My Clinical Notes
Renal tubular acidosis
- This is a metabolic acidosis due to impaired acid secretion by the kidney
- There is a hyperchoraemic metabolic acidosis with normal anion gap
Type I
- Distal RTA due to inability the excrete H+ ions and generate acidic urine in the distal tubule, even in states of severe acidosis
- It may complicate many renal disorders
- Features include;
- Rickets or osteomalacia due to buffering of H+ with calcium in bone
- Nephrocalcinosis with renal calculi
- This is due to a combination of hypercalciuria from bone, reduced urinary citrate (which inhibits calcium phosphate precipitation) which is reabsopbed to act as a buffer for H+ and an alkaline urine
- It is also associated with hypokalaemia as there isn’t H+ to exchange for Na so K+ is exchanged instead
- Causes;
- Idiopathic
- Genetic;
- Ehlers-Danlos
- Marfan’s
- Autoimmune disease;
- SLE
- Sjogren’s
- Autoimmune hepatitis
- Nephrocalcinosis
- Hypercalcaemia
- Medullary sponge kidney
- Tubulointerstitial disease
- Chronic pyelonephritis
- Chronic interstitial nephritis
- Obstructive uropathy
- Renal transplant rejection
- Drugs;
- Lithium
- Amphotericin
- Diagnosis
- Acid load – oral ammonium chloride – there is a failure to acidify the urine beyond pH 5.5
- Treatment is with oral sodium bicarbonate or citrate
Type II
- Proximal RTA due to a defect in bicarbonate reabsorption in the proximal tubule resulting in excess bicarbonate in the urine
- The tubules are able to reabsorb some bicarbonate so can acidify urine during systemic acidosis
- It is rarer than type I
- May be an isolated thing or may be associated with Fanconi’s anaemia
- Hypokalaemia is common – the bicarbonate of the urine causes and osmotic diuresis causing increased flow rate to the distal tubule and therefore increased K+ excretion
- Causes;
- Idiopathic
- Fanconi’s syndrome
- Tubulointerstitial disease
- Myeloma
- Interstitial nephritis
- Drugs
- Lead and other heavy metals
- Acetazolamine
- Out of date tetracycline
- Diagnosis
- Give an IV sodium bicarbonate load – high excretion in the urine
- Treatment is with high doses of bicarbonate
Type III
- Very rare – combination of Type I and Type II
Type IV
- Due to hyporeninaemic hypoaldosteronism
- Hypoaldosteronism causes hyperkalaemia and acidosis (reduced K+ and H+ excretion)
- Causes;
- Mild renal impairment
- Causes of hypoaldosteronism
- Drugs;
- K+ sparing diuretics
- NSAIDs
- ACEI/ARB
Fanconi’s syndrome
- May be genetic or acquired – heavy metal poisoning, drugs, renal diseases
- Disturbance of the proximal tubule which does all the reabsorbing so there is defective reabsorption of;
- Amino acids
- Potassium
- Phosphate (leading to hypophosphataemic rickets and osteomalacia)
- Glucose (glucosuria)
- Bicarbonate (Type II RTA)
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