Tag: acute kidney injury

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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.

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Antibiotics and AKI for #MADID18 (now with video)

Last fall, Dr. Davis (@IDPharmProf) asked if I would be interested in speaking about antibiotic induced AKI. She was thinking of submitting an idea for a session on kidney disease and antibiotics. Later, she told me I would be sharing the stage with Bruce Mueller (@BAMPharmD), who would be talking about antibiotic dosing during AKI and CRT. This felt like agreeing to doing some Karaoke and then being told you are being paired-up with Frank Sinatra.

I did my best, but compared to Dr. Mueller, the only difference between me and Bozo was the red nose and floppy shoes.

Here is a screencast of the presentation and the slides for you to peruse. But if you ever get a chance to hear Dr. Mueller, don’t miss it. He is really good.

 

 

Keynote: MAD-ID Antibiotic Induced Acute Kidney Injury

PowerPoint: MAD-ID Antibiotic Induced Acute Kidney Injury

PDF: MAD-ID Antibiotic Induced Acute Kidney Injury

 

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Cardiorenal Syndrome. Revised

I gave the cardiology fellows at St John Hospital and Medical Center a lecture on cardiorenal syndrome this morning. I revised and expanded the lecture I used for the residents:

It could still use a slide or two on the various loop diuretics and their uses.

We also had an interesting discussion on the data suggesting that loop diuretics maybe harmful in acute decompensated heart failure. I should include a couple of slides on that.

Overall a significant upgrade. You can find the lecture in the usual place.

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Cardiorenal syndrome

On the first Friday of every month I give a lecture to the residents at St. John Hospital and Medical Center. I like to do an electrolyte lecture but for March the chief resident asked me to talk about cardiorenal syndrome. In researching the lecture I came across this article by Claudio Ronco.

The article defines cardiorenal syndrome as any condition with simultaneous kidney and heart failure. He then goes on to subdivide cardiorenal syndrome into 5 types:

  1. Acute heart failure causing acute renal failure
  2. Chronic heart failure causing chronic kidney disease
  3. Acute kidney injury causing any type of acute cardiac dysfunction (including arrhythmia)
  4. Chronic kidney disease causing any chronic cardiac disease
  5. Any systemic condition that causes renal and cardiac dysfuction (e.g. sepsis)

This is terrible. Cardiorenal syndrome used to signify the unique cause of acute kidney injury where the decrease in function is due to apparent volume depletion in a patient that obviously overloaded. It named the only scenario where acute kidney injury responded to diuresis. It was unique and specific. Ronco comes along and says, yes I like your version of cardiorenal syndrome so I will make it type 1 in my new all purpose definition of cardiorenal syndrome. Now whenever there is cardiac dysfunction and simultaneous kidney dysfunction we can just call it cardiorenal syndrome.

It doesn’t have to be this way look at the example of hepatorenal syndrome. The syndrome does not refere to just any situation with simultaneous renal and liver dysfunction. It is a very specific diagnosis that only occurs with chronic liver disease and ascites. The patients must be oliguric, there is no non-oliguric HRS. Patients must be sodium avid and unresponsive to fluids and albumin. Additionally the patients cannot have laboratory or imaging evidence for an alternative cause of renal failure. Because of this definition hepatorenal syndrome identifies a very specific disorder, with a specific pathophysiology and unique prognosis and treatment options.

Ronco takes the beautiful and evocative name cardiorenal syndrome, strips it of all specificity and then tries to restore it by tacking on five different types. The fifth type 5 is the one that makes my brain explode. Sepsis, really? Acute kidney injury from sepsis that happens in the same patient who also suffers from sepsis induced cardiomyopathy should now be considered to have cardiorenal syndrome? Ronco is a man who has spent his life studying sepsis and acute renal failure, I can’t believe he is actually referring to that condition as CRS type 5.

I’m not buying what Ronco’s selling. Cardiorenal syndrome begins and ends with type 1 for me.

FYI: Here is the lecture (Keynote, PDF). It still needs some work. I’d like to add a section on ultrafiltration and I need to include the NEJM article on furosemide that was published yesterday.

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second lecture of the year: acute kidney injury

This is a significant upgrade from the version I posted a couple of years ago. I put the lecture together right before the ATN trial was published. I finally got around to updating the presentation to include that data. I also updated the NGAL section and added some data on avoiding volume overload.

I used a number of the posts on the blog to allow me to rapidly update the presentation. I was pleased with how well my ATN commentary/review stood up.

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Volume, a new target for dialysis and acute renal failure?

One of the major advancements in nephrology in the first decade of the 21ast century was the rejection of Kt/V as a treatment target in dialysis. In a field that is lacking in randomized clinical trials we had three well done randomized clinical trials designed to verify the mounds of observational data. In all three Kt/V as an expression of dose failed.

Chronic hemodialysis: HEMO

  • eKt/V of 1.05 vs 1.45 (or a spKt/V of 1.2 vs 1.6) 

Peritoneal dialysis: ADEMEX

  • Increase in PD dose such that they move from less than 40% at Kt/V of 2.0 to 83% at Kt/V of 2.0

Dialytic support for acute renal failure: VA/NIH ATN trial

  • 3 days a week dialysis versus 6 days a week all at a single-pool Kt/V of 1.2 to 1.4 per session
  • Hemodynamicly unstable patients were randomized to one of two levels of CVVH 20 or 35 ml/kg/hour of total CRT effluent
All three looked at variations on Kt/V tuned to the individual clinical scenario. Varying Kt/V in each of these clinical scanrio made not a whif of difference to the patients.

In the aftermath of such intellectual carnage nephrology is desperately seeking a replacement. My experience with nocturnal dialysis and the amazing work coming out of Canada makes home hemo look like the most appealing option. Getting results comparable to transplant makes it look like an entirely new modality compared to traditional in-center hemo.
One of the aspects that made Kt/V so appealing was how it was a useful in any situation involving dialysis. (The lessons from NCDS study on chronic in-center hemodialysis guided the definition of adequate dialysis for ARF in the ATN trial)

What lessons does home hemo have to teach acute renal failure in the ICU? What lessons does it have for peritoneal dialysis. One could argue that one of the central problems in modern dialysis is fluid management. Too many of my patients are chronically fluid overloaded leading to hypertension and over worked hearts. Home hemo corrects hypertension. Is solving that cardiovascular problem accounting for much of the improved clinical outcomes?

If that is the case, then there is a clear lesson that we can take from home hemo and apply to the ICU. 
Don’t let your patients get volume overloaded
We covered this in journal club last thursday: Fluid Overload and Mortality in Children Receiving Continuous Renal Replacement Therapy

The study is a retrospective interpretation of registry data on children with acute renal failure receiving continuous renal replacement therapy. Each patient was given a fluid overload score by calculating a percentage overload:

They divided patients into three strata:

  1. <10% overload
  2. 10-20% overload
  3. ≥20% overload
They also used percentage overload as a continuous variable for the primary multivariate analysis.
The primary data is shown in table 2.
It should be immediatly obvious that the patients with more volume overload were sicker, they had signifigantly:
  • longer ICU stay
  • higher mortality
  • more multi-organ dysfunction
  • more likely to be intubated
  • more inotropes
  • more sepsis
  • higher PRISM score
For that reason I am not going to spend time discussing the univariate analysis and go straight to the multivariate analysis:

Worse fluid overload severity remained independently associated with mortality (OR, 1.03; 95% CI, 1.01-1.05). The relationship was satisfactorily linear and the OR suggests a 3% increase in mortality for each 1% increase in degree of fluid overload at CRRT initiation.

That is impressive. If the results hold up and aplies to adults it should scare the crap out of anyone who regularly rounds in the ICU. Think of a typical 80 kg adult who has total input of 2,400 mL (100 mL/hr) and has 1,600 mL of urine output, 67 mL/hour. That is a positive balance of 800 mL or 1% of body weight. If that goes on for 3 days and then the patient becomes oliguric with only 400 mL of urine output for two days (2,000 mL positive per day) before initiating CRT. That patient would be up 6,400 mL or 8% of bodyweight: Those relatively innocuous seeming numbers would represent a 24% increase in mortality compared to someone with matched ins and outs. Yowsa!
This is an observational study and it is important not to accept he results as truth but it is certainly a suggestive lead.
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lowest FeNa I have ever seen

I was consulted on a patient with autoimmune hepatitis and acute kidney injury. The patient has ascites and was admitted with a small bowel obstruction.

I’m not sure if it is actually the lowest but it is remarkably low:

serum Na 147 mmol/L
serum Creatinine 1.77 mg/dL

urine Na <10
urine Cr 148

I assumed a urine sodium of 5 mmol/L

FENa= 0.04%

This is 4 molecules of sodium excreted for every 10,000 filtered. Amazing.