Month: August 2026

Hi Dr. Topf,

I hope you’re doing well! I was reviewing S11: Sodium Metabolism, and I think I’m having some trouble understanding why euvolemic hyponatremia is non-edematous while hypervolemic hyponatremia is edematous. I was wondering if you could please help me correct my thought process.

Voume status is a total body sodium issue (more sodium, more edema)

Hypo- and hypernatremia is a total body water issue (more water more hyponatremia)

For euvolemic hyponatremia, such as SIADH, my understanding is that excess ADH causes water retention, which lowers serum sodium and plasma osmolality. The resulting osmotic gradient causes some of the excess water to shift from the ECF into the ICF. I was thinking that because the retained water is distributed between both compartments in the same 2/3:1/3 ratio, there isn’t a significant enough increase in ECF volume to produce edema?

Nope, these patients do not get edema and are clinically euvolemic, though if you put them on  scale they will be heavier, it is just that the extra volume is not clinically evident.

Where I become confused is with hypervolemic hyponatremia. I understand the example of heart failure: the hearts not pumping well, our organs aren’t getting perfused and so to increase blood volume we activate RAAS and ADH, causing retention of both sodium and water. However, if the serum osmolality is also low because this is a hyponatremia, shouldn’t there still be an osmotic gradient causing some of the retained water to move into the ICF, just as it does in SIADH? What makes the ECF expand enough in hypervolemic hyponatremia to produce edema?

With the increase in total body sodium all of that volume goes to the extracellular compartment, since sodium is an extracellular ion

However the retained water from the ADH does distribute across both the intracellular and extracellular compartment in a 2/3rds : 1/3rd ratio.

The ECF expands due to the RAAS induced retention of Na

I’m also confused by the statement that hypervolemic hyponatremia involves an increase in total body sodium. If decreased renal perfusion activates RAAS, and theres increased sodium reabsorption rather than sodium loss in the urine, don’t we see a net increase in sodium. So if there’s more sodium reabsorption I think I don’t get how this is a hyponatremia or is it considered a hyponatremia because even though there’s a net increase in sodium is the water increase out pacing it where the overall concentration is is low making it a hyponatremia?

There is increased retention of Na, that is what causes the hypervolemia, and there is a net retention of water, that is what causes the hyponatremia. Yes, the increase in water retention outpaces the sodium retention.

I feel like I’m missing something or thinking through this wrong somewhere so any help is super appreciated!

I think you get it better than you thought.

Thank you so much for your time and help!

Best Regards,
XXXXX

Occam’s razor: when evaluating multiple competing theories, the simpler explanation of an entity is to be preferred.

Solid logic, but not infallible.

This week I took care of a patient with a serum calcium of 17.5 mg/dL. Calciums that high are almost always malignant in nature. But we did the internal medicine thing and ran the algorithm. First branch point, “Is this PTH dependent or independent hypercalcemia?” The PTH came back at 220 pg/mL. Primary hyperparathyroidism. Case closed…or not.

A calcium of 17.5 mg/dL is extraordinarily high for primary hyperparathyroidism. In fact it would have been the highest calcium I had ever seen in primary hyperparathyroidism. I learned as a fellow, that whenever you think “this is the worst case of X I have ever seen, consider that maybe it is not the worst case of X but rather a more pedestrian case of Y.” Maybe, instead of the worst case of primary hyperparathyroidism this was two diseases instead of one.

Hickam’s dictum: Patients can have as many diseases as they damn well please.

The workup revealed a kappa/lambda ratio of 250 to 1. The patient didn’t just have primary hyperparathyroidism. They had primary hyperparathyroidism and multiple myeloma (or MGRS, the bone marrow biopsy is still pending).

The myeloma amplified the hyperparathyroidism beyond reason.

When you see the most dramatic presentation of a common codition, don’t just marvel at its severity, but ask yourself could this be somehting else entirely?

Sometimes Occam loses and Hickam wins.