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Letters to the Editor |
Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Research and Training Hospital, Istanbul, Turkey
Received 29 March 2008; accepted 23 April 2008.
* Corresponding author. Address: At
f bey sokak Derya 85 sitesi, 2. Ksm A blok, Kat: 3, D: 11 Acbadem, 34660, Istanbul, Turkey. Tel.: +90 216 545 28 58. (Email: mdumantepe{at}gmail.com).
Key Words: Acute kidney injury • Cardiopulmonary bypass • Creatinine • IL-18
I read with great interest the article titled ‘Does furosemide prevent renal dysfunction in high-risk cardiac surgical patients? Results of a double-blinded prospective randomised trial’ [1]. First of all I would like to thank the authors for their efforts and then add a few things to the topic. We concur with the authors that perioperative urinary output more than 1 ml/kg/h is not an outstanding reflection of renal function after cardiopulmonary bypass. In that situation most of us think everything is all right. As the authors mentioned, lots of factors are responsible for acute kidney injury (AKI) for high-risk patients. Detection of AKI based on perioperative urinary output and several unreliable laboratory markers like serum creatinine underestimates the underlying renal status. Serum creatinine, although used routinely in clinical practice and in clinical trials, is a poor marker of renal dysfunction and an increase in which is not directly related to tubular injury in AKI. There is also a delay in the detectable increase in serum creatinine as a result of the time required for its accumulation and equilibration. Changes in creatinine can be nonspecific and may occur as a result of increased muscle mass and nutrition which are nonrenal factors. The alterations in serum creatinine are not particularly sensitive or specific for small changes in glomerular filtration rate [2].
Because of the vital importance of earlier targeting of therapies, many markers have been explored for early diagnosis of AKI. Although the initial studies on some molecules such as tubular enzymes, growth factors, adhesion molecules, and some cytokines were promising, the larger and the more detailed studies have shown an inadequate sensitivity or specificity to advocate its clinical use. Recently described molecules such as kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, cysteine-rich protein 61 and IL-18 have demonstrated compelling results as markers of AKI at the preclinical level [2,3,5]. However, none of these molecules except lipocalin have been systematically explored in humans AKI. In a recent study, it was demonstrated that neutrophil gelatinase-associated lipocalin in the urine increases in pediatric patients after cardiac surgery before the increase in serum creatinine [2]. Nevertheless, the study did not comment on the severity or outcomes of AKI in these children. It has also been reported that serum cystatin C seems to increase 24–48 h before creatinine in patients with AKI but cystatin C is a marker of clearance and not a marker of renal tubular injury [4].
Over and above being a marker of renal tubular injury, urine IL-18 is an attractive test for further development as it is fast, reliable, accurate, and inexpensive. As compared with other markers, IL-18 has the advantage that it can be readily measured by commercially available ELISA kits. Availability of commercial kits can considerably hasten the development of the test for routine clinical use [5].
Footnotes
The authors of the original paper [1] were invited to comment on this Letter to the Editor but declined the offer.
References
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