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Hanging with @melhoenig About to learn about Adrenal Physiology from @AnandVaidya17 at @harvardmed (two #NephMadness veterans)
Starts with a very Canadian video of a moose licking a truck. Does the moose have Addison disease? (hey Michelle, @AnandVaidya17 calls it Addison's)
Now Wyoming big horn sheep licking cars. He suspects that this is normal behavior of animals that live in an environment without much sodium.
Hyperaldo can come in many forms. Talking about a volume depleted hiker with a PRA of 8, Aldo of 30. ARR of 3.75. Secondary hyper aldo due to volume depletion.
Woman ate 3 banana, fruit salad, 3 potatoes. ldo is 30 with PRA of 1.2, ARR of 25. Also secondary hyper aldo driven by the potassium load.
38 yr old with 158/92, K of 3.2 with Also of 30 and PRA of <0.6. RAA 50+, this is primary hyperaldo.
57 year old CHF, BP of 158/92. PRA 3.2. ALdo 30, ARR of 9.4. Renin dependent aldosteronism. Rhis is pathology even though the axis is working normally.
Nice image here. I like how he abstracted away the loop.
mTORC2 allows for aldo independent K excretion in the CCD.
Potassium excretion
Lung fish may be the first species to have aldosterone. There were unique receptors (cortisol and aldo receptors) before there was aldo. Cortisol bound both receptors. Aldo developed when we left the ocean and needed to be sodium avid.
Humans have learned to cultivate sodium. So we don't crave sodium (but we like it). Talking about the Yanomami People maintain an ancient diet with very little sodium. 2 mmol/day, 200 mmol of K per day. Their PRA is in the teens. Aldo of 75 mcg per day.
Those high aldo levels are not toxic to the Yanomami
ACEi would be particularly toxic to these people, hence the Brazilian Pit Viper venom.
Poem to summarize the salt and water hormones
On to Primary Hyper Aldo. Suppressed renin means no proximal sodium reabsorption. Lots of distal delivery of sodium. Reabsorb that sodium and excrete potassium. leads to hypertension, hypokalemia, metabolic alkalosis.
Feed rats a high sodium diet, aldo falls, blood pressure goes up. No cardiac fibrosis.

Then repeat with L-NAME (NO antagonist) and AngII: fibrosis myocardial damage

Then repeat with L-NAME (NO antagonist) and AngII and eplerenone: no fibrosis myocardial damage
Then repeat with L-NAME (NO antagonist) and AngII but low sodium and no eplerenone: no fibrosis myocardial damage
On to Addison Disease. Patient named John Kennedy. He was one of the first people to be treated with cortisone. Showing pictures of JFK getting sicker until he was about 35 and then looking better when cortisone becomes available. Pics suggest cushingnoid appearence from over Tx
It’s so simple. Perhaps you need a refresher course
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