SUMMARY
Acidemia stimulates renal ammonia production and excretion. This adaptive response allows increased H+ secretion and generation of new bicarbonate. To determine whether a relationship existed between urine ammonium (NH4+) concentration and excretion and urine anion gap (Na+ + K+ − Cl−), ammonium chloride (NH4Cl) was administered per os for 5 days to induce systemic acidemia in 12 healthy Beagles. During NH4C1 administration, a strong, statistically significant (P < 0.0001) relationship was apparent between urine NH4+ concentration measured in millimoles per liter and urine anion gap.
Regression equation: urine [NH4+] = 8.2 − 0.416 × urine anion gap; r = −0.897.
A statistically significant (P = 0.0001) relationship existed between urine NH4+ excretion measured in millimoles per kilogram of body weight per day and urine anion gap.
Regression equation: urine NH4+ excretion = 0.74 − 0.38 × urine anion gap; r = −0.768.
As urine NH4+ concentration or excretion increased, urine anion gap became more negative. Before NH4Cl administration (no systemic acidemia), a weak, but statistically significant (P = 0.015) relationship was observed between urine NH4+ concentration and urine anion gap.
Regression equation: urine [NH4+] = 65.2 − 0.141 × urine anion gap; r = −0.41.
However, a relationship was not evident between urine NH4+ excretion and urine anion gap before NH4Cl administration. Hence, urine anion gap is a reliable index of urine NH4+ concentration and excretion only in dogs with metabolic acidosis. In human beings with distal renal tubular acidosis, NH4+ excretion is inappropriately low and results in a positive urine anion gap. Therefore, as a reliable index of NH4+ excretion, urine anion gap may represent an easy and rapid method to aid in the diagnosis of distal renal tubular acidosis in dogs.
