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renal tubular acidosis (RTA)


  • RTA is a group of conditions which cause a chronic metabolic acidosis due to either:
    • impaired ability to secrete hydrogen ions in the distal convoluted tubule (type I RTA)
    • impaired ability to absorb bicarbonate in the proximal convoluted tubule (type II RTA)
    • physiological reduction in distal tubular ammonium excretion, secondary to hypoaldosteronism (type IV RTA)
  • renal tubular acidosis was first described in 1935 by Lightwood
  • most common causes of RTA seen in the ED are:
    • chronic renal disease
    • toluene toxicity ⇒ hypokalaemia + rhabdomyolysis
    • inherited renal transport disorders
    • heavy metal toxicity
    • lithium

type I RTA


  • urinary pH > 5.3 in a patient with serum bicarbonate ⇐ 20mmol/L

clinical features

  • inability to reduce urinary pH below 5.3
  • decreased urinary citrate and hypercalciuria contributes to urolithiasis, nephrocalcinosis and rickets/osteomalacia
  • normal anion gap metabolic acidosis (although less severe cases may not cause acidosis “incomplete dRTA” diagnosed via the Short Ammonium Chloride Test)



  • Rx with citrated bicarbonate decreases systemic acidosis and may prevent renal calculi formation and secondary bone disease

type II RTA

clinical features

  • can generate acidic urine thus acidosis less severe than type I RTA
  • may be isolated or part of a syndrome of features called Fanconi syndrome:
    • polyuria, polydipsia, pRTA, phosphaturia, glycosuria, aminoaciduria, uricosuria, hypokalaemia, hyperchloremia and tubular proteinuria ⇒ osteomalacia due to phosphate wasting


type III RTA

  • a rare, transient, juvenile pattern of combined proximal and distal RTA
  • also seen in carbonic anhydrase II deficiency

type IV RTA (hyperkalaemic)

  • type 4 RTA is not actually a tubular disorder at all and nor does it have a clinical syndrome similar to the other types of RTA described above.
  • it was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic acidosis due to a physiological reduction in distal tubular ammonium excretion, which is secondary to hypoaldosteronism.
  • its cardinal feature is hyperkalemia, and measured urinary acidification is normal.


hyporeninaemic hypoaldosteronism
aldosterone resistance
primary aldosterone deficiency (rare)
  • primary adrenal insufficiency
  • congenital adrenal hyperplasia
  • aldosterone synthase deficiency
rta.txt · Last modified: 2010/01/18 03:38 by

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