The Clinical Etymologist
The Clinical Etymologist is a podcast devoted to curiosity, lifelong learning, and the quiet joy of medicine. Hosted by Dr. Kim—a general internist and self-appointed Clinical Etymologist—each episode explores the words we use in medicine to diagnose, to heal, and to make sense of the human condition. With a blend of language, history, clinical insight, and his unique sense of humor, Dr. Kim uncovers the hidden roots of medical terms—from the eponyms we invoke to the metaphors we overlook. This is a space for curious souls who still believe learning can be meaningful and fun.
The Clinical Etymologist
Sodium Conundrum
Use Left/Right to seek, Home/End to jump to start or end. Hold shift to jump forward or backward.
In this episode of The Clinical Etymologist™, Dr. Kim returns to the mystery of hyponatremia through the lens of soda, sodium, and the kidney’s inner logic. From the ancient chemistry of soda water to the modern lab value of serum sodium, Jennifer the Padawan learns that hyponatremia is usually less about salt and more about water. Together, they review how ADH explains urine osmolality, while aldosterone and effective circulating volume explain urine sodium. Along the way, they untangle SIADH and other pathologies. By the end, the algorithm becomes physiology: the kidney only asks, should I keep sodium, or should I let it go?
You're listening to The Clinical Etymologist, a podcast where medicine meets meaning, created by Dr. Simon Kim, a general internist with a passion for the strange, fascinating, and sometimes hilarious roots of medical terminology.
SPEAKER_00Long time ago, in a teaching hospital far, far away. I returned to the doctor's lounge after rounds, still thinking about Jennifer's question. The patient's sodium was 122. Jennifer wanted an algorithm. I wanted physiology, and my kidneys apparently wanted sugar. So I opened the fridge and found a bright orange can of fanta sitting there, glowing like radioactive happiness. I couldn't find expiration date, which meant either it was very fresh or expired long time ago. I took a cautious sip. Then I looked at the label sodium thirty five milligrams. I paused. Interesting, I said. Jennifer looked at me.
SPEAKER_02Dr. Kim, if you don't mind, what is interesting?
SPEAKER_00This, I said, holding up the fanta can. Soda. She blinked.
SPEAKER_02Dr. Kim, are we doing product placement now?
SPEAKER_00Not yet, but I am willing to discuss with any future sponsors, but I digress. No, I said, deepening my voice. We are doing etymology. I turned the can slowly in my hand. Soda. Sodium. Same family. Same ancient story. The word sodium comes from soda, which originally referred to alkaline substances obtained from certain plants and mineral deposits. This story is older than the periodic table, I said. Older than modern chemistry. The ancient Egyptians used natron, a naturally occurring sodium-rich mineral mixture, for cleaning and for mummification. Jennifer looked at the can again.
SPEAKER_02So before sodium was a lab value, it was a practical substance.
SPEAKER_00Exactly, I said. Before anyone knew sodium was an element, people already knew that soda could clean, preserve, dissolve, and transform things. Chemistry often begins long before anyone understands the chemistry. Jennifer looked at the orange can again.
SPEAKER_02So why are these drinks called soda drinks?
SPEAKER_00Because before soda became a sweet drink in a can, I said, it was chemistry in a glass. Early carbonated drinks came from soda water. Water that in its earliest form often came from natural mineral springs or wells. As groundwater passed through limestone and other mineral-rich rocks, it dissolved carbon dioxide and alkaline salts, including sodium bicarbonate. When this mineral water emerged under pressure, it could naturally sparkle. People noticed that these spring waters tasted sharp, fizzy, and slightly alkaline, and many believed they had medicinal properties. Then pharmacists and drink makers added that magical ingredient, I mean sugar, like sweet syrups and flavors to soda water. Over time the name was shortened. Soda water became soda. I took another sip of the probably expired orange soda, feeling sugar levels surging in my central nervous system. Before we go down that soda rabbit hole, we must return to our discussion. More specifically, we are here to ask one question. Jennifer's eyes widened in anticipation. What does the kidney think about hyponatremia? In previous episode The Sodium Doom, we reviewed that posterior pituitary releases ADH in response to high tonicity sensed by hypothalamus and to drop in blood volume sensed by carotid sinus and aortic arch. The low blood volume over eyes low tonicity. This makes sense. Perfect tonicity will not help if one's blood volume is gone. But what do kidneys say about all this? For that we must review how aldosterone works. I turned to my Padawan. Jennifer, tell me what aldosterone is.
SPEAKER_02It is a steroid hormone. It is made in the zona glomerulosa of the adrenal cortex.
SPEAKER_00Good, I said. And what regulates it?
SPEAKER_02It is mainly regulated by the renin angiotensin aldosterone system. When the kidney senses low perfusion pressure, or when the macula densa senses low sodium chloride delivery, or when sympathetic tone increases through beta-1 receptors, the juxtaglomerular cells release renin. Renin converts angiotensinogen from the liver into angiotensin 1. Then angiotensin converting enzyme, mostly in the pulmonary vascular endothelium, converts angiotensin 1 into angiotensin 2. Angiotensin 2 then stimulates aldosterone release from the adrenal cortex.
SPEAKER_00That is brilliant. Another factor is that high potassium level stimulates aldosterone release. So, what does this hormone do?
SPEAKER_02It acts on the distal tubule in collecting duct, especially the principal cells. It promotes sodium reabsorption and potassium secretion. And in the alpha-intercalated cells, aldosterone promotes hydrogen ion secretion, which is why excess aldosterone can cause metabolic alkalosis.
SPEAKER_00Jennifer, you must have had a fantastic tutor for your nephrology block. I am curious. Who was it?
SPEAKER_02It was you, Dr. Kim.
SPEAKER_00Honestly, I did not remember. I blushed a little then continued. Very good, Jennifer. You have excellent recall. So, to recap, ADH tells the story of why the body is holding on to water. Sometimes because the serum is too concentrated, and sometimes because the circulation feels threatened. Through those amazing aquaporin channels, ADH determines whether the urine becomes concentrated or dilute. Aldosterone tells a different story, what the kidney thinks about sodium and effective circulating volume. Can you build on this, Jennifer?
SPEAKER_02I will try. ADH explains the urine osmolality. Aldosterone helps explain the urine sodium. If the kidney thinks effective circulating volume is low, it activates the renin angiotensin aldosterone system. Aldosterone tells the distal nephron to reabsorb sodium so the kidney holds on to sodium and the urine sodium becomes low.
SPEAKER_00That is spot on, Jennifer. The body is overloaded, but the kidney feels underfilled. Now, what about when urine sodium is high, like greater than 40? What does that indicate?
SPEAKER_02It means the kidney sees no need to conserve sodium, so either the effective circulating volume is not low, or the kidney cannot conserve sodium properly, or something is forcing sodium loss.
SPEAKER_00Good. Give me examples.
SPEAKER_02In syndrome of inappropriate ADH, ADH is inappropriately high, so the urine is concentrated, but the arterial circulation is not truly underfilled. So RAS and aldosterone are not strongly activated, and the kidney is not desperately holding on to sodium. That is why urine sodium is often high, often above 40.
SPEAKER_00Yes, that is why it is called inappropriate. In SIADH, ADH is not doing something mysterious. It is doing exactly what ADH normally does. It inserts aquaporens, holds onto water, and makes the urine concentrated. The inappropriate part is the context. The patient is not hypertonic and the circulation is not truly threatened. There is no good physiological reason for ADH to be active, yet it is active anyway, so inappropriate, Jennifer continued.
SPEAKER_02Also, Dr. Kim, high urine sodium can also happen when the patient is volume depleted and the kidney is losing sodium anyway, like with diuretics or some forms of acute kidney injury. The problem is that the kidney is unable to conserve sodium or it is being pharmacologically forced to waste it.
SPEAKER_00What about adrenal insufficiency, hypothyroidism, and cerebral salt wasting? Any ideas why they have high sodium?
SPEAKER_02To be honest, I just memorize them. But I will try to explain based on what I know. First, hypothyroidism. Low thyroid, especially severe hypothyroidism, can lower cardiac output in GFR. If the kidney receives less effective arterial blood flow, the body may respond by increasing ADH. ADH then holds on to free water, so the sodium falls by dilution. But this is not classic salt and volume depletion like vomiting or diarrhea, so ras and aldosterone are usually not dramatically activated. Therefore, the urine sodium is often not very low. It may be relatively high.
SPEAKER_00What about adrenal insufficiency?
SPEAKER_02Okay, Dr. Kim, I could work this out. In primary adrenal insufficiency, aldosterone is low. Without aldosterone, the distal nephron cannot reabsorb sodium properly. So the kidney wastes sodium, urine sodium becomes high, the patient becomes volume depleted, and potassium may also rise. This volume depletion turns on ADHD.
SPEAKER_00Excellent, I said. And cortisol?
SPEAKER_02Cortisol normally suppresses CRH. When cortisol is low, that break is removed and CRH rises. CRH causes release of ACTH and ADH. So primary adrenal insufficiency creates a double whammy. First, low aldosterone causes renal sodium wasting, high urine sodium, volume depletion, and often hyperkalemia. That volume depletion stimulates ADH. Second, low cortisol itself increases ADH activity. More ADH means more free water retention, so the hyponutremia worsens.
SPEAKER_00Beautiful, I said. Unless you remember the adrenal gland. And clinically, SIADH patient will look evolemic or the mild hypovolemic.
SPEAKER_02Oh yes, 30 slash 20 slash 10 rule.
SPEAKER_00I knew then that Jennifer was a secret listener of the clinical etymologist. What about second and tertiary adrenal insufficiency?
SPEAKER_02In secondary and tertiary adrenal insufficiency, cortisol is low, but aldosterone is usually preserved because RAAS is intact. So these patients usually do not have the same salt-wasting hypercolimic volume-depleted picture as primary adrenal insufficiency. Their hyponatremia is mainly from low cortisol, increasing ADH activity and impairing free water excretion. Urine sodium may still be relatively high because the kidney is not maximally sodium avid.
SPEAKER_00Now tell me about the cerebral salt wasting. Jennifer frowned.
SPEAKER_02That one always confused me.
SPEAKER_00It confuses everyone, and the confusion is the key to understanding this confusing diagnosis. Bottom line is that the brain is confused. Brain doesn't listen to the kidney, and the physician is confused. I have seen cerebral salt wasting once when moonlighting at a neurosurgical ICU many years ago. Cerebral salt wastingly happens in patients with intracranial disease. The kidney wastes salt, meaning sodium, because of increased natriuritic peptides and altered sympathetic input from the diseased or injured brain. The patient becomes truly volume depleted. The body senses this and releases ADH. Urine osmolality is high, but the kidney keeps producing urine and keeps wasting sodium because that is what the brain tells the kidney to do. So, high urine sodium. If they named it cerebral-induced renal salt wasting, this would have made more sense, but I am just an internist. So how would you treat this cerebral salt wasting, Jennifer?
SPEAKER_02Hmm, I suppose we treat the underlying brain injury, but in the meantime, because the kidney is losing sodium and water, we have to replace both Congrats, Jennifer, you got it.
SPEAKER_00That is how we treat it. I looked at Jennifer with pride. Jennifer, you are no longer memorizing the algorithm. You are reading the physiology. So let's look at your patient's labs.
SPEAKER_02Okay, Dr. Kim. Her sodium was 122, potassium 4, choleroid 100 B U N normal, and oh no. Dr. Kim, they are from yesterday. The team did not order labs for today. Jennifer, what do you think we should do? Well, I would like to order repeat labs now, including repeat electrolytes, serum osmolality, urine osmolality, urine sodium, glucose, BUN, creatinine, TSH, and morning cortisol if clinically appropriate.
SPEAKER_00Sounds good. Enter them on the Skynet and let's review when results are back. In the meantime, anything else you want to tell the attending nurse? Address code, status? No. At least not yet. Ask her to do accurate ins outs. And why?
SPEAKER_02You are looking out for any change in ADH. If ADH is turned off, patient will start not not peeing.
SPEAKER_00I picked up another probably expired Fanta can. Channeling inner Sir Isaac Newton holding the celestial orb. I pontificated. The drink is called soda. The lab calls it sodium. The periodic table calls it natrium. But the kidney does not care what we call it. I threw it at the garbage can, narrowing missing it. Basketball was never my forte. The kidney only asks, should I keep it or should I let it go?
SPEAKER_01If you like this episode, share it with a curious friend. As a novice podcaster, Dr. Kim, despite his busy schedule, is still constructing the official website where you'll be able to subscribe, leave a review, explore show notes, and connect further. But that will come soon. Stay tuned. Until next time, channel your inner etymologist because every diagnosis has a backstory and every word has a pulse.
Podcasts we love
Check out these other fine podcasts recommended by us, not an algorithm.
Deep Questions with Cal Newport
Cal Newport