered bicarbonate load that exceeds the reduced proximal reabsorptive capacity; this most commonly occurs when alkali is given for the diagnosis or treatment of this disorder.
• In patients presenting with a normal anion gap metabolic acidosis, two scenarios can produce a misleading elevation in the urine pH that incorrectly suggests the presence of RTA:
  • Urinary tract infections with urea-splitting organisms may increase the urine pH because urea is converted to ammonia and bicarbonate.
    • Thus, assessment of the urine pH should include a urinalysis and, if indicated, a urine culture.
  • Severe volume depletion (which indirectly and reversibly limits hydrogen ion secretion by reducing distal sodium delivery) can impair urine acidification.
    • Thus, reliable interpretation of an inappropriately high urine pH requires that the urine sodium concentration be greater than 25 meq/L.

Urine ammonium excretion

• Urine ammonium excretion is reduced in distal RTA Thus, either direct measurement or indirect estimation of the urine ammonium concentration can be helpful in establishing the correct diagnosis.
• Urinary NH4 excretion cannot be directly measured in most clinical laboratories. However, an indirect estimate can be obtained by measurement of the urine anion gap and/or the urine osmolal gap.
• Estimation of NH4 excretion is not useful in patients with proximal RTA.

Laboratory Findings
Common laboratory findings		Other tests to consider
Test	Finding	Test	Finding
Serum HCO3	↓	Serum aldosterone	Low in aldosterone deficiency states Normal/ high in aldosterone resistance
Serum Chloride	↑	Urine anion gap	Absence of ammonia
Serum Na	Normal	Measurement of fractional urine bicarbonate excreation	Bicarbonateuria in proximal RTA
Serum Potassium	Variable	Furesimide test	pH >5.5 and elevated potassium (distal RTA) pH >5.5 and normal potassium (aldosterone deficiency)
Arterial Ph	↓	Urine glucose	Urine glucose + Serum glucose normal Fanconi syndrome
Serum anion gap	Normal	Fractional excretion of amino acids
Urine Ph	>5.5	Urine HCO3 infusion	PCO2 does not rise in distal RTA