Tag: cardiorenal syndrome

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The failure of creatinine as a marker of AKI

  • If you went to a national nephrology meeting in the 2000’s and walked into a lecture on clinical AKI there were two obligatory sections that would be part of the talk.
    1. The first would be how poor creatinine was as a marker for AKI. The expert at the front of the room would explain that creatinine was a lagging indicator and that by the time the creatinine had begun to climb the injury was yesterday’s news. Identifying AKI by a bump in the creatinine would force you to always be reactive rather than proactive. This discussion would then lead to a plea for better markers of AKI, followed by descriptions of NGAL, KIM-1, and other promising AKI assays of the future.The second would be a complaint about the lack of a consensus definition of AKI. The speaker would point to 35 different definitions of AKI in the literature, from highly sensitive (25% bumps in serum creatinine) to perfectly specific (need for acute dialysis during the hospitalization).
Oh 2002, how I miss you… (https://www.ncbi.nlm.nih.gov/pubmed/12454534)

Depending on the exact year of the talk, they would then talk about the RIFLE criteria, or to the AKIN modifications to the RIFLE criteria, or to KDIGO’s modifications to AKIN. The speaker would always point to a future where we had a consensus definition of acute kidney injury so that we could start to move forward with a cohesive literature where one paper could be compared to another. What was always odd about these talks was that the second part of the lecture, about the emerging creatinine-based consensus definitions of AKI must have been browsing Facebook during the earlier part of the lecture about the futility of creatinine-based definitions of AKI.

But the consensus did emerge. Despite all the experts warning us about the problems with small changes in creatinine defining AKI, that is the world we live in. One problem with this definition recently emerged in a discussion of cardiorenal syndrome. This article by Testani et al found that:

The group experiencing hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater reductions in filling pressures (p<0.05 for all). Hemoconcentration was strongly associated with WRF (OR=5.3, p<0.001) whereas change in right atrial pressure (p=0.36) and change in pulmonary capillary wedge pressure (p=0.53) were not. Patients with hemoconcentration had significantly lower 180 day mortality (HR=0.31, p=0.013). This relationship persisted after adjustment for baseline

We should not have a situation where increased risk of AKI (yes, I know the definition of worsening renal function, WRF, does not perfectly overlap with Stage 1 AKI, but work with me) is also associated with improved 180 day mortality. By defining AKI around changes in AKI we have deputized nephrologists to be the creatinine police and make decisions on treating patients based on what effect it has on short-term changes in GFR which may or may not have anything to do with long-term outcomes. In the above study, using serum creatinine to guide therapy leads to insufficient diuresis, poor fluid removal, and poor 180 day outcomes.

The Twitter discussion about this was particularly enlightening. Take a look.

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Cardiorenal conference in New York: #NephCards2018

You probably know Kenar Jhaveri. He is the founder of NephronPower and the first editor of AJKDblog. He is a professor of Medicine at Hofstra Northwell School of Medicine on Long Island. Kenar is a good friend and one of the great nephrology educators.

He is sponsoring a cardiorenal symposium in March. I’d love to go but I’ll be most of the way to Everest Basecamp at that time. If you have some spare conference time, you should check out The Heart-Kidney Connection.

There will be mad tweeting so in mid-March tune your Twitter machine to #nephcards2018

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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.