Acute Tubular Necrosis Question

[as8906]

On firecracker/first aid 2015, it says that there is an increase in FENa with acute tubular necrosis. I understand this; the tubules aren't working properly so sodium is not being reabsorbed and more ends up in the urine.

But then there is that mnemonic device "MAD HUNGER", and the "N" stands for "Na+/H2O retention (HF, pulmonary edema, hypertension)". How is there both sodium wasting and sodium retention?

Is it because there is progression to sodium retention? Does it start out with wasting of sodium and progress to retention?

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[jqueb29]

I've temporarily brain-dumped all my kidney stuff for neuro currently so someone correct if this is wrong: with ATN, you have less overall filtration of sodium since you have less functioning nephrons. However, for the sodium that actually does get filtered (a below normal amount), there is less reabsorption of this sodium (remember, FENa only refers to how much is excreted as a fraction of how much was filtered, not how much is present overall in serum).

 

[as8906]

Hey thanks a lot man, that makes sense. I got another answer to this question that considers two types of ATN, I'll copy/paste it here for the sake of completion and in case anyone else looks this up:

2 types of ATN: Oliguric and non oliguric. Both have minimal tubule reabsorption and waste electrolytes. Oliguric has low GFR and makes little urine so what little the tubules get is typically wasted. Body retains fluid and electrolytes. Non oliguric has high GFR and tubules do waste and patient tends not to accumulate fluids and electrolytes (easier to manage).