Thread by @BukuRenal

A #medtwitter tweetorial thread!

✳️ Why do we sometimes recommend oral sodium bicarbonate in CKD?

When GFR declines then sulphates, phosphates & small organic anions build up.

💥This causes a metabolic acidosis in CKD - the ‘R’ in GOLDMARK (see photo)

#MedEd #nephtwitter

The acidaemia in CKD (may) cause:
➡️ Bone demineralisation
➡️ Faster CKD progression
➡️ Protein & muscle catabolism
➡️ Hyperkalaemic tendency

These flow diagrams always make cause & effect appear certain - in reality there is a fair bit more uncertainty (from Dobre 2020 NDT)

The decreased pH in CKD can be improved by:
✅ Stopping smoking
✅ Increasing intake of base-producing foods
✅ Giving furosemide

However, when these measures become insufficient then we consider ‘topping up’ with oral bicarbonate to help prevent the complications above.

So how do we give bicarb tablets?

In UK often use 500mg sodium bicarbonate tablets, starting at
3/day & then titrating.

(Note each tablet has 6mmol of HCO3. Compare this to the 150mmol of HCO3 in 1L of IV 1.26% sodium bicarb - hence why tablets don’t do much in acute setting!)

Problems:
❌ Tablet burden
❌ Abdominal cramps, burping
❌ Mixed evidence for efficacy (as with lots of things in renal…)
❌ No one knows exactly what level of serum bicarb to start treatment or what level to target….. as ever keen to hear the opinions of wider #nephtwitter!

Bonus tweet! When do we give IV bicarb in renal?

Consider 1.26% IV bicarb if meets checklist👇
✅ AKI is causing ⬇️pH (not ⬆️lactate etc.)
✅ Hyperkalaemic (not monotherapy, as adjunct)
✅ Fluid status = room for volume
✅ Patient can ⬆️RR (to blow off CO2 formed)
✅ Calcium OK