Robert Albright, DO
An ICU Doc's Take on Kidneys, Hydration, Sodium
Another of the interesting people I’ve coached is Dr. Bob Albright of the Mayo Clinic in Rochester, MN.
Bob’s a Kidney Doc with a specialty in ICU Medicine. If something goes seriously wrong on race day, Bob’s who you want to be treating you.
I called Bob to discuss one of my favorite reads from 2022, Jason Koop’s book, Training Essentials for Ultrarunning1. The book contains a 3x3 matrix (Table 14.4) on athlete hydration and sodium status.
If you have a medical background, and find yourself treating any athlete who may be hyponatremic (article below), Bob recommends you look into immediately giving 100-150 cc of 3% saline solution. Bob notes, “it burns a little going in, but you won’t hurt anyone.”
For the rest us, Dr. Albright has some homework for us.
Learn our sweat rate2 - our rate of loss will change over time and based on the climate we experience.
Learn our absorption rate - sweat rate is only part of our race day hydration strategy. Another important factor is the rate that we can uptake fluids and calories. This needs to be trained and documented. There are a wide range of uptake rates based on fitness and conditions. Pacing strategy must take into account uptake rates, as well as underlying fitness.
Know who we are - as well as tracking net volume losses, know how we perform for a given set of conditions. When conditions are extreme, or fitness unproven, use caution. As Bob told me once… “you don’t want me as your doctor.”
Sodium - we now know endurance athletes don’t need a ton of sodium. Additionally, we know that placing ourselves on, essentially, a high-sodium diet can have negative consequences. When figuring out sodium intake rates for performance, be sure to discuss the health impacts of these rates with your primary care physician.3
That’s the big picture. To get into the detail, I’m going to share four articles that Bob has published previously.
Hyponatremia & Sodium Intake
Hydration
Rhabdo
Late Night Top Ten Kidney List
Hyponatremia, By Bob Albright
Most endurance athletes know a few things about low serum sodium levels (hyponatremia). They know it’s common, they know it is caused by drinking too much water and they know that supplementing sodium will treat and/or prevent the problem. Hmm, well, what we “know” may hurt us.
Actually the incidence of documented hyponatremia among endurance athletes is extremely low. The clinical signs and symptoms attributed to hyponatremia are very diverse, and often (especially with respect to cramping) turn out to be unrelated as the measured sodium levels turn out to be normal. Presuming any unusual symptom we experience during endurance sports is due to hyponatremia may mask other more serious issues.
Many have laid the blame for hyponatremia at the feet of excess water ingestion, often along with inadequate sodium supplementation. While it is true that, as a group, the athletes diagnosed with hyponatremia tended to have ingested more water and were out on course longer, the direct causal link needs to be examined much more carefully.
The human body is a marvelous survival machine. Our species can thrive in deserts, rain forests and most anything in between. While much of our adaptation may be due to our ability to modify our immediate environment, I argue it’s because of our kidneys!
We have an incredible ability to maintain internal balance of blood chemistry. In fact our blood’s density (osmolality) varies by less than 0.01% under physiologic circumstances. Sodium is the principle agent which contributes over 96% of our serum’s density (osmolality). We jealously guard our osmolality via receptors in the brainstem. These osmoreceptors will become stimulated if the osmolality rises even slightly. Think dehydration; a huge salt load; or enough sugar / fat. This will trigger the very powerful stimulus to DRINK. Ingestion of water (if it is absorbed—more on that later) will “dilute” the blood restoring balance. Additionally, the increase in osmolality also triggers the release of a compound known as vasopressin (anti-diuretic hormone- ADH) from the pituitary gland (brainstem). This compound instructs the kidneys to IMMEDIATELY begin maximum urinary concentration via conservation of water.
Vice versa is true as well. If our body’s sodium level decreases even slightly, the ADH will shut off and thirst is abolished. Our kidneys can excrete more than 13 liters per day of water without one single point change in the sodium level!
Whoa! So how in the world does an athlete drinking far less than 13 liters become hyponatremic?
Before we get to that, we need to remember my prior point that we are marvelous survival machines. We regulate the concentration of the bloodstream separately from maintaining adequate organ perfusion. Perhaps the major threat to our existence is low effective circulating volume in our blood vessels. The brainstem and major blood vessels have receptors which respond to low flow states and stimulate the body’s compensatory mechanisms to restore circulation. We maintain this “effective volume” by means of enhancing the cardiovascular system’s efficiency. This occurs via adaptations of heart rate, cardiac pumping volume and vessel tone (ie. opening or constricting of the vessel beds); and the interplay of, you guessed it, the kidneys!
Our kidneys sense delivery of blood flow. When the kidneys are under perfused, they react by triggering increase in blood pressure and sodium retention, thus restoring the normal situation. Vice versa, if we eat a tremendous load of salt—without the low volume issue—we simply excrete the salt! These effects are not guided by blood concentrations of sodium, but by whether or not we need to conserve or release sodium and hence fluid.
But isn’t there any cross over in the system?
A key point in the understanding of hyponatremia among athletes relates to the extremes of physiology which occur. When effective circulating volume declines below a critical threshold (greater than 15 % decrease in volume—which could be due to SEVERE dehydration) stimulation of sodium resorption (via the kidneys), increases in heart rate, enhanced cardiac pumping function and blood vessel constriction occurs. However, the brainstem contributes an additional adaptation, which is a “good news / bad news” situation. Severely compromised effective circulating volume triggers the release of vasopressin – ADH. This is explained by our need to restore the circulation via any means necessary in these dire situations. So, in order to persevere our life (good news) we become hyponatremic (bad news).
Athletes in this situation are very, very dehydrated. Their mucous membranes will be dry; they will have a fast heart rate; and, usually, low blood pressure. They will have lost significant weight from the start of the event.
When this situation occurs, restoration of the circulating volume is mandated ASAP! Usually intravenous saline (0.9%) is the fluid of choice. Once the circulation is restored, the stimulus for vasopressin-ADH release ceases, and the low sodium concentration is quickly corrected by the kidneys as they get rid of all the free water.
OK, so how does this happen to folks who are NOT depleted from an effective circulating volume perspective?
The answer lies in the release of vasopressin- ADH from a “non-osmolality” stimulus. Fear, pain, nausea, vomiting, shortness of breath (in general - all significant physiologic stressors) are potent causes for release of vasopressin and ADH!
Medical professionals call this SIADH (syndrome of inappropriate antidiuretic hormone). To make maters worse, non-steroidal anti-inflammatory drugs (NSAIDs) block water excretion hence - making the sodium concentration even lower. Additionally, certain medications such as the commonly-prescribed Selective Serotonin Reuptake inhibitors (SSRI drugs for depression) are well documented stimulators of vasopressin- ADH release!
The symptoms of confusion, vision changes, lethargy, weakness and headache are no less evident than among the athletes with VERY low volume but its cause and treatment are vastly different.
So, take one part anxious athlete, one part going a bit too hard (or too long), add pain, nausea and maybe too much water –like fluids on the course and viola! Hyponatremia.
This is by far the most common scenario seen at endurance events. The treatment for these type athletes is hypertonic (very dense, high osmolality, 3%) saline IV solutions. These solutions are required to “overwhelm” the kidney’s tendency to retain water, while using the kidney’s natural tendency to excrete the sodium load. The kidney does not need to save the sodium; given the absence of low effective circulating volume.
Drinking water alone does not cause this problem, nor can it simply be remedied by eating lots of sodium. An issue which is often ignored is the rate of absorption of both water and solutes (anything suspended in the water). During intense muscular exertion, blood flow is preferentially sent to the muscles. This leaves less for digestion and fluid/solute absorption. Therefore assuming ingestion of a certain amount of sodium or water will get taken into the circulation is an uncertain assumption at best.
What is the athlete to do?
1. Be as well trained for the upcoming event as possible.
2. Match your expectations (and pacing) to your training.
3. Be as acclimatized to the environment as possible.
4. When nausea, or other “digestion problems” occur, slow down, allow the gut to regain function.
5. Replace your sodium losses: note each liter of sweat has only 40-80 mmol/liter of sodium, at most. For most of us, 200-400 mg. sodium per hour is more than sufficient (assuming we are absorbing it).
6. Avoid severe dehydration (seems a no brainer—but see above) water only may be fine for shorter events (< 90 min. or so).
7. NO NSAIDs!
8. Caution - ask your physician about SSRI agents and endurance activities.
9. Weigh yourself prior to your event and write it down on you race number—this will help guide the medical personnel to give the correct therapy if you do develop hyponatremia
10. Get tested: If you have experienced serious hyponatremia (or think you have), it’s worthwhile to see a physician who may order an electrolyte (blood chemistry) screen during a race simulation workout. This can be facilitated by having a prescription written for the blood testing, which can be given to the lab personnel at the testing facility (often a lab at a hospital) at your convienience. If hyponatremia is confirmed, a more thorough evaluation is warranted. Your physician may even wish to check specific urine chemistries, as well as, serum adrenal and thyroid function testing.
I do need to emphasize, not all unusual symptoms we experience during our events are hyponatremia-related, and getting a cause and treatment sorted out is well worth it.
Hydration, By Bob Albright
Water, water everywhere, but not a drop to drink
Water, water everywhere and all the boards did shrink…
Many of us are products of a liberal arts education and recall these lines from a poem about a guy on a boat, for whom the bell eventually tolled (apologies for mixing two macabre poems). He most likely succumbed to a fate many of us can relate to, albeit on a much less severe scale. He likely met his end due to dehydration. Remember that to compound matters, he chose very poorly when he eventually drank from the sea.
Huh? Has the nephron guy gone round the bend due to high altitude, stress-induced delirium?
Maybe.
But first let me do my best to explain a central physiologic concept near and dear to all our hearts (and brains, muscles and other non-beating organs): osmolality and how it relates to the need to drink, prevention of dehydration and maintenance of general health (thus avoiding the Ancient Mariner’s fate).
Osmolality is generally defined as the amount of solutes, or particles (dissolved substances) per unit of volume measurement. It can be thought of as how dense a solution is. Osmolality becomes critical to us as multicellular organisms as our cells are encased by membranes which have the peculiar characteristic of being permeable to water. What this means is many of our body’s cells can behave like the science experiment we all did in school where we had a container of water separated into two compartments with a cellophane membrane (permeable to water but not salt) separating the compartment. As salt was added to one side of the membrane, the water level rose in the sodium side. Ah yes, osmosis.
We may even determine the forces driving water one way or another depending on the differences between osmolality inside of cells versus outside the cells. The area outside cells is either the bloodstream or the space between cells also known as the interstitum. Water will generally move easily from inside to outside of cells, or vice versa, based largely on these density or osmolality changes (forces).
This becomes a critical issue when we remember that if brain cells become swollen, they will put pressure on their neighbors and as there is no room to expand inside our brain cases (skulls) this leads to compromised blood flow due to internal skull pressure exceeding the blood pressure -- no blood flow = very bad. A negative pressure, for example if the bloodstream is more dense than the cells, will lead to water leaving the cells and cell shrinkage. This causes the cells of the brain particularly to tear away from their nerve connections -- known as myelinolysis. This is a disastrous consequence of severe dehydration and is a proximate cause of death.
How do we protect ourselves from this fate?
We maintain an osmolality of 286 mOsm/L within and outside of our cells at all times. This is accomplished with the input of two important systems: our “osmoreceptors” located in our brainstem and the contribution of our kidneys. Actually, the kidneys are really only responding to a signal from the brainstem -- vasopressin (AKA anti-diuretic hormone or ADH). ADH is released by the brainstem under influence of rising bloodstream density (osmolality) which in turn directly triggers thirst and facilitates the kidneys retention of free water. This results in decreasing the density back to normal. Conversely, with excess intake of water, no ADH is released and our kidneys excrete the excess water very quickly.
The capacity of our bodies to handle these extremes is illustrated best by understanding that we can drink up to 14 liters or as little as a half liter and still maintain internal balance.
So, how much do I need to drink?
A simple answer may be, “listen to your body.”
More specifically, we need approximately one liter of water per day for usual respiration, and “life.” This amount increases with fever, low oxygen levels (due to increased breathing rate) or excess perspiration -- the latter being certainly familiar to all of us during racing season. Tried and true methods of determining sweat rate are well known and are effective. Drinking beyond these needs simply kicks in the compensation of our kidneys getting rid of the excess water.
Can what I drink (or eat) be too dense?
No, this does not occur under normal circumstances (that is, ingestion of food with access to water or other liquids). When we eat something dense, it is absorbed (after a bit of digestion), we become thirsty and the ADH mechanism kicks in and all is right with the world. However, when we race, we are sending the blood to the musculoskeletal system, slowing digestion. As our nutrients lay in the stomach and intestines they exert the osmotic force described above -- resulting in the athlete’s nemesis bloating, sloshing or even nausea, vomiting or diarrhea. Many sports drink manufacturers have recognized this and tailor their products to prevent this by keeping the osmolality (density) below that of our bloodstreams (<300 mOsm/L). Diluting the nutrients we take in will work as well -- a big sip of water with that gel please.
How come the Ancient Mariner died, and what’s the deal with drinking seawater?
The osmolality of seawater is >2000 mOsm/L, which explains why ocean swims with the inevitable drink from the sea can be such a problem from a nausea perspective for athletes.
So, here’s hoping that that bell never tolls for thee.
Rhabdo, By Bob Albright
Looking at the title, you might think this is about a Vietnam-era special forces dude who’s been wronged, but it’s actually about what can be a life-threatening medical condition. There has been a lot of interest in this condition recently in the mainstream media. Are endurance athletes at risk?
Rhabdomyolysis (aka Rhabdo) is the medical term for the destruction of muscle tissue. This is not your average delayed onset muscle soreness (DOMS), nor is that nagging pain you feel in your quads after a huge load of eccentric stress. This is the actual death of muscle cells (myocytes) causing the release of the compound myoglobin and other muscle cell constituents into the circulation.
Muscles are bundled together and encased in connective tissue sheaths. When cell death occurs, the muscle units will swell, which is a dangerous situation, leading to high pressure within the muscle sheaths. This high compartment pressure may lead to even more damage due to ischemia as the high pressure exceeds blood pressure and more destruction ensues. This situation requires attention immediately, as with a surgical procedure the muscles can often be saved.
Elevated amounts of myoglobin in the blood (myoglobinemia) will lead to high amounts of myoglobin being filtered through the kidneys and into the urine (myoglobinuria). Herein lays one of the major dangers: sudden kidney shutdown, known as acute kidney injury (AKI).
AKI leads to metabolic derangements which range from mild to immediately life threatening. High potassium level (hyperkalemia) represents the worst complication, as it may lead to cardiac standstill.
Causes of rhabdomyolysis are myriad, and can be grouped into ischemic (insufficient blood flow), traumatic (crush injury), inherited, infectious and toxic/metabolic.
As endurance athletes I think it’s worth focusing on a few issues.
Heat or cold stress: Both extremes of temperature can be deadly to our muscles. Heat stroke is just as dangerous as frostbite.
Trauma: Not only do we need to keep the rubber side down and stay away from collapsing buildings, but do not forget the infamous scene from Caddyshack where the clergyman is having the best golf game of his life… in the thunderstorm…
Toxins/Drugs: This is not a big one among the clean-living types reading this, but excess alcohol, cocaine, amphetamines and snake/scorpion bites (rattlers mainly) all have colorful associations with athletes and rhabdomyolysis. Very rarely, high dose statin therapy has caused rhabdomyolysis. This risk is increased with certain drug combinations (gemfibrozil, amlodipine and a statin as examples).
Metabolic: The nemesis of the endurance athlete -- hyponatremia, low phosphorus levels (rare, but typically due to nutritional disorders along with alcohol abuse), and low potassium levels have been associated with rhabdomyolysis. Do not forget the major cause of hyponatremia is the body’s excess production of antidiuretic hormone, which is in turn stimulated by extreme stress and inhibited by prostaglandins. ADH leads to the kidneys saving water and diluting the body’s sodium level…
Blah, blah, blah… so what? Well, NSAIDs block prostaglandins, so, NSAIDs increase your risk for hyponatremia. When low sodium is caused by extreme dehydration, NSAIDs also prevent the body from opening up critical vascular beds, perhaps taking a muscle injury right past nagging ache to muscle cell death. There are many other metabolic issues one can explore with the wonders of the interwebs as well.
Inherited: Some folks inherit unusual changes in how cells use oxygen and fatty acids (mitochondrial defects) which manifest themselves as muscle cell death with exertion. This is not usually subtle, but depending on the person’s prior activity level, an unusual effort may lead to a rhabdomyolysis episode. Those with sickle cell disease (a blood disorder) need also to be cautious with exertion associated with possible dehydration, as these stresses lead to sickle crisis.
How do we prevent this?
Prevention is clearly the usual answer to most medical conditions. Dialing in your training, nutrition and fluid strategy is critical as well. So, as I’m mentioned in past columns, NO NSAIDs and be sensible about training in extreme weather.
How is it treated?
Much depends upon the severity and any complications that develop. Oral or IV fluids may be sufficient, but occasionally, hospitalization and even surgery may be required.
How will I know if I have it?
Keep an eye on your urine character and quantity. Cola-colored urine is never normal. This should prompt rest, fluids and a call to your provider if your urine does not clear within hours. Severe muscle pain accompanied by swelling of the extremity or discoloration of the painful area or signs of poor blood supply to the limb downstream should prompt you to go to the ER or med tent ASAP! Many times these situations are associated with feeling extremely ill in general as well. Get help! Dehydration and low blood pressure can make this bad situation worse.
Late Night Top Ten Kidney List, By Bob Albright
Since I’m on call these two weeks and indeed, doing this late at night, I think I’m okay on the title. What are the top 10 things you can do to prevent ever seeing the likes of me in a professional encounter?
Your kidneys are responsible for maintaining the internal metabolic control of electrolytes, acid/base, volume status, blood pressure, hormonal status (vitamin D and EPO) and management of waste products. When your kidneys are failing, there is not a single system in the body which is not impacted.
How can one keep the kidneys healthy?
[cue the Late Night Orchestra]
Number 10: Stay wet. Do not walk around dehydrated all day long. We don’t need to be guzzling back dozens of bottles a day, but keep the urine a pale yellow color and drink when you are thirsty. Chronic dehydration leads to a myriad of kidney problems.
Number 9: Get checked out if you are having trouble getting the stream started or stopped, or you seem to have trouble emptying your bladder. Don’t let the “plumbing” ruin the processor.
Number 8: Don’t blow off blood in the urine. This seems a “no brainer” but you’d be surprised. It is very important to sort out the source of any urinary bleeding.
Number 7: Know your family history. One of the most common inherited conditions out there is autosomal dominant polycystic kidney disease. Ask your folks!
Number 6: Take your medications, especially for hypertension. If you are having side effects, let your provider know as, most times, an alternative is possible. Hypertension is the number one kidney killer!
Number 5: Do not smoke. Smoking is an independent, powerful risk factor for development of both cancer of the kidney and urinary tract as well as kidney failure. If you do smoke, let someone help you with quitting. You are up against an empire of doom with nearly limitless resources -- enlist some allies!
Number 4: Stay Lean. Overweight means higher blood sugar and blood pressure. Diabetes is the second killer of kidneys -- and the majority of diabetes is preventable by being lean.
Number 3: Be very careful with non-steroidal anti-inflammatory agents (NSAIDs). While these agents are quite beneficial for many with normal kidneys and pain/inflammation, they have a dark side. Their ability to decrease pain and inflammation are directly due to blockage of prostaglandins. However, prostaglandins also open blood vessels. So, do not use these agents if you are engaging in an activity where good blood flow may be important. I need to also point out the tendency of these agents to amplify or even cause low sodium levels (hyponatremia). Maybe acetaminophen is a good option to consider?
Number 2: Get a fasting blood glucose level. As I said before, most of type 2 diabetes is preventable. Often, knowing that you are at risk (if the glucose level is greater than 100) is a powerful motivator for lifestyle changes.
And the number one way not to have one of my ilk as a doctor...
Get your blood pressure checked. Hypertension is the number one leading cause of kidney disease in our country. It is silent and it is deadly. Get checked, if it’s high, there are many effective strategies to achieve goal blood pressure. Most of these are not even medications. Your goal: keep the systolic (upper number) less than 120 and the diastolic (lower number) less than 80.
Perhaps the most frustrating aspect of my chosen field of medicine (nephrology) is most of the patient’s problems were, at least at one point in the past, preventable. I do not do frustration well, you might not like me when I’m frustrated…
Here’s to us never meeting.
Back To Table of Contents
If you buy Jason’s book then the first thing to do is open to Page 328 (2nd Edition) and read… Avoid These Things. There’s four things to avoid: (1) low energy availability, (2) hard workouts when fasted/depleted, (3) hard workouts at the end of a long run and (4) long runs without fuel. It’s a running book so insert your own sport when you read this outstanding section.
Simple test for you on Page 300 of Jason’s book. Personally, I do pre/post weigh-ins for a variety of sessions to track my losses. I also track my morning weight over time as chronic dehydration can arrive gradually during the summer months.
If you’re looking for guidance on sodium intake rates then see Page 301 of Jason’s book. Separate from intake for athletic performance, be sure to discuss your strategy with your Primary Care Physician.
This should be a required read for all involved in endurance sports. Thanks