To the Editor:
We read with interest the Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury.1 The authors present a 59-yr-old patient with the only preoperative medication an angiotensin-converting enzyme inhibitor for hypertension, who suffers acute kidney injury (AKI), after prolonged (9 h) abdominal surgery for recurrent ovarian cancer. The patient received a crystalloid infusion at a rate of 24 ml kg−1 h−1 as well as neosynephrine (0.35 µg kg–1 min−1) intraoperatively to maintain a mean arterial pressure of 70 mmHg. Nevertheless, the patient suffered oliguria intraoperatively and was found to be “mottled” and suffered anuria with associated AKI, postoperatively. We write to further emphasize that preoperative therapy with either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker may pose a higher risk for postoperative AKI. In addition, we wish to underscore the use of norepinephrine as a suitable therapy for perioperative hypotension in such patients.
In a recent retrospective study of perioperative risk factors for the development of AKI after lung resection (n = 1,129), Ishikawa et al.2 demonstrated that patients developing similarly defined AKI were more likely to be taking angiotensin-converting enzyme inhibitor or angiotensin receptor blocker preoperatively. Multivariate analysis demonstrated that preoperative therapy with an angiotensin receptor blocker was an independent predictor of AKI in such patients.
The development of hypotension in patients receiving angiotensin-converting enzyme inhibitor is widely recognized; however, there has been no demonstrated association of the extent, or duration of hypotension with the development of AKI.3,4 Nevertheless, the medical community tries to minimize the potential for AKI by administering vasopressors.4
In the refractory hypotension that the authors described in the Case Scenario,1 the ideal agent would appear to be norepinephrine rather than neosynephrine (phenylephrine). This is because administered norepinephrine having both (α1 and β1) effects would replace the well-known decreased circulating catecholamine levels associated with the induction of anesthesia and would tend to maintain cardiac output, whereas phenylephrine, with purely α1 activity, would tend to decrease cardiac output.