HLA-Matched Kidney Transplantation in

the Era of Modern Immunosuppressive

Therapy
Arun Amatya, MD; Sandy Florman, MD; Anil Paramesh, MD; Anup Amatya, PhD Jennifer McGee, MD; Mary Killackey, MD;
Quing Ren, MD; Brent Alper, MD; Jean Heneghan, MS; Eric Simon, MD; Karen Sullivan, PhD; Douglas Slakey, MD; Rubin Zhang, MD
Drs. Amatya, Ren, Alper, Heneghan, Simon, Sullivan, and Zhang are with the Department of Medicine, and Drs. Florman,
Paramesh, McGee, Killackey, and Slakey are with the Department of Surgery, School of Medicine, Tulane University in New
Orleans, Louisiana; Dr. Amatya is also with the Center for Health Statistics, University of Illinois at Chicago.

BACKGROUND: The effect of HLA match on renal graft survival has become controversial as has the policy of
mandatory sharing of kidneys.
METHOD: We performed a retrospective analysis of HLA matched (M) and mismatched (MM) kidney transplants in
our center. Tacrolimus, mycophenolic acid, and steroids were used as maintenance therapy and basiliximab induction was added for high-risk patients.
RESULT: A total of 229 kidney transplants were included with median follow-up of 5.1 years. The 5-year deathcensored graft survival by Kaplan-Meier method was significantly higher in the M group than in the MM group for
deceased-donor kidney transplants (log-rank, p .018). This graft survival advantage was detected in patients with
a peak panel reactive antibody (PRA) greater than 20% (p .023), but not in those with a PRA level of less than 20%
(p .32). The graft survival was not statistically different for live donor kidney transplants (p .077). A mismatched
kidney was an independent risk for graft loss (hazard ratio: 2.27, 95% confidence interval: 1.0095.09, p .047)
and acute rejection was a significant cause of graft loss in mismatched deceased-donor transplants (p .035).
CONCLUSION: Acute rejection remains a significant cause of graft loss in HLA-6-antigen mismatched deceaseddonor kidney transplants. Our data support mandatory sharing of HLA-matched kidneys in sensitized patients with
a PRA level greater than 20%.

DOI: 10.1002/dat.20439

DR3, DR4 to recipient A2, A3, B8, B13,

DR3, DR4: donor has homozygous antigen A2 and is phenotypically matched
to recipient).7 It was again expanded in
March 1995 to zero mismatched kidneys (e.g., donor A2, B8, B13, DR3,
DR4 to recipient A2, A3, B8, B13, DR3,
DR4: failure to identify the 2nd A is usually due to the presence of homozygous
antigen).8
The lower incidence of rejection and
the better graft survival of these HLAmatched kidneys was demonstrated in earlier studies.7-11 However, a recent analysis
indicated that the impact of HLA matching has steadily declined as more potent
immunosuppressive agents have been
used.12 It has also been suggested that
the mandatory sharing beyond the local
allocation area for low sensitized patients

with a panel reactive antibody (PRA) level

less than 20% created logistical inefficiencies and tended to benefit white patients
more than African American patients.13 In
January 2009, UNOS updated its policy
that HLA-matched kidneys continue to
be nationally shared for sensitized adult
patients with PRA levels greater than
20%, and the locally matched patients
have the highest priority regardless of
PRA level.
In this study, we analyzed the outcome
of all HLA-matched kidney transplants that
received potent immunotherapy with tacrolimus (TAC), mycophenolic acid (MFA),
and steroids. We sought to answer the
question of whether the aforementioned
changes in policy would be supported using
a single centers data in this era of modern
immunosuppressive regimens.

idney transplant is the preferred

treatment for selected patients
with end-stage renal disease,
as it prolongs life expectancy,
improves quality of life, and decreases
cost of long-term medical care compared
with maintenance dialysis treatment.1-5
The best method of allocating the limited number of available deceased-donor
kidneys remains controversial.6 In 1987,
the United Network for Organ Sharing
(UNOS) established a national program
of sharing HLA-matched deceased-donor
kidneys (3 pairs of HLA-A, B, and DR
antigens identical in both donor and recipient). Superior graft survival was welldocumented with these shared kidneys.7 In
August 1990, the HLA-matching criteria
was expanded to phenotypically matched
kidneys (e.g., donor A2, A2, B8, B13,

May 2010 Dialysis & Transplantation 1

HLA-Matched Kidney Transplantation

TABLE I. Transplant recipient characteristics of HLA-matched (M) and

HLA-mismatched (MM) kidneys (mean SD).
M

MM

Immunosuppressive therapy
Our standard triple immunosuppression regimen consisted of steroids, TAC,
and MFA. High risk patients defined as
prior transplant recipients, HLA-6-antigen
mismatch, and those with PRA levels greater than 20% received basiliximab induction
therapy. Intravenous methylprednisolone
was administrated prior to reperfusion and
tapered to maintenance oral prednisone.
TAC doses were adjusted to keep the 12hour trough levels between 10 to 12 ng/mL
for the first 3 months, 7 to 10 ng/mL for the
remainder of the first year, and 4 to 7 ng/
mL thereafter. Each patient received either
mycophenolate mofetil (MMF) at 1 gram
or enteric coated sodium mycophenolate
(Myfortic) at 720 mg twice daily.

(n 73)

(n 98)

p-value

48.33 14.96

45.25 15.17

.23

Female

33 (45.2%)

36 (36.7%)

.26

Male

40 (54.8%)

62 (63.3%)

African American

24 (32.9%)

72 (73.5%)

White

49 (67.1%)

23 (23.5%)

Others

0 (0%)

1 (3%)

26.9 6.04

27.36 6.76

.64

37.90 41.70

21.83 33.8

.01

Rejection

14 (19.2%)

11 (11.2%)

.14

CIT (hours)

18.91 6.56

17.45 6.96

.17

WIT (minutes)

28.92 6.1

29.86 8.52

.41

Acute rejection was confirmed by kidney

biopsy. The severity of rejection was defined
according to Banff criteria. Rejection of
grade 1 or below was initially treated with
IV methylprednisolone. Thymoglobulin
was used for steroid resistant rejection, or
as initial therapy for any rejection of Banff
grade 2 or higher. Thymoglobulin, plasmapheresis, and intravenous immune globulin
(IVIG) were used for antibody mediated
rejection. Standard antifungal, antibacterial, and cytomegalovirus prophylaxis were
administered per protocol.
Outcomes measures included: (1)
death-censored graft survivals over 5 years,
(2) incidence of biopsy confirmed and
treated acute rejection, (3) quality of graft
function as assessed by estimated glomerular filtration rate (eGFR) using the
Modification of Diet in Renal Disease
equation, and (4) etiologies for the graft
loss. Renal graft loss was defined by primary non-function or loss of renal function
requiring chronic dialysis. Patient death
included all mortalities from the time of
kidney transplantation. Death with a functioning graft (DWFG) was excluded from
graft survival estimate (death-censored).
Graft failure was excluded from graft function calculation.

Deceased-donor
Kidneys

Age (years)
Sex

Race

BMI
Peak PRA (%)
Previous Transplants

<.0001

(n 26)

(n 32)

p-value

36.81 12.45

39.88 15.99

.53

Female

11 (42.3%)

13 (40.6%)

.92

Male

15 (57.7%)

19 (59.4%)

Live Kidneys

Age (years)
Sex

Race
African American

4 (15.4%)

13 (40.6%)

White

20 (74.1%)

17 (54.8%)

Others

2 (7.4%)

2 (6.5%)

BMI

27.66 6.81

27.18 7.64

.82

Peak PRA (%)

17.23 30.33

9.75 21.17

.29

5 (19.2%)

0 (0%)

.01

CIT (hours)

2.75 6.38

1.61 3.72

.43

WIT (minutes)

28.05 7.07

27.23 7.47

.67

Previous Transplants

Materials and Method

Study population
We retrospectively compared the outcomes
of HLA-matched and HLA-mismatched
kidney transplants from January 1997 to
December 2007. Any kidney transplant
recipient who also received a pancreas,
liver, or heart transplant was excluded
from this study. Based on the 6 antigens at
HLA-A, B, and DR loci, the HLA-matched
group (M group) included all of the HLA
2 Dialysis & Transplantation May 2010

.23

identical, phenotypically matched, and

zero mismatched kidneys. The HLA-mismatched group (MM group) was used as
comparison and it represented no match
at any of the 6 HLA antigens (6-antigen
mismatch). Both kidney transplants from
deceased donors and living donors were
studied for graft survival analysis, and
deceased-donor kidney transplants were
further subgrouped into those with peak
PRA levels greater than 20% and those
less than 20%.

Statistical methods
Statistical analyses were performed using
SAS version 9.1.3 software (Cary, North
Carolina). A 2 or Fisher exact test was used
for count data and a t-test for continuous

MM

p-value

Deceased-Donor Kidneys Graft Function

eGFR at 1 year

56.12 18.75

60.53 21.71

.18

eGFR at 3 year

58.89 21.1

55.88 24.43

.53

eGFR at 5 year

60.93 22.16

60.47 28.23

.94

10 (55.5%)

9 (28.1%)

.1

5 (27.7%)

7 (21.8%)

.9

Causes of Graft Loss

DWFG
CAN
Rejections

0 (0%)

9 (28.1%)

.035

3 (16.6%)

7 (21.8%)

.70

eGFR at 1 year

57.31 15.83

61.2 26.75

.53

eGFR at 3 year

56.43 16.74

58.21 20.33

.77

eGFR at 5 year

54.62 20.51

58.45 25.51

.68

DWFG

2 (33.3%)

2 (22.2%)

.53

CAN

2 (33.3%)

3 (33.3%)

.62

Others
Live Kidneys

Graft Function

Causes of Graft Failure

Acute Rejections
Others

0 (0%)

3 (33.3%)

.22

2 (33.3%)

1 (11.1%)

.25

measures. Product-limit estimates of survival curves were generated by KaplanMeier method and the survival difference
was analyzed by log-rank test. A multivariable Cox proportional hazard regression
analysis with a stepwise variable selection
was performed to examine the risk factors
for the graft loss. A p-value < .05 was considered statistically significant.

Results
A total of 229 consecutive kidney transplants that met the study criteria were identified during the 11-year period. Median
follow-up was 5.1 years (range, 12.1
132 months) as of December 2008 and
all were transplanted more than 1 year
before this study. Table I summarizes the
transplant recipient demographic characteristics of the 2 groups. There was no
difference in age, sex, body mass index
(BMI), warm ischemia time (WIT), or cold

ischemia time (CIT) in either deceaseddonor kidney transplants or live-kidney

transplants between the 2 groups. However,
African American ethnicity represented an
overwhelmingly higher proportion in the
MM group, while white ethnicity was the
majority of the M group (p < .0001). The
peak PRA was significantly higher in the
M group than the MM group for deceaseddonor kidney transplants. These different
distributions become less significant in live
donor kidney transplants (Table I).
There were no differences in the graft
function as measured by eGFR between the
M and MM groups for both deceased-donor
and live-kidney transplants (Table II). The
5-year cumulative incidence of biopsy confirmed and clinically treated acute rejection
were significantly higher in the MM group
than in the M group for both deceased-donor
(Figure 1A, 27.6% versus 9.6%, p .003)
and live-kidney transplants (Figure 1B,
34.4% versus 3.8%, p .01). The relative risk (RR) of acute rejection was 2.94

(95% confidence interval [CI]: 1.326.23,

p .003) in mismatched deceased-donor
kidney transplants, and 9.09 (95% CI:
1.2364.9, p .01) in mismatched livekidney transplants.
The 5-year death-censored graft survival estimated by the Kaplan-Meier method was significantly higher in the M group
than in the MM group for deceased-donor
kidney transplants (Figure 2). The estimated deceased-donor graft survivals at 1,
3, and 5-years were 100%, 89%, and 84%
in the M group, and 93%, 79%, and 70%
in the MM group (log-rank, p .018). We
further sub-analyzed deceased-donor graft
survivals by their peak PRA levels (PRA
<20% versus >20%). There was no survival
difference between the M and MM groups
for PRA levels less than 20% (Figure 3A).
The estimated graft survival at 1, 3, and 5years were 100%, 82%, and 78% in the M
group, and 94%, 81%, and 69% in the MM
group (log-rank, p .32). However, for
sensitized patients with PRA levels greater
than 20%, HLA-matched deceased-donor
kidney transplants had a superior graft
survival compared with mismatched transplants (Figure 3B). The estimated graft
survival at 1, 3, and 5-years were 100%,
96%, and 90% in the M group, and 88%,
75%, and 75% in the MM group (log-rank,
p .023). For live-kidney transplants, there
was no statistical significance in the graft
survival between the M and MM groups
(Figure 4). The estimated living-donor
graft survival at 1, 3, and 5-years were
100%, 100%, and 89% in the M group,
and 93%, 81%, and 72% in the MM group
(log-rank, p .077). The causes of graft
loss are summarized in Table II. DWGF
and chronic allograft nephropathy (CAN)
were the main causes of graft loss. Acute
rejection did not cause any graft loss in
the M groups of both deceased-donor and
live donor kidneys, but it was an important cause of graft loss in the MM groups,
especially in the deceased-donor kidney
transplants (p .035).
The risk factors for graft loss were also
examined by Coxs proportional hazard
regression analysis and significant risk factors were further analyzed by a stepwise
variable selection model. The risk factors
included recipient age, sex, race, BMI,
PRA, previous transplant, CIT, WIT, and
mismatched kidneys. Mismatched kidneys
and recipient age were found to be

TABLE II. Graft function and causes of graft loss between HLAmatched (M) and HLA-mismatched (MM) kidney transplants (mean
SD).

May 2010 Dialysis & Transplantation 3

HLA-Matched Kidney Transplantation

independent risk factors for graft loss in

deceased-donor kidney transplants with
a hazard ratio (HR) of 2.27 (95% CI:
1.0095.09, p .047) and 0.96 (95% CI:
0.0930.97, p .0001), respectively. After
adjusting for acute rejection, the effect of
mismatched kidneys loses statistical significance (HR: 1.84, 95% CI: 0.844.21,
p .142) indicating a mediating effect.

Discussion

FIGURE 1. The cumulative incidences of acute rejection between HLA-matched (M) and HLAmismatched (MM) kidney transplants according to donor origins. (A) Deceased donors; (B) living
donors.

FIGURE 2. Kaplan-Meier estimated death-censored graft survival between HLA-matched (M) and
HLA-mismatched (MM) deceased-donor kidney transplants.
4 Dialysis & Transplantation May 2010

Earlier studies demonstrated superior graft

survival of HLA-matched kidney transplants
compared with mismatched transplants.7-11
This was mainly due to the lower incidence
of rejection and graft loss from rejection in
the matched kidneys. Over the last decade,
several potent immunosuppressive agents
have been introduced into clinical practice
that have significantly reduced the incidence
of rejection and improved graft survival.14
A recent analysis suggested that the impact
of HLA match on graft survival has steadily declined.12 All of our patients received
modern triple immunosuppressive agents
as maintenance therapy. Our data indicated
that HLA-matched deceased-donor kidney
transplants still had significantly better 5year graft survival than the mismatched
deceased-donor transplants. However, this
survival advantage was limited to the sensitized patients with PRA levels greater
than 20%, and there was no survival difference in patients with PRA levels less than
20%. Our result supports UNOSs recently
updated policy that mandatory sharing of
HLA-matched kidneys should continue for
sensitized adults with PRA levels greater
than 20%. The intent was to increase kidney
transplants for sensitized patients who otherwise would not receive an organ offer or
have difficulty in matching an offered organ.
Previous data have indicated that 65.7% of
matched kidneys are allocated to the candidates with PRA levels less than 20%.13
We also found that there were a significantly higher proportion of African
American patients (73.5%) in the MM group
with more white patients (67.1%) in the M
group, which supports the notion that sharing of matched kidneys benefited the white
patients more than the African American
patients.13 The peak PRA level was higher
in the M group than the MM group, suggesting that kidney sharing may increase kidney

FIGURE 4. Kaplan-Meier estimated death-censored graft survival between HLA-matched (M) and
HLA-mismatched (MM) living donor kidney transplants.

FIGURE 3. Kaplan-Meier estimated death-censored graft survival between HLA-matched (M) and
HLA-mismatched (MM) deceased-donor kidney transplants according to the panel reactive antibodies (PRA). (A) PRA <20%; (B) PRA >20%.

transplantation in sensitized patients. The

UNOS policy of sharing has been frequently
criticized for the inevitably longer CIT and
more severe ischemic injury in the shared
kidneys.15 However, we did not find significantly longer CIT in the M group compared
with the MM group. The graft function,
as measured by eGFR, was also similar
between the M group and the MM group.
The living-donor kidney transplants
provided better short-term (1-year) and
long term (5-year) graft survival than the
deceased-donor kidney transplants in both
the M and the MM groups. We did not see a
significant survival difference between the
M and MM groups for live donor kidney
transplants. This illustrates that the effect
of HLA match is less consequential in live
donor than in deceased-donor kidney transplants.16-18 Living unrelated donor kidney
transplants have better graft survival than
deceased-donor kidney transplants despite
more HLA mismatches in the former category.17-20 This has been explained by the
fact that living-donor kidneys are usually
healthier and have less ischemic injury than
deceased-donor kidneys.17,21
The cumulative incidence of acute
rejection was significantly higher in the MM
group than the M group with a RR of 2.94
for rejection in mismatched deceased-donor
kidneys and a RR of 9.09 in mismatched live
donor kidneys. Our rejection rates were similar to the rates reported previously.16,22,23
Acute rejection did not cause any graft loss
in the M groups of both deceased-donor and
live donor kidney transplants, but it was a
significant cause of graft loss in the MM
groups. Interestingly, HLA-mismatch was
initially found to be an independent risk for
graft loss in deceased-donor kidney transplants with a HR of 2.27. When adjusted for
acute rejection, the effect of mismatch lost
significance, suggests that acute rejection is
the mediating factor of HLA mismatch for
graft loss in deceased-donor kidney transplants. An interleukin-2 receptor antibody
(basiliximab) was used as an induction for
our high risk patients including all patients
in the MM group. It was suggested that
more potent induction therapy with thymoglobulin can decrease the incidence of acute
rejection and may prolong graft survival in
high risk patients.24-26 Therefore, induction
with a T-cell depleting antibody should be
considered for HLA-6-antigen mismatched
deceased-donor kidney transplants.
May 2010 Dialysis & Transplantation 5

HLA-Matched Kidney Transplantation

This study provides the first singlecenter data examining the effect of HLA
match on long-term graft survival. Among
the strengths of this study is the fact that
our patients were treated with 1 modern
immunosuppressive regimen, the previous
studies were based on either pooled multicenter data or UNOS data, and different
immunosuppressive protocols were used
in different transplant centers. Our study
is limited by its retrospective nature and
relatively small sample size in a single
center that prevents the study of the impact
of various HLA mismatching (1 to 5 HLAantigen mismatch).
Our data indicate that mandatory sharing
of HLA-matched kidneys remains beneficial
for sensitized patients with PRA levels greater than 20%. It not only increases the access
of kidney transplantation, but also provides
superior long-term graft survival in sensitized patients. The impact of HLA match has
become less consequential in low sensitized
patients as well as living-donor kidney transplants. Acute rejection remains a significant
cause of graft loss in HLA-6-antigen mismatched deceased-donor kidney transplants
who were treated by basiliximab induction
and tacrolimus, mycophenolic acid, and steroids as maintenance. More potent induction therapy may be needed to reduce the
incidence of rejection and to improve graft
survival in those high risk patients.

Acknowledgments
We thank the members of the Tulane
Abdominal Transplant Institute for maintaining the transplant data base. D&T

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