Hyponatremia: You Ain't Worth the SALT in My Tears

In this podcast, Dr. Kimberlee Thielen, an internal medicine physician and nephrologist with Kidney Specialists of Minnesota, discusses hyponatremia, more specifically a water balance issue.
Enjoy the podcast!
Objectives:     Upon completion of this podcast, participants should be able to:
Define how sodium effects the body.
Identify signs and symptoms of hyponatremia.
Explain the 4 goals for hospitalized patients with hyponatremia.
Select proper treatment modalities for individuals with identified hyponatremia. 
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SHOW NOTES:
CHAPTER 1: When we are talking about hyponatremia we are not talking about Na+ problems but rather a water balance issue.
The normal amount of Na+ in the plasma water is usually 136-142 meq/L.
The body's Na+ balance is important for volume regulation which is controlled by renin angiotensin/Aldosterone system. This is different than the body's water balance which is maintained by antidiuretic hormone (ADH).
Normal physiology of water balance requires ADH which involves the hypothalamus-post pituitary and the kidneys.
To understand hyponatremia you need to first understand the physiology of water balance and where ADH is produced. ADH is produced in post pituitary and released by 2 physiologic stimulators: (1) elevated serum osmolality, (2) decrease circulating volume.
The majority of serum osms are made up of sodium. When your Na+ is high there are osmoreceptors in your hypothalamus that sense increased extracellular serum Na+ which synthesizes ADH which is released once again from the post-pituitary.
The posterior pituitary can also synthesize ADH 2nd low volume status regardless of serum osmolality.
Parasympathetic response from left atrium, aortic arch & carotids sense the low volume status or volume contraction with decrease arterial blood flow thereby stimulating a vagus nerve response which leads to the posterior pituitary releasing ADH.
ADH once released acts at the renal collecting tubule via cyclic AMP which inserts water channels called aquaporins in the collecting tubules flowing via the medullary interstitial osmotic gradient. Next water moves from the intratubular space to the medullary interstitial space thereby concentrating the osmolality. So the further you travel through the kidney more water is removed from intratubular space to medullary interstitium concentrating the urine.
A normal healthy person can concentrate their urine upwards of 1200 milli osms and dilute it to around 60 milli osms, which narrows as we age, likely to nephron drop.
We all tend to lose some GFR as we age.
Nephron Drop Out attrition of nephron units that scar up generally due to athrescleortic disease.
ADH- insert aquaporins into collecting tubules - based on osmolality of urine and interstitial water will flow down the osmotic gradient through the aquaporins. Collecting tubules as they go deeper into the kidney the medullary interstitial osmotic gradient increases. The water that is reclaimed is through a complex peritubular capillary network returning to the venous system.
CHAPTER 2: Hyponatremia in most patients is going to be hypo-osmolar hyponatremia.
When talking about hyponatremia we are generally talking about a serum Na+ less than 135 mew which once again is a water balance issue.
Most cases of hyperosmolar hyponatremia are clinical relevant and usually caused by hyperglycemia, prostate or uterine surgery, glycine, sorbitol, mannitol, IVIG. You get an increased osmolar state in the blood which pulls water from intracellular space leads to hyponatremia.
Pseudohyponatremia are iso-osmolar and generally a laboratory artifact. Can have your lab run serum Na+ via direct ion selective electrode measurement to obtain true Na+ level.
What is hypo-osmolar hyponatremia? Causes are divided into 3 categories: (1) water intoxication, (2) SIADH, (3) volume stimulated ADH.
You can differentiate by 2 urine tests: Test #1- Urine Osmolality which we would expect to be low or max dilute.  Test #2 is Urine Sodium.
Water Intox - The urine Osms are maximally dilute.
SIADH and Volume stimulate ADH urine osms not max dilute. Urine sodium is low in volume stimulated ADH and generally >40 meq per/L in SIADH. Which is due to the kidney seeing itself as euvolemic. So this will cause the release of sodium into the urine.
In volume stimulated ADH the kidney perceives itself ischemic or underperfused. So the urine Na+