Non-anion gap acidosis

  • Non-anion gap metabolic acidosis -> All hinges on the balance between Chloride and Bicarbonate anions
  • Can either occur 1) via exogenous acid (H+) which pulls (HCO3-)  down or 2) Loss of (HCO3) from fistulae or diarrhea or etc
    • For Topf’s lecture on non-anion gap metabolic acidosis, we use the model #2/loss of (HCO3-)
    • Can lose (HCO3-) from GI tract, from renals, or from the addition of chloride/”chloride intoxication”
    • Chloride intoxication options: HCl, chloride gas, early renal failure, dilutional acidosis

Renal tubular acidoses

  • Fail to absorb the bicarb initially filtered by the kidney, RTA 2
  • Fail of kidney to synthesize new bicarb to replace the lost bicarb from metabolism, RTA 1
  • Stow the hydrogen ions from ammonia, RTA 4
    • The last two mechanisms seem linked (in my own analysis)…

Screen Shot 2018-01-03 at 15.20.43.png

Screen Shot 2018-01-03 at 15.21.55.png

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*Main role of the kidney in bicarb management is reabsorptionits job is reabsorb thousands of millimoles of the filtered bicarb -> see above image, 3,456 mmol/day

*Ancillary/side-job is the synthesize a small amount of bicarb to replace bicarb that’s lost in the daily acid load -> see image above, 50-100 mmol/day

Screen Shot 2018-01-03 at 15.11.03.png

  • Commentary on the ancillary job of synthesizing small amount of bicarb:
    • Key point is that body uses either ammonium or a titratable acid (like dihydrogen phosphate, H2PO4-) to collect the H+ that’s excreted when the bicarb is synthesized

RTA 2

  • Acetazolamide
  • Multiple myeloma
  • Lead toxicity
  • Mercury poisoning
  • Wilson’s disease
  • Hyperparathyroidism

Consequences of loss of more bicarb in the urine -> K+ is lost to maintain electroneutrality (?)

Also, consequences of bone disease -> bone buffers the acidosis


RTA 1 -> Occurs b/c of failure at any of the following steps for urinary acidification (i.e. failure to produce new bicarb)

  • Consequences are bone buffering
  • Renal stones -> 2/2 increased urinary pH and hypercalciuria

Screen Shot 2018-01-03 at 15.34.05.png

  • RTA 1: Voltage-dependent -> Problem with the Na+ transporter (?)
    • Only distal RTA that has hyperkalemia
    • Differentiate from RTA 4 by response to fludrocortisone
  • RTA 1: H+ secretion problem
    • Most common cause of distal RTA
    • Lithium
    • Pyelonephritis
    • Sickle cell
    • Also, Wilson’s, Multiple Myeloma like the RTA 2
  • RTA 1: Gradient defect
    • Usually from Amphotericin B

RTA 4

  • Problem with the NH3 which is needed excrete excess H+ as NH4+ ion -> ammonium in urine means there’s no RTA <- i.e. if there’s no urine anion gap (or, it’s neg), then you’re secreting NH4+ in the urine/you don’t have RTA 4.

How to diagnose the etiology of non-gap metabolic acidosis -> get that urine anion gap!

Look for H+ clearance via looking for urinary ammonium (NH4+)

  • Do this via urinary anion gap
  • Normal/negative urinary anion gap means there’s ammonium in the urine = you’ve r/o RTA 4

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Check out Joel Topf’s excellent renal blog, Precious Bodily Fluids

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