Journal Club: Campath and ACE/ARB and AKI in CABG

The first article was an analysis of campath for induction with tacrolimus.

Patients were randomized to either

  • Methylpred 250 mg and Campath 20 mg immediately following surgery followed by Tacrolimus Group
  • Tacrolimus, prednisone, and MMF (no induction therapy)

Primary outcome was biopsy proven rejection at 6 months.
Secondary outcome was biopsy-proven rejection at 12 months, time to first rejection, patient and graft survival, incidence of corticosteroid resistant rejection.

n= 131 deceased donor, kidney transplant in patients with PRA ≤ 25%. All patients were receiving their first kidney. Age 18-65.

No episodes of humoral rejection was found in either group.

The figure above I think is particularly informative as it becomes obvious that all the difference is in the first month. This is a study of induction vs. no induction and they demonstrate a huge reduction in early rejection with induction.

Big picture: large reduction early reduction but no difference in serum creatinine at one year.

The second article was a retrospective analysis of the risk of acute kidney injury based the presence or absence of ACEi/ARB.

A VA study looking at chronic use of ACEi or ARB and the risk of acute kidney injury following cardiovascular surgery. SUNY Buffalo looked at 1,358 patients with CV surgery from 2001-2005. 50% were on ACE/ARB

  • 40% had AKI (essentialy all Modified RIFLE: Stage 1, Cr rise ≥0.3 or 50-100%)
  • 7 patients Stage 2 (Cr rise 2-3x the baseline)
  • 2 patients Stage 3 (Cr greater than 4 or >3x the baseline)

They found that use of ACEi/ARB had a 27.6% increase in risk of AKI.

Of note 18% of the patients who had AKI, their creatinine had not returned to baseline at 3 months post surgery and still qualified as AKI. This does not jive with the natural history of AKI, especialy relatively mild AKI. This makes me wonder if the baseline creatinine were abnormally low in some of the patients and the increase documented was not AKI but actually resolution of the creatine falling.

The primary concearn I have is that the study had 543 patients with AKI and only 9 had more than a doubling of creatinine. They used a very sensitive definition of AKI and like any test, when you increase the sensitivity you decrease the specificity. It is very possible that a large proportion of those patients defined as AKI didn’t actually have AKI, throwing the study into doubt.

2 Replies to “Journal Club: Campath and ACE/ARB and AKI in CABG”

  1. I appreciate your work here.
    I read the article and shared it with our CT surgeons as soon as it came out. I do a lot of work in the cardiothoracic ICU and deal with a great deal of patients… I can say that I have routinely been taking off ACEi/ARBs pre-op for quite sometime. Although we all recognize they are excellent drugs there is enough of a hit to renal hemodynamics intraop for CABG to leave them out of the equation and resume postop when stable, just prior to discharge.

    Again, keep up all the good work you are doing here!

  2. Dr. Prince, thanks for your follow-up. We had a heated discussion at the end of journal club regarding stopping ACEi/ARB. I agree with you, though I don’t find the evidence in the article terribly compelling, the physiology makes sense and without a compelling reason to continue the drugs, they should be stopped.

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