Renal tubular acidosis has come up a few times in the past papers. It is usually a way to call the candidate's attention to solvent abuse (toluene causes RTA Type 1), or an excuse to ask about the urinary anion gap.

Previous SAQs on the subject of renal tubular acidosis have included the following:

This topic is explored in greater detail in the section on acid-base disturbances, and specifically in the discussion of the diagnostic approach to normal anion gap metabolic acidosis. Those chapters may extend beyond the needs of the poor crazed exam candidate. Instead of adding even more reading material to one's pile, the following brief tables may suffice.

Characteristic Features of Renal Tubular Acidosis

Type 1

  • Severe acidosis
  • Severe hypokalemia
  • Urinary pH is usually very alkaline
  • Renal calculi
  • A frusemide dose fails to acidify the urine

Type 2

  • Moderate acidosis
  • Moderate hypokalemia
  • Urinary pH is not especially alkaline
  • A bicarbonate dose is rapidly excreted

     

Type 4

  • Mild acidosis
  • Hyperkalemia
  • Urinary pH is usually less than 5.5

 

Causes of Renal Tubular Acidosis

Type 1

Autoimmune diseases

Hypercalciuric conditions

Miscellaneous conditions

Drugs

Type 2

Congential

  • Fanconi syndrome

Acquired

  • MGUS / light chain disease
  • Vitamin D deficience
  • Hyperparathyroidism
  • Amyloidosis

Drugs

  • Acetazolamide
  • Topiramate
  • Tenofovir
  • Ifosfamide
  • Aminoglycosides
  • Lead poisoning
  • cadmium poisoning
  • mercury  poisoning
  • copper poisoning

Type 4

Failure of renin secretion

  • Diabetes and diabetic nephropathy
  • NSAIDs
  • NSAID-related interstitial nephritis
  • Glomerulonephritis

Angiotensin system failure

  • ACE-inhibitors
  • Angiotensin-2 receptor blockers
  • Heparin

Decreased aldosterone secretion

  • Primary hypoaldosteronism
  • Primary adrenal insufficiency
  • Secondary hypoaldosteronism
  • Steroid use
  • NSAIDs
  • Critical illness

Aldosterone receptor malfunction

ENaC sodim channel blockade