Tag: antibiotic

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Antibiotics and AKI for #MADID18 (now with video)

Last fall, Dr. Davis (@IDPharmProf) asked if I would be interested in speaking about antibiotic induced AKI. She was thinking of submitting an idea for a session on kidney disease and antibiotics. Later, she told me I would be sharing the stage with Bruce Mueller (@BAMPharmD), who would be talking about antibiotic dosing during AKI and CRT. This felt like agreeing to doing some Karaoke and then being told you are being paired-up with Frank Sinatra.

I did my best, but compared to Dr. Mueller, the only difference between me and Bozo was the red nose and floppy shoes.

Here is a screencast of the presentation and the slides for you to peruse. But if you ever get a chance to hear Dr. Mueller, don’t miss it. He is really good.

 

 

Keynote: MAD-ID Antibiotic Induced Acute Kidney Injury

PowerPoint: MAD-ID Antibiotic Induced Acute Kidney Injury

PDF: MAD-ID Antibiotic Induced Acute Kidney Injury

 

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You knew that proteinuria is protective against amphotericin induced hypokalemia. Right?

All of you #NephMadness players crying into your coffee about Proteinuria getting beat out by Patient Reported Outcomes need to understand that proteinuria isn’t always bad*.

*I am being sarcastic here, proteinuria is always bad, and the only reason I am writing this post is because of this interesting quirk where it appears to be protective.

Proteinuria protects against amphotericin b induced hypokalemia. In patients on amphotericin, heavy proteinuria, a protein concentration of 3 g/L (3+ on dipstick), is protective against amphotericin b induced hypokalemia.

The study was done on normal formulations (as opposed to liposomal preparations) of amphotericin B.

Amphotericin B is highly protein bound. With standard doses, the normal amphotericin concentration in the urine will be 1-2 micromol/L. With 3+ urine protein, the albuminuria concentration is over 40 micromol/L, and this is apparently enough to bind and neutralize amphotericin’s collecting duct toxicity. Amphotericin’s anti-fungal property comes from its ability to tear open fungi cell membranes. Unfortunately it does a doozy on the membranes of the collecting tubules as well, allowing potassium to flow down its contraction gradient from the cells to the tubular fluid (and out in the urine). Similarly hydrogen flow from the tubular fluid back into the cells causing metabolic acidosis. It is an unusual cause of renal potassium loss without increased aldosterone levels.

For you #NephMadness geeks, toad bladder was instrumental to working out the mechanism for amphotericin induced hypokalemia.