Renal tubular acidosis (RTA):RecognizeTheAmmonium defect and pHorget the urine pH

Abstract

To maintain acid-base balance, the kidney must generate new bicarbonate by metabolizing glutamine and excreting ammonium (NH₄ ⁺). During chronic metabolic acidosis, the kidney should respond by increasing the rate of excretion of NH₄ ⁺ to 200–300 mmol/day. If the rate of excretion of NH₄ ⁺ is much lower, the kidney is responsible for causing or perpetuating the chronic metabolic acidosis. Thus, the first step in the assessment of hyperchloraemic metabolic acidosis is to evaluate the rate of excretion of NH₄ ⁺. It is important to recognize that the urine pH may be misleading when initially assessing the cause of this acidosis, as it does not necessarily reflect the rate of excretion of NH₄ ⁺. If proximal renal tubular acidosis (RTA) is excluded, low NH₄ ⁺ excretion disease may be broadly classified into problems of NH₄ ⁺ production and problems of NH₄ ⁺ transfer to the urine; the latter being due to either interstitial disease or disorders of hydrogen ion secretion. The measurement of the urine pH at this stage may identify which problem predominates. This approach returns the focus of the investigation of RTA from urine pH to urine NH₄ ⁺.