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]

Overview

The diagnosis of renal tubular acidosis should be considered in any patient presenting with metabolic acidosis.The first step in diagnosing metabolic acidosis includes measuring the blood pH. The next steps includes measurement of urine pH and estimation of urinary ammonium excretion.

Laboratory Findings

The diagnosis of renal tubular acidosis should be considered in any patient presenting with metabolic acidosis.The first step in diagnosing metabolic acidosis includes measuring the blood pH. The next steps includes measurement of urine pH and estimation of urinary ammonium excretion.

Urine PH

• Patients with normal renal function and normal renal acidification mechanisms who develop acidosis usually have a urine pH of 5.3 or less.
• In most cases of distal renal tubular acidosis, 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) renal tubular acidosis.
• However, the urine pH can be reduced below 5.5 in occasional patients (2 of 17 in one study) with distal renal tubular acidosis.
• In contrast to the persistently elevated urine pH in distal , the urine pH is variable in proximal renal tubular acidosis, a disorder characterized by diminished proximal bicarbonate reabsorption.
• The urine pH will be inappropriately elevated if patients with proximal renal tubular acidosis 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 renal tubular acidosis:
  • 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 renal tubular acidosis 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 renal tubular acidosis.

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 renal tubular acidosis
Serum Potassium	Variable	Furesimide test	pH >5.5 and elevated potassium (distal renal tubular acidosis) 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 renal tubular acidosis