Synopsis
Classify renal tubular acidosis from acid-base and potassium physiology, identify reversible causes, and replace alkali safely without missing an electrolyte emergency.
- RTA is a renal acidification defect that usually causes a normal-anion-gap, hyperchloraemic metabolic acidosis out of proportion to any reduction in glomerular filtration.
- First confirm genuine metabolic acidosis and exclude gastrointestinal bicarbonate loss, chloride-rich fluid administration, ketoacidosis masked by mixed disorders, toxins and advanced CKD.
- Distal type 1 RTA impairs urinary hydrogen secretion, often leaves urine inappropriately alkaline during systemic acidosis, and is associated with hypokalaemia, hypocitraturia, stones and nephrocalcinosis.
Key red flags
Mild metabolic acidosis with persistent hyperkalaemia in diabetic or interstitial CKD, especially during RAAS or ENaC-blocking therapy, suggests type 4 physiology.
Investigation priorities
Confirm metabolic acidosis and assess severity and respiratory compensation.
Management branches
Routine chemistry shows a low bicarbonate concentration.
- Repeat or obtain a blood gas when artefact or respiratory alkalosis is possible, while checking chloride, potassium, renal function, glucose, lactate and ketones.
- Calculate and albumin-adjust the anion gap, then seek diarrhoea, urinary diversion, saline administration, toxins and reduced-GFR explanations.
Key medicines
Sodium bicarbonateFor chronic renal tubular acidosis, initiate and titrate using the current BNF and specialist plan; the required dose varies substantially with subtype and ongoing bicarbonate loss.
Potassium citrate with potassium bicarbonateUse only through a renal or metabolic stone service, divided and titrated to potassium, bicarbonate and urine citrate using the live BNF product guidance.