Renal Tubular Acidosis and Uraemic Acidosis


Metabolic acidosis occurs in both acute and chronic renal disorders

  • the anion gap may be elevated or normal
  • damage to glomeruli and tubules: high anion gap due to failure to excrete acid anions
  • damage to the tubules only: normal anion gap (RTA or hyperchloraemic type), GFR may be normal or only minimally affected

Uraemic acidosis

  • renal failure causes metabolic acidosis through the accumulation of acidic anions such as phosphate and sulfate

Renal tubular acidosis

  • causes are numerous
  • primary problem is the inability to acidify the urine and excrete acid
  • may be incomplete and only develop in the presence of an acid load

Type 1 distal

Type 2 proximal

Type 4


reduced H+ excretion in distal tubule

impaired HCO3 reabsorption in proximal tubule

impaired cation exchange in distal tubule

hyperchloremic NAGMA




minimum urine pH


(but usually >5.5 before acidosis becomes established)


plasma HCO3


usually >15

usually >15

plasma K




renal stones





  • caused by failure to excrete acid anions (phosphate and sulphate)due to decreased number of functional nephrons
  • GRF < 20ml/min
  • low plasma HCO3
  • patients often survive a long time and get chronic complications such as bone demineralisation


  • ‘classic’ RTA
  • aka distal
  • reduced secretion of H+ in distal tubule -> inability to maximally acidify the urine


  • hereditary
  • autoimmune (Sjogrens, SLE, thyroiditis)
  • nephrocalcinosis (e.g. primary hyperparathyroidism, vitamin D intoxification)
  • drugs/toxins (e.g. amphotericin B, toluene inhalation)
  • obstructive nephropathy


  • urine pH remains >5.5 despite severe acidaemia (HCO3 < 15mmol/L)
  • may require an acid load test to see whether urinary pH remains > 5.5
  • hyperchloraemic acidosis + alkaline urine + renal stone formation
  • secondary hyperaldosteronism -> increased K+ loss in urine


  • NaHCO3 (corrects Na+ deficit, ECF volume and corrects hypokalaemia)
  • sodium and potassium citrate solutions can be useful if hypokalaemia persistent
  • citrate also binds Ca2+ in the urine and can help to prevent renal stones


  • aka proximal
  • termed proximal because the main problem is impaired reabsorption of bicarbonate in the proximal tubule
  • at normal plasma HCO3, 15% of filtered HCO3 is excreted in the urine -> in acidosis when HCO3 levels are low the urine can become HCO3 free
  • symptoms take place when there is an increase in plasma HCO3 -> proximal tubule cannot reabsorb the increased filtered load -> delivered to distal tubule and is unable to be reabsorbed -> urinary loss of HCO3
  • results = metabolic acidosis with an inappropriately high urinary pH + hyperchloraemia (Cl- replaces HCO3 in circulation)
  • with increased distal tubular Na+ delivery -> hyperaldosteronism -> K+ wasting


  • proximal tubular defects: affects reabsorption of glucose, phosphate and amino acids
  • hereditary
  • vitamin D deficiency
  • cystinosis
  • lead nephropathy
  • amyloidosis
  • medullary cystic disease


  • metabolic acidosis (usually not as severe as distal RTA)
  • plasma HCO3 usually > 15mmol/L
  • high urinary HCO3 (inappropriate)
  • hypokalaemia
  • during the NH4Cl loading test urinary pH drops < 5.5


  •  treat underlying disorder
  • NaHCO3 and K+ supplementation not always necessary (if required will require large doses)
  • thiazide diuretics (some patients respond to this which results in increased proximal HCO3 reabsorption)


  • associated with renal failure caused by disorders affecting the renal interstitium and tubules
  • GFR >20mL/min (unlike uraemic acidosis)
  • always associated with hyperkalaemia (unlike others)
  • defect in cation-exchange in the distal tubule with reduced secretion of both H+ and K+
  • associated with: Addison’s disease or post bilateral adrenalectomy
  • acidosis not common unless there is associated renal damage affect the distal tubule
  • the H+ pump in the tubule is not abnormal so that patients with this disorder are able to decrease their urinary pH to < 5.5 in response to the acidosis

References and Links

Journal articles and textbooks

  • Bersten AD, Soni N. Oh’s Intensive Care Manual (6th edition), Butterworth-Heinemann 2009. [Google Books Preview]

Social media and web resources

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