Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a group of tubular transport disorders in which the kidneys cannot excrete acid adequately or reclaim filtered bicarbonate, even though glomerular filtration is normal or only mildly reduced. The result is a normal-anion-gap metabolic acidosis, also called hyperchloraemic metabolic acidosis: bicarbonate falls and chloride rises to maintain electrical neutrality, rather than unmeasured acids accumulating as they do in uraemia, ketoacidosis, or lactic acidosis. Calculate the anion gap from the serum sodium, chloride, and bicarbonate: Na − (Cl + HCO₃). Interpret it using the laboratory’s reference range. In Canadian laboratories, these values are generally reported in mmol/L; for sodium, chloride, potassium, and bicarbonate, the numeric values are equivalent to mEq/L. The first bedside clues are the bicarbonate, potassium, chloride, creatinine, and the patient’s neuromuscular status. Hypokalaemia may cause fatigue, muscle cramps, weakness, ileus, or dysrhythmia. Hyperkalaemia may be clinically silent until conduction deteriorates. Severe acidaemia can produce tachypnoea or Kussmaul respirations, nausea, reduced cardiac contractility, hypotension, and altered mental status. A normal or near-normal estimated GFR with persistent hyperchloraemic acidosis should prompt consideration of RTA. Reduced...