Category: Tweetorial

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New Tweetorial: Comparing diffusive versus convective clearance

I have been workshopping this one for awhile in my mind and today I carved out a few hours to create it.

It starts here

Part of the inspiration for this came from an epic message on the Channel Your Enthusiasm back channel by Roger Rodby

Here is the draft of the script.

Diffusive vs Convective clearance

I was teaching the third year medical students about acute kidney injury and the lecture begins with a brief history of extracorporeal dialysis for AKI. And I asked a student what extracorporeal dialysis was, and he correctly identified it as “dialysis outside the body.”

Since the ironclad law of the Socratic Method is that every correct answer is rewarded with another, harder, question, I replied, “Can you think of any example of intracorporeal dialysis?” The right answer is peritoneal dialysis, but he said , “The kidney?”

And off on a tangent we went…
Does the kidney even do dialysis? No. The kidney does not use diffusion to clean the blood. Clearance is provided by convection at the glomerulus. Plasma is squeezed through the slit diaphragms of the podocytes in the glomerulus but besides the lack of protein, the solute composition on both sides of that membrane is essentially identical.

The kidney does not clear the blood by diffusion, the defining characteristic of dialysis, but rather by convection. How does that work? Glad you asked. Take Creatinine. The creatinine on both sides of the podocyte is the same, 4.4 mg/dL in this example.

4.4 mg per dL x a GFR of 25 mL per minute x 1440 minutes in a day divided my 100 mL in a dL comes to 1584 mg of creatinine filtered.

That is just about the amount of creatinine produced by a typical person a day. 

So convective clearance can clear all of the creatinine produced everyday, the additional creatinine secreted in the proximal tubule is just gravy. 

What about sodium? 

138 mEq/L x a GFR of 25 mL per minute x 1440 minutes in a day divided by 1000 mL in a L comes to 4968 mE of creatinine filtered. 

This is a problem since we only consume around 100-200 mEq of sodium a day. So this where the tubules earn their stripes by reabsorbing all the excess filtered sodium to keep us from peeing ourselves to death.

So these two examples demonstrate an important principle of convective clearance, it is better for clearing things at a high concentration than at a low concentration. In fact, a GFR of 1 is enough to clear a typical sodium daily load.

138 x 1 ml/min x 1440 min/day divided by 1000 ml/L = 198 mEq/day

This why even a tiny residual renal function makes a huge difference in dialysis patients. 

But that same GFR of 1 would only clear 

4.4 x 1 ml/min x 1440 divided by 100 ml/dL = 63 mg of creatinine only about 4% of the daily creatinine load.*

*This calculation is highly dependant on the serum Cr concentration, which would be a lot higher than 4.4 if the GFR was 1, but since a GFR of 1 in incompatible with life, the patient would also be getting renal replacement therapy, so it is hard to know where the serum Cr would actually be.

So after explaining that the kidney didn’t actually do dialysis, or anything remotely close to dialysis. I asked if there was an organ that did do dialysis? Or, more specifrically, used diffusion for clearance.
Answers from the crowd: 

Liver > nope

Spleen > nope

Skin > nope

And finally, Lung? Yup.

The lung clears carbon dioxide from the body and absorbs oxygen by setting up a setting where the gasses move down their respective concentration gradients across a semipermeable membrane. You know, like dialysis.

A ventilator is not really like an artificial lung, in the way a dialysis machine replaces the core function of a kidney. It provides flow, but no clearance. We still are dependent on the alveolar membrane for oxygen absorption and carbon dioxide clearance. 

But ECMO is an artificial lung and fully replaces the alveoli and uses the principles of dialysis to clear carbon dioxide and move oxygen into the blood. So at some level, ECMO is closer to the lung than dialysis is to the kidney. 

One final note on this thread is in regards to dialysis and convection. The kidneys work by convective clearance but our primary means of replacing them is by diffusive clearance. However this summer we saw a randomized controlled trial of modifying dialysis to use convection rather than diffusion…and the result? Significant reduction in total mortality. 

We don’t get a lot of wins in dialysis, so when we get one, we pay attention.

The script isn’t exact because I have to do some edits to meet the character limits of tweets.

Here are the Keynote slides that I used to create the gifs.

Diffusion v Convection
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I don’t come to laud the urinary anion gap, I come to bury it

While preparing for the electrolyte session for Epic Pathshala I added a new twist. For the first time I added the concept that Jaime Uribarri has been shouting for the last few years regarding the use of urinary anion gap. I first saw Dr. Uribarri at NKF Clinical at Boston in 2022. He gave a great lunch-time presentation on the utility (more specifically, the lack of urility) of urine anion gap. Perfect counter programming to Richard Sterns’ lecture on managing electrolyte disorders with the assistance of the BUMP (basic urine metabolic panel) (NDT).

Dr. Uribarri’s thoughts were crystalized in two recent articles:

  1. The Urine Anion Gap: Common Misconceptions
  2. Beyond the Urine Anion Gap: In Support of the Direct Measurement of Urinary Ammonium

The tweetorial can be found here:

Part One

Part Two

Here is my rough script that I use to write the tweets

This is going to be a long arc and it has a point but it is going to take a bit to get there.  #Tweetorial #MedThread #Electrolytes #AcidBase 1/11

Let’s start with acid base balance. Metabolizing proteins, specifically the sulfur containing amino acids, methionine and cysteine, generates hydrogen sulfide (H2S). This acid cannot be cleared by the lungs. #OnlyTheKidneys can clear this acid. 2/11

This acid load, generated by normal metabolism that must be excreted by the kidneys is the daily acid load. When patients with advanced CKD develop progressive metabolic acidosis it is because they are failing to clear the daily acid load. 3/11

On a “western diet” (I.e. carnivorous diet) it is about 50-100 mEq of acid (H+ ions) a day. 4/11

Boy it would be easy if we could excrete this as free hydrogen ions, alas that would require a urine pH of around 1 (50 mEq H+ in 2 liters of urine). At a minimal urine pH of 4.5, we would need to make 1200 liters of urine a day to clear the daily acid load. 5/11

So the kidney has to smuggle the hydrogen out as something other than free hydrogen. There are two solutions to this:

  1. Titratable Acid
  2. Ammonium 6/11

Titratable acid is just H2PO4–. Most of the daily acid load is excreted this way. The problem is that it is fixed by phosphate intake. We cannot manufacture new phosphate open the spot when we encounter a large acid load, so we cannot ramp up phosphate excretion to deal with an acid load.** 7/11

**Actually that is not entirely true. In addition to the serum bicarbonate, the bones are called upon to buffer an acid load. And as they are dissolved buffering acid (not an ideal state) they release phosphate which clears the acid from the body. 8/11

So when faced with a large acid load we call on system two: ammonium. The physiologists have two models for how this works. In one the production of NH4 from glycine produces two bicarbonate, the other urinary NH3 accepts a hydrogen ion to form NH4. 9/11

We’ll let the physiologists argue over these two models, for our purpose the only thing you need to know is that a healthy renal response to acidosis is an increase in urinary ammonium to excrete the excess daily acid load. 10/11

The problem comes from the fact that when you order a urine ammonium the labs tells you to pound sand. They won’t do it.They can use the same instrument they use to measure serum ammonia (though they would need to dilute the urine sample 40:1). Because the lab wouldn’t measure urine anion gap lead to 40 year distraction called the urinary anion gap… 11/11

Okay, on to part two. 

Let’s review, the kidneys excrete 50-100 mEq of H+ ions every day as what we call, “The daily acid load”

Most of the daily acid load is excreted as H2PO4–, AKA Titratable acid

An insignificant < 1% is excreted as free hydrogen and that can be detected as urine pH.

And most importantly, for our purposes, in the face of an acid load, that excess acid is excreted as NH4+ 1/

Clinical labs generally refuse to measure urinary ammonium so doctors have been forced to scramble to find ways to “estimate” urinary ammonium. 2/

In 1986 electrolyte legend, Mitch Halperin published this paper which discovered an amazingly tight correlation between urinary anion gap and urinary ammonium.  3/

This makes sense. The typically measured urine electrolytes are sodium, potassium, and chloride. If there are a lot of positively charged ammoniums in the urine, the urine chloride better increase to balance those cations out. Can’t have people peeing sparks. 4/

Discoveries are made in JCI, but standard of care changes with NEJM. And sure enough, 2 years later, NEJM published this “proof” of the urinary anion gap. What an amazing time that the NEJM would publish 60 person physiology studies 😍 5/

So for forty years this schema ruled the nephrology wards.

Patients with non-anion gap metabolic acidosis would have urine electrolytes checked in order to see if their kidneys were responding appropriately. 

A negative urine anion gap indicated a rich supply of urinary ammonium indicating a healthy renal response and would direct physicians to look to the gut for the cause of metabolic acidosis.

A positive urinary anion gap indicated a kidney that was unable to excrete excess ammonium and suggests a diagnosis of distal or hyperkalemic (type 1 or 4) RTA. 

But a few years ago Dr. Uribe began making noises that this whole urinary anion gap went against fundamental laws of nature. Na,Ley that urinary na, k, and cl are not there to merely balance charges but that their urinary excretion is dependent on dietary intake.

Uribe pointed out that patients would have volume depletion(due to extra-renal sodium losses) and as a result would lower urine Na, resulting in the negative gap. Similarly in the healthy controls ion Batille’s study, they had been loaded with oral NH3Cl. The excess chloride he argues would make the urinary anion gap negative. 

He then points to studies of DKA, respiratory acidosis, and systemic acidification that all result in increases in urine ammonium but do not make the urine anion gap more negative.

And here is the Keynote presentation I used to generate the images

Keynote

PowerPoint

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Adding more meetings to the meeting

Kidney Week is approaching. After a two year hiatus we are going to meet in person again in less than a month. I am very excited. NephJC and the NSMC will have a great presence and it should be fun.

You can take a peak at the line up here: #NephJC is going to be busy at #KidneyWk. Join us!

But I think ASN and the Kidney Week planning committee could be doing more to increase engagement. To make the event more fun.

I took a crack at it in this tweetorial

Modest proposal for @ASNKidney #KidneyWk.

Sunday is the least attended day of the conference. It is a half day and most people leave that morning and miss the whole day.

Sunday’s Plenary session should begin at 9 not 8 to encourage people to go out and socialize Saturday night and to make room for…

7:30 AM Sunday have 5k run/walk. Do a different kind of social event. Raise money for a local charity. Let nephrologists form teams. @VUMCKidney team. @arkanalabs @goKDIGO all could have shirts and shared a moment.

These national meetings need to move past charging hundreds of dollars for slideshows and be more about being with your people.

Originally tweeted by Joel M. Topf, MD FACP (@kidney_boy) on October 12, 2022.

There are 41 sessions on Thursday.

41 on Friday

30 on Saturday

and 8 on Sunday

Adjusting the schedule on Sunday truly is a model proposal. I would love to see ASN try some new ideas at Kidney Week.

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Another hyponatremia Tweetorial

This was a great case. The full the tweetorial is unrolled below.

🧂 Hyponatremia #CaseReport #Tweetorial

(and a gif for the people who want to rename this hyperhydronemia)

Chug Water GIF

Patient came to the hospital with abdominal pain, nausea, and vomiting. Patient has alcohol use disorder. Last drink was about a day prior to admission.

After arrival to the ER the patient has a seizure.

gross james van der beek GIF

Besides the weirdly elevated anion gap, and the hypokalemia, the initial labs just show some AKI. I don’t have an ABG but I suspect combined metabolic alkalosis and lactic acidosis.

This can be demonstrated by looking at the Delta Ratio which compares the change in bicarb to the change in anion gap. The ratio should be 1. If it is less than 1, there is an additional non-anion gap metabolic acidosis, > 2 additional metabolic alkalosis

A delta ratio of 6 is crazy high.

Kate Mckinnon Snl GIF by Saturday Night Live

A related calculation, called the “bicarb before” can tell you the serum bicarb without the anion gap acidosis, so if the patient has two disorders it allows you to look at the metabolic alkalosis (or non-anion gap metabolic acidosis) without the anion gap metabolic acidosis.

The “bicarb before” comes to a mostly unbelieable serum bicarb of 60.

But the reason I was intrigued by the case are the next two labs that come 10 and 20 hours after the initial labs…The sodium drops to 125 despite getting 150 an hour of 0.9% NS and the patient making 3600 ml of urine.

Additionally the full force of the metbolic alkalosis is revealed with the bicarb shooting from 29 to 41. I suspect this is due to vomiting. The urine chloride < 20 is consistent with this. This is Cl responsive metabolic alkalosis. It will (eventually) respond to the NS.

The urine also has a massive anion gap, around 90. What is the unmeasured anion?

(BTW the answer is bicarbonate)

But what is driving down the sodium? The patient appears volume depleted, and the steadily improving serum creatinine points to a patient with pre-renal AKI.

In volume depletion hyponatremia, giving fluid improves the serum sodium, it doesn’t make it worse. Also these patients do not typically make 3600 ml of urine

In it is highly unusual to make that much urine and have the sodium fall, usually that kind of urine output is associated with arising sodium. A hint to what is happenning can be found in the electrolyte free water clearance (Clefw).

The high urine sodium and really high urine potassium makes the urine essentially isotonic to plasma. Even though the patient is making 3.6 liters, it is like taking ladles of soup from a big pot, no matter how many ladles you take out it doesn’t change how salty the soup is.

pot wo GIF

Because the electrolyte free water is close to zero, those 3.6 liters of urine are not afffecting the serum sodium at all. So why is the sodium falling? I suspect this is due to the patient drinking (unrecorded) water.

So what would you do if faced with a falling sodium in a volume depleted patient?

I chose Tolvaptan plus continued 0.9% NS at 150/hr. The following day, the labs look…better.

I think this patient had nausea induced ADH in addition to severe metabolic alkalosis and volume deficiency. I found it interesting.

Originally tweeted by Joel M. Topf, MD FACP (@kidney_boy) on July 30, 2021.

What I loved about it is that the full lab interpretation required six different equations:

  • Anion Gap
    • the rare case of a relevant anion gap despite an increased serum bicarb
  • Gap Gap analysis
    • First the Delta Ratio
    • Then the Bicarbonate Before
  • Urine chloride in metabolic alkalosis
    • <20 mEq/L is chloride responsive
  • Urina anion gap
    • People think it is just for RTAs…not true
  • Electrolyte free water clearance

And I got great comments from Twitter. Some highlights:

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Hyponatremia tweetorial

This is a basic approach to hyponatremia. (link if you would prefer to see the tweets on twitter)

1/ This is like the Bat Signal for me… #Tweetorial #Hyponatremia #LoudlyForThePeopleAtTheBackOfTheRoom

https://twitter.com/tonlajr/status/1304011343226437637
Batman Michael Keaton GIF

2/ The first question in hyponatremia is…

👏Is👏the👏patient👏seizing?👏

If you have a patient with cerebral edema from acute hyponatremia you need to 3% Saline first and ask questions later.

Matthew Smith Doctor Who GIF

3/ If patients have hyponatremia and have severe symptoms it is 150 ml of 3% then recheck the sodium and give another 150 ml of 3% (I’m using the European guidelines)

https://eje.bioscientifica.com/view/journals/eje/170/3/G1.xml

3b/ Be careful with vomiting there 👆🏻

This means if the hyponatremia is causing the vomiting, then you have severe symptoms and it is 3% time. But if the vomiting is causing the hyponatremia, that doesn’t automatically indicate severe symptoms and you will need to dig deeper.

4/ The goal of acute mgmt is to raise the Na by 5 or stop the symptoms, which ever is quicker. If you have raised the Na by 5 and they are still seizing, then it is probably not the low Na causing the seizure and you need to 👀 deeper. Algorithm from

https://eje.bioscientifica.com/view/journals/eje/170/3/G1.xml

5/ But when @tonlajr asked about the approach to sodium he wanted to know abot dx, not acute mgmt so…onward to diagnosis!

Glory Roomba GIF

6/ I am goin to be walking you through this algorithm:

https://twitter.com/hashamsarwar/status/1304476073627914240?s=20

Step one check the serum osmolarity (and get a repeat sodium, just to make sure it wasn’t a lab error)

7/ Since we are looking at a low sodium we expect a low osmolarity (don’t worry about the difference between osmolality and osmolarity, anyone who is a stickler about that is being a dick)

If we don’t find a low osmolality something weird is going on:

7b/ Low sodium with a normal osmolarity: Lab error from too much protein (IVIG, multiple myeloma) or too much fat (High lipids or triglys) in the blood. This throws off some lab machines.

(Specifically but not point of care iStats or ABG laboratories)

7c/ Low sodium with a high osmolality: this is usually due to hyperglycemia (but can be seen with mannitol, glycine and other edge cases). The hyponatremia is real, but due to another osmotically active particle (glucose in most cases) the are no consequences to the hyponatremia

7/d It is not as simple as that (it never is).
Read this manuscript journal📖: https://pubmed.ncbi.nlm.nih.gov/26002851/
or listen to this podcast🎧:

EMCrit 242 – ED Nephrology with Joel Topf aka KidneyBoy

8/ So that leaves the true hyponatremia. Low sodium and low osmolarity. The branch point here is:

What is the urine osmolarity?

The urine osmolarity tells us if the kidney is causing the hyponatremia or just unable to correct the hyponatremia (despite the best intentions)

9/ The urine osmolarity is less than 100 (maybe up to 150 or 200 if the patient has CKD). This indicates a lack of ADH and a kidney that is doing its best to correct the hyponatremia. The problem is not the character of the urine but the amount. Right urine, not enough.

9b/ The differential for low sodium, low serum and urine osmolarity is short:

• Oliguric kidney failure
• Tea and Toast
• Beer Drinkers potomania
• Psychogenic polydipsia

* Recovering from volume depletion hyponatremia

9c/ In low Na, low serum and urine osmolarity the urine is getting rid of excess water but the kidney cannot make enough urine because:

• Kidney failure (low GFR)
• T & T / Beer drinkers (lack of solute)
• Psychogen polydipsia (you are drinking faster than you are peeing)

10 Low sodium, low serum osm, high urine osm. This is ADH dependant hyponatremia. The kidney, stimulated by ADH, is causing the hyponatremia by generating free water. Making more urine here, just makes the Na fall further.

10b/ ADH can be 𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝗶𝗰 due to low volume or a perceived low volume state:

Low volume states: GI losses like diarrhea or vomiting; renal losses like diuretics

High volume/low perceived volume: heart failure, liver failure, nephrotic syndrome

10c/ ADH can be 𝗻𝗼𝗻-𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝗶𝗰 (euvolemic):

Adrenal insufficiency
Hypothyroidism (probably doesn’t exist, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470237/)
SIADH (it’s usually this)

10d/ To differentiate these you can try to use a physical exam to determine volume status but doctors suck at it.

https://pubmed.ncbi.nlm.nih.gov/3674097/

10e/ Instead (or in addition) Check urine sodium and serum uric acid:

Urine sodium low, uric acid high in hypovolemic and hypervolemic hyponatremia

Urine sodium high and uric acid low in euvolemic hyponatremia

Originally tweeted by Joel M. Topf, MD FACP (@kidney_boy) on September 12, 2020.

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Mini-Tweetorial on Metformin Associated Lactic Acidosis (MALA)

How small can you make a tweetorial? This one is only 5 tweets.

A lot of patients are on metformin and a lot of people get lactic acidosis. One does not always cause the other.

But in this case I think the metformin did cause the lactic acidosis. The patient did not have sepsis. There wasn’t any dead bowel, shock, or other typical cause of lactic acidosis. And thanks for asking, the thiamine was normal, they were not being poisoned with arsenic. No aspirin toxicity. No malignancy causing an occult type B lactic acidosis.

They had acute tubular necrosis causing acute kidney injury.

The lactate was sky high

Perfusion was intact. Blood pressures were in the 160s.

And they were taking a coupe grams of metformin a day. The thing about a creatinine of 8 is you need to have a GFR of around zero for almost week to get there. So imagine the patient has about 14 grams of metformin on board.

I think this was MALA.

I think this patient should have gotten hemodialysis.

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Contrast Associated or Contrast Induced Nephropathy? Who the hell knows. St John Ascension Grand Rounds

Everyone talks about the importance of mentors in career development, but there is another type of Fairy God Mother that doesn’t get as much press but can be just as important, this is the Sponsor. A sponsor doesn’t give advice and guide you like a mentor does, but when opportunities come up they think of you and put your name forward.

The most important sponsor in my career has been Chief of Medicine at Ascension St John, Lou Saravolatz. As a fellow, Dr. Saravolatz discovered a bug now known as Methicillin Resistant Staph Aureus (remind me, what world changing research are you doing in your fellowship?). But as Chief of Medicine he has been my (and a host of other docs) sponsor. Dr Saravolatz invited me to give my first grand rounds presentation in 2003. A talk on contrast nephropathy.

Today, I gave another talk on contrast nephropathy. Here are the files. I will try to get a video with my narration up in the next few days.

Keynote

Powerpoint (I just export the Keynote presentation to Powerpoint so I suspect many of the animations are crap. It is here just to preempt the chorus of Twitter requests for it)

PDF

Here is a video of this presentation Rutgers Robert Wood Johnson Department of Medicine grand rounds.

I also am posting the talk bit-by-bit as #Tweetorials.

The first:

The second

The third

The fourth

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Pseudohyperkalemia: the tweetorial

Last week I posted a tweetorial on pseudohyperkalemia due to CLL and a high white blood cell count.

This case peaked with a potassium of 9.5. Pretty frightening, but that was nothing compared to the potassium of 15.5 I saw in 2014. Details here.

I had another case of pseudohyperkalemia in 2011. That one was due to thrombocytosis.

In response to my Tweetorial, Yash Chivate shared a case of pseudohyperkalemia of his own.

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Things we do for no reason (#TWDFNR ) in AKI

Last week I wrote this tweetorial

I had been thinking about this for a long time.

When you hear #TWDFNR talks about AKI the two things that are usually hammered are:

  1. The uselessness of the FENa and other urinary excretion indices.
  2. The low yield of the kidney ultrasound.

I actually like both of those tests, despite the pundit class dumping on them.

The FENa is vilified because in trials that look at its ability to separate out purely hemodynamic decreases in GFR from acute tubular necrosis it does poorly. This is especially disappointing because all of the board exams and med student level lectures on FENa says this is just what the test is all about. I concede that FENa in isolation is a bad test to determine the etiology of AKI. But as part of the global assessment of the patient, getting a FENa can be incredibly powerful.

Saying the FENa is useless is like testing to see if a blinded physician given only an aucultory exam could diagnose community acquired pneumonia. I think there is a good chance auscultation would fail that hurdle. But that doesn’t mean we should abandon our stethoscopes. The auscultory exam is one of a number of studies we do when assessing a patient who may have pneumonia. It is a valuable part of the global patient assessment.

Similarly, the FENa is part of my global assessment of a patient.

For example, I have a patient with cirrhosis and acute kidney injury. I look at the urine and see a mixture of hyaline casts and granular casts. Now, you need to be careful about granular casts in cirrhosis. As the bilirubin climbs, it can stain innocent hyaline casts to look brown, and they can start to look somewhat like muddy-brown casts. I don’t think that is what is happening on this slide, because I can see simultaneous dirty brown and hyaline casts. Then we checked the urine sodium and it was 50. This is off diuretics. This is remarkably high for a patient with cirrhosis and ascites. But there it is. The urine sodium is high and in agreement with U/A findings. I make a diagnosis of acute tubular necrosis.

Not the patient’s urine, but those are some nice muddy brown casts.

It’s an N of 1, but that’s all we have in clinical medicine, one N of 1 study after another.

The kidney ultrasound story is a much simpler than the FENa story. The argument that kidney ultrasound is of low yield and low cost effectiveness is due to the exrtemely low yield of U/S to find obstruction. In almost every case that you find obstruction, you suspected obstruction, and using it in cases without a clinical suspicion is like Acestes aiming at a non-existent target.

But the thing is, the treatment of obstruction is not dialysis, and if you fail to identify and correct the obstruction, no mixture of IV fluids, avoiding nephrotoxins, and regulating blood pressure will fix the obstruction. That obstruction will lead to renal failure and dialysis. In a world of $60,000 a month maintenance therapies, I refuse to miss even one easily correctable (but otherwise irreversible) cause of kidney failure.

The real #TWDFNR in AKI are:

  • Urinary protein to creatinine ratio
  • Intact PTH

The fallacy of the Protein Creatinine ratio was the subject of the afore mentioned tweetorial.

Some great comments and discussion from the tweetorial:

The problem with PTH in AKI is that it is useless. I see fellows and attendings ordering this and I have no idea what to do with it. Some people try to use the KDIGO PTH guidelines for ESKD. This seems to be totally evidence-less. PTH is an acute phase reactant in AKI. Part of the AKI syndrome is a drop in calcium, and after that PTH rises, just like it is supposed to. I don’t see any reason to suppose this secondary hyperparathyroidism is pathologic. I have seen some people order it to try to distinguish acute from chronic CKD. The reasoning being, that chronic kidney disease would have a high PTH and acute would not. This is not the case both acute and chronic kidney disease can have secondary hyperparathyroidism.

Stop ordering PTH in AKI. Stop checking urinary protein to creatinine ratio and start doing urinalysis and microscopy.