Correspondence
and not truly representative of physicians practicing in the United
States, Canada, Europe, Australia, and New Zealand.
Participant selection was not random, and the opinions of physi-
cians in other parts of the world (eg, Asia, Africa, and South America)
were not sought. The opinions of nonphysician professionals, such as
transplant nurses/coordinators, also were overlooked. We share the
concern that incentives perhaps could reduce the selflessness of organ
donation, but various forms of compensation for donors in Iran,
Ireland, Israel, Singapore, and Saudi Arabia have not destroyed their
altruistic systems of living or deceased organ donation.2-4
It puzzles us that mixed motivations are seen as such a threat
when it comes to organ donors while we pay military personnel,
firefighters, and others who take considerably greater risks for their
services to humanity. Moreover, in an analogous situation that
involves health care professionals and healthy participants, we
allow payment to women who donate their eggs or become sur-
rogate mothers. The moral issues raised by accepting a system that
includes controlled compensation should be weighed against the
morality of allowing as many as 18 patient deaths per day when
there are people who would be willing to help if only a legal
compensation system were in place.5
Alireza Hamidian Jahromi, MD, MRCS1
Sigrid Fry-Revere, JD, PhD,2 Bahar Bastani, MD3
1
Louisiana State University Health Sciences Center, Shreveport
Louisiana
2
Center for Ethical Solutions, Lovettsville, Virginia
3
Saint Louis University School of Medicine, St Louis, Missouri
Acknowledgements
Financial Disclosure: The authors declare that they have no
relevant financial interests.
References
1. Tong A, Chapman JR, Wong G, Craig JC. Perspectives of
transplant physicians and surgeons on reimbursement, compen-
sation, and incentives for living kidney donors. Am J Kidney Dis.
2014;64:484-485.
2. Khatami SM, Mahdavi-Mazdeh M. Perfect is the enemy of
good: the Iranian system of paid donation. Am J Transplant. 2014;14:
1222-1223.
3. Fry-Revere S. Stop organ trafficking now: articles pertaining
to medical, political, ethical, and cultural aspects of kidney
donation. http://www.stoporgantraffickingnow.org/?page_id=196.
Accessed December 19, 2014.
4. Global Observatory on Donation and Transplantation (GODT)
data. http://www.transplant-observatory.org. Accessed December 19,
2014.
5. US Government information on organ and tissue donation and
transplantation. http://www.organdonor.gov/about/data.html. Accessed
December 19, 2014.
Tong et al declined to respond.
Ó 2015 by the National Kidney Foundation, Inc.
http://dx.doi.org/10.1053/j.ajkd.2014.06.040
Pseudo–Acute Kidney Injury Secondary
to Intravenous Dexamethasone
To the Editor:
A 64-year-old woman was admitted to our hospital due to a severe
asthma attack. On admission, her serum creatinine and serum urea
nitrogen levels were 0.75 mg/dL and 20.9 mg/dL, respectively.
Intravenous therapy with dexamethasone was initiated for treatment
of the asthma attack. The next day, serum creatinine level increased
to 4.63 mg/dL (corresponding to estimated glomerular filtration rate
344
Box 1. Drugs That Can Cause Pseudoelevation in Serum
Creatinine Concentration
Sources of Extrinsic Creatinine
8 mg creatinine in dexamethasone, 3.3 mg
16 mg creatinine in hydrocortisone, 100 mg
37.5 mg creatinine in azasetron hydrochloride, 10 mg
Analytical Interference
5-Fluorocytosine
Cefoxitin
of 8.1 mL/min/1.73 m2), and a nephrologist was consulted for acute
kidney injury (AKI). Extensive examinations were performed, but
only serum creatinine level supported the diagnosis of AKI (serum
urea nitrogen was 14.9 mg/dL). Later, we learned that the blood
sample had been drawn by a physician in training and was obtained
from the patient’s left cubital vein, with tourniquet applied, at the
same time that dexamethasone was being infused into the left dorsal
hand vein. Then we noticed that dexamethasone contains creatinine
as a buffer. Thus, approximately 1 hour later, a new blood sample
was obtained from the patient’s right arm; serum creatinine level was
normal in this sample.
From case reports and drug information, we compiled a list of
medications that can cause pseudoelevation of serum creatinine
concentration (Box 1).1-4 To help offset chemical and physical
instability, dexamethasone, hydrocortisone, and azasetron hydro-
chloride contain creatinine as a buffer.5 The 5-fluorocytosine mole-
cule interacts with creatinine iminohydrolase, causing spuriously high
creatinine concentrations measured by the enzymatic method.3 In
addition, pseudo-AKI can result from cefoxitin interference with the
Jaffe method for creatinine measurement.4 Our findings warn clini-
cians to consider exogenous creatinine and other drugs that influence
creatinine measurement as a possible cause of pseudo-AKI.
Minami Nakajima, MD, Tsuyoshi Inoue, MD, PhD
Hideki Kato, MD, PhD, Masaomi Nangaku, MD, PhD
The University of Tokyo Graduate School of Medicine
Tokyo, Japan
Acknowledgements
Financial Disclosure: The authors declare that they have no
relevant financial interests.
References
1. Darby D, So J, Russell J, Monaghan PJ. Spuriously raised
serum creatinine associated with an excipient present in an intrave-
nous dexamethasone formulation. Ann Clin Biochem. 2012;49(pt 3):
292-294.
2. Makiishi T, Yamamoto S, Maeda S. Case of suspected
pseudo-elevation of serum creatinine immediately after intra-
articular injection into a wrist joint of a pharmaceutical prepara-
tion of dexamethasone containing creatinine as a buffer. Nihon
Jinzo Gakkai Shi. 2011;53(2):200-206.
3. Mitchell RT, Marshall LH, Lefkowitz LB Jr, Stratton CW.
Falsely elevated serum creatinine levels secondary to the presence
of 5-fluorocytosine. Am J Clin Pathol. 1985;84(2):251-253.
4. Sherman RA, Eisinger RP, Weinstein MP, Samel J. Cefoxitin-
induced pseudo acute renal failure. Clin Ther. 1981;4(2):114-117.
5. Akers MJ. Excipient-drug interactions in parenteral formu-
lations. J Pharm Sci. 2002;91(11):2283-2300.
Received August 5, 2014. Accepted in revised form September 29,
2014. Originally published online November 13, 2014.
Ó 2015 by the National Kidney Foundation, Inc.
http://dx.doi.org/10.1053/j.ajkd.2014.09.020
Am J Kidney Dis. 2015;65(2):342-347