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The increasing rate of societal obesity is also affecting the transplant world through obesity in candidates and donors as well as its posttransplant repercussions. Being overweight and obese has been shown to have significant effects on both short- and long-term complications as well as patient and graft survival. However, much of the comorbidity can be controlled or prevented with careful patient selection and aggressive management. A team approach to managing obesity and its comorbidities both pre- and posttransplant is essential for successful transplant outcomes. Complicating understanding the results of obesity research is the inclusion different weight categories, use of listing vs transplant weights, patient populations large enough for statistical power, and changes in transplant management, especially immunosuppression protocols, anti-infection protocols, and operative techniques. Much more research is needed regarding many elements, including safe weight loss before transplantation, prevention of weight gain after transplant, genomic influences, and the role of bariatric surgery in the transplant process.
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Nutrition in Clinical Practice
Volume 29 Number 2
April 2014 171 –191
© 2014 American Society
for Parenteral and Enteral Nutrition
DOI: 10.1177/0884533613518585
hosted at
Invited Review
Obesity—is it a simple equation of intake being more than out-
put with the result being weight gain? Is all obesity the same? Is
it the obesity or the comorbidities associated with obesity that
influence our health outcomes? These same questions apply to
obese transplant candidates and recipients as well. Obesity has
long been recognized as a factor that affects overall health and
outcomes from disease and surgery and can affect survival.
Much research has been undertaken to discern the effect of obe-
sity on transplant candidates and recipients. Given the limited
resources of organs, all transplant programs are obligated to be
good stewards to provide organs to the recipients with the best
opportunities for patient and graft survival. However, non-
researched-based prejudices toward obesity are not acceptable
when making life-sustaining decisions for individuals.
One of the difficulties in comparing the effect of obesity
and outcomes is that the definition of obesity has changed
since the start of transplantation. The currently accepted terms
and body mass index (BMI) ranges per the World Health
Organization classifications are the standard (see Table 1). We
have adjusted study data or terms where feasible to be consis-
tent with these descriptors and weight ranges.
In this review, we attempt to review the current literature
regarding the effect of obesity on transplantation, which may
occur in 3 general areas: perioperative complications, short-
term complications (within 3–6 months posttransplant), and
long-term complications. In addition, we look at the data avail-
able to determine if and when transplant candidates can or
should lose weight, as well as information about the effect of
weight changes both before and after transplant and, briefly,
the role of bariatric surgery in solid organ transplantation. We
conclude with a discussion about what weight criteria or
considerations might be, and we make recommendations for
weight management patient care.
518585NCPXXX10.1177/0884533613518585Nutrition in Clinical PracticeDiCecco and Francisco-Ziller
From 1Mayo Clinic, Rochester, Minnesota.
Financial disclosure: None declared.
This article originally appeared online on February 6, 2014.
Corresponding Author:
Sara R. DiCecco, MS, RD, LD, Mayo Clinic Hospital- Rochester
Methodist Campus, 201 West Center Street, Rochester, MN 55902, USA.
Obesity and Organ Transplantation: Successes, Failures,
and Opportunities
Sara R. DiCecco, MS, RD, LD1; and Nickie Francisco-Ziller, RD, LD1
The increasing rate of societal obesity is also affecting the transplant world through obesity in candidates and donors as well as its
posttransplant repercussions. Being overweight and obese has been shown to have significant effects on both short- and long-term
complications as well as patient and graft survival. However, much of the comorbidity can be controlled or prevented with careful patient
selection and aggressive management. A team approach to managing obesity and its comorbidities both pre- and posttransplant is essential
for successful transplant outcomes. Complicating understanding the results of obesity research is the inclusion different weight categories,
use of listing vs transplant weights, patient populations large enough for statistical power, and changes in transplant management,
especially immunosuppression protocols, anti-infection protocols, and operative techniques. Much more research is needed regarding
many elements, including safe weight loss before transplantation, prevention of weight gain after transplant, genomic influences, and the
role of bariatric surgery in the transplant process. (Nutr Clin Pract. 2014;29:171-191)
obesity; weight reduction programs; body mass index; weight loss; organ failure; organ transplant; bariatric surgery
Table 1. World Health Organization Classification of Weight
Weight Status Body Mass Index, kg/m2
Underweight < 18.5
Normal range 18.5-24.9
Overweight 25-29.9
Class I 30-34.9
Class II 35-39.9
Class III >40
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172 Nutrition in Clinical Practice 29(2)
What Is the Effect of Obesity on
Transplant Outcomes?
Kidney Transplantation
With kidney transplantation as the oldest and most common
type of organ transplant, much has been studied on the effect of
weight and weight changes on transplant outcomes, especially
in consideration of the “obesity paradox,” wherein obese
patients may have better survival or a protective effect from
obesity while on hemodialysis yet more complications, cost,
and worse outcomes with transplantation.2 Table 2 delineates
selected reports of obesity research completed for kidney
transplantation. Several studies generally agree that the inci-
dence of obesity in pretransplant candidates is increasing in
comparable rates seen in the general population and has gener-
ally increased over the evolution of transplantation.2,3 In addi-
tion, several groups have noted that the obese population,
while listed, tends to have decreased access to transplant as
shown by a correlation between rising BMI and increased rates
of being bypassed for an organ as well as generally longer wait
time.4 This was also noted by Patibandla et al, finding that
while being diabetic reduced access and listing for transplant,
the effect was influenced by increased BMI and other comor-
bidities rather than diabetes itself.5
In reviewing data from nearly 15,000 maintenance hemodi-
alysis patients, Molnar et al found a 35% mortality for obese
patients while awaiting kidney transplantation due to cardio-
vascular causes; those with lower BMI, lower muscle mass,
and/or unintentional losses had a higher mortality as well.6 In
describing weight changes while listed for kidney transplanta-
tion, Schold et al showed that nearly one-third of patients
changed their weight classifications between listing and trans-
plant, with 25% of the obese patients losing enough weight to
change their obesity class.2 Losing weight while listed for
transplantation did not directly influence posttransplant mor-
tality or graft loss; instead, it was the rapid weight gains or
losses that were significantly associated with graft loss in the
nonobese. From calculation of hazard ratios, the authors found
that for every kilogram of weight gain, there was a protective
effect on mortality, while each kilogram of weight loss
increased the risk of death after transplantation. They surmised
that the reason for the weight loss, whether intentional or not,
was the key influencer of outcome. In describing those who
tended to gain weight pretransplant, more were female, dia-
betic, and/or on intermittent hemodialysis. In addition, Molnar
et al noted that those obese patients who rapidly lost weight
before transplant regained the weight such that very little long-
term benefit was seen.6
The demographic profile of kidney transplant candidates
seems to indicate that obesity is more common among the
older population,7-10 more common in diabetics,5,10-12 and yet
seems to be divided between whether it trends to male9,12 or
female sex.4,7,8,10 Racial differences, when studied, have also
noted an increased incidence of obesity in African Americans4,7
and some indigenous populations.12
After transplantation, the data seem to trend that being
overweight or obese increases the risk of delayed graft func-
tion (DGF) of the new kidney and the incidence of wound
complications (infections, dehiscence). DGF may significantly
complicate the posttransplant course (morbidity, mortality,
length of stay, and cost) as a result of either ischemic reperfu-
sion or immunologic injury to the graft.6,8-20 Kolonko et al, in
their analysis of posttransplant pulsatility and resistance
indexes, found that the obese patients had higher renal vascular
resistance (an indicator of vascular stiffness), which was linked
to the incidence of DGF, and they recommended considering
this when interpreting testing results.18 Conversely, Bardonnaud
et al, while in agreement with others that pretransplant obesity
was associated with DGF and longer length of stay, reported
that their 5-year patient and graft survival was comparable
to nonobese recipients, with the acknowledgment that they
do a systematic cardiovascular assessment before listing for
In other short-term complications, Bennett et al noted that
the increased risk of surgical wound complications became sig-
nificant for those with BMI > 40.11 Also, Kuo et al noted that
pretransplant obese patients (BMI > 30) had overall increased
incidence of posttransplant wound complications.21 However,
in those who lost weight before transplant, the act of losing
more than 10 kg acted as an independent variable in predicting
wound complications. Less conclusive are the data regarding
the effect of obesity on the incidence of acute rejection, with
Gore et al,7 Chang et al,16 and Weissenbacher et al19 finding an
increased incidence in the obese recipients, while Pirsch et al
and Bennett et al did not.11,14 Several groups have noted an
increased creatinine level initially in their obese patients, but
this normalizes relatively quickly after transplantation.8,22 A
Japanese group, in its research regarding the risk factors for the
development of new-onset diabetes after transplant (NODAT),
found that both the rate of weight gain and the increase in body
fat posttransplantation are associated with an increased risk of
developing NODAT after hospital dismissal.23,24
The long-term benefit of kidney transplantation vs dialysis
at most weight classes seems obvious; however, Patibandla et
al noted that the benefit of transplant disappears for those with
a BMI > 41.5 The data of Glanton et al3 and Pelletier et al25
concur, with the latter authors recommending that this is per-
haps the point where bariatric surgery should be considered.
Results regarding patient and graft survival are variable with
multiple groups reporting that obesity does reduce patient and/
or graft survival at 1 year, 5 years, or longer.7,9,11,16,19,26-28
Meanwhile, several groups have reported no significant differ-
ences in patient or graft survival long-term.8,13,17,21,29 Meier-
Kriesche and colleagues’ elegant statistical analysis of almost
52,000 patients from the U.S. Renal Data System database
divided patients into BMI groups in 2-kg/m2 increments.28
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Table 2. Kidney Transplantation: Selected Weight Studies and Results.2-22,26,27,30,31,33,35
Reference Patients BMI Categories, No. (%) Outcomes
Holley15 46 obese vs normal-
weight controls
33 (72) class I/II
13 (28) class III
Obese: worse initial graft function and ultimately lower graft survival, longer LOS, longer surgical
times. Obese also had significantly more wound complications and increased incidence of new-onset
diabetes after transplant requiring insulin.
Merion13 263 (Univ of Michigan) 223 (85) nonobese (< 120%
ideal body weight)
40 (15) obese (> 120% ideal
body weight)
Increased rate of wound infections in obese (17.5%) vs nonobese (6.3%). No significant difference in
hypertension, rejection episodes, graft or patient survival at 3 y.
Pirsch14 584 (Univ of Wisconsin) 466 (80) BMI < 27.5
59 (10) BMI 27.5-30
59 (10) BMI > 30
Obese: DGF was significantly higher and was not influenced by preservation injury. No significant
differences in acute rejection occurred; however, a decrease in graft survival, especially from
immunologic causes, was a trend. Wound and urologic complications were higher in BMI > 27.
Johnson17 493 (Australia) 434 (88) BMI < 30
59 (12) BMI > 30
Obese: wound breakdown and infections more common in obese. BMI was independent predictor for
wound breakdown. Graft and survival were comparable at 5 y in carefully screened patients.
Glanton37443 obese, waitlisted
(U.S. Renal Data
All with BMI > 30 Obese tx recipients had much better survival than waitlisted patients. Death rates: obese living donor
1.9/100 patient years, obese deceased donor 3.3/100 patient years, and obese listed patients 6.6/100
patient years. Survival benefit disappeared for those patients with BMI > 41. Obese: deaths trended to
be associated with infection and coronary artery disease.
Gore727,377 (UNOS/SRTR) 1042 (4) underweight
12,089 (44) normal weight
8765 (32) overweight
3891 (14) class I
1590 (6) class II/III
Obesity associated with older age, female sex, African American race, less living donor tx, and more
comorbidities. Obese: 7% increased risk of DGF, more acute rejection, longer LOS, and decreased
overall graft survival.
Chang16 5684 (Australia) 218 (4) underweight
2719 (48) normal weight
1880 (33) overweight
867 (15) BMI > 30
Overweight and obesity were associated with DGF and rejection in first 6 months. Obesity: associated
not with decreased kidney outcomes but with factors such as coronary artery disease that led to
decreased graft and patient survival.
Schold2162,284 (UNOS) 15,255 (9) underweight
60,370 (37) normal weight
51,282 (32) overweight
24,342 (15) class I
11,035 (6.8) class II/III
Weight changes while listed: nearly one-third of patients changed classification between listing and
tx. One-fourth of obese lost weight enough to change BMI category. Weight gainers tended to be
female, Db, and on intermittent hemodialysis. Weight loss on waitlist did not influence post-tx
mortality or graft loss. Rapid pre-tx weight loss was associated with increased weight gain after
tx, so no long-term benefit seen. Nonobese: both rapid weight gain or loss pre-tx had significant
association with graft loss.
Segev4132,353 (UNOS
Standard Transplant
Analysis and
48,349 (37) normal weight
45,411 (34) overweight
25,509 (19) class I
9479 (7) class II
3605 (3) class III
Obese: trend to be female and/or African American. Mean waiting time increased with each BMI
category, as did likelihood of being passed over. Mean waitlist times: normal weight, 39 mo;
overweight, 40 mo; class I, 42 mo; class II, 51 mo. Class III had 59-mo wait and were 22%– 23%
more likely to be bypassed for transplant.
Furriel8448 (Portugal) 295 (66) normal weight
127 (28) overweight
26 (6) BMI > 30
Obese: more women, older. Overweight and obese had initial higher Cr, more DGF, longer operating
room time, and more surgical wound complications post-tx (lymphocele and wound dehiscence).
No differences in LOS, graft or patient survival, or rejection, with trend to less chronic rejection and
graft loss in obese.
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Reference Patients BMI Categories, No. (%) Outcomes
Molnar614,632 (maintenance
hemodialysis, DaVita)
1523 (11) BMI < 20
4903 (33) normal weight
4274 (29) overweight
2348 (16) class I
1584 (11) class II/III
35% overall death rate while waiting. Survival was affected by low BMI or unintentional weight
loss. Worst survival: low muscle mass/high BMI. Best survival: high muscle mass/low BMI. Each
increase of 1 kg/m2 BMI decreased death rate (0.96), while each kg decrease in dry weight increased
death hazard ratio (1.06). So, 5-kg weight gain = 20% better survival, while 3- to 5-kg loss = 31%
and > 5-kg loss = 51% higher death rate within all patients.
Molnar20 11,836 (SRTR/DaVita) Hemodialysis receiving
first tx
Pre-tx BMI predicted DGF—each 6.0-kg/m2 increase of BMI (a linear relationship) was associated
with a 30% higher risk of DGF, which increased as BMIs increased, so that those with BMI > 35 had
an 87% higher risk of DGF than those with BMI < 35. The association between BMI and DGF was
stronger in non-Db and extended donor criteria recipients.
Hoogeveen26 1810 (Netherlands) 305 (17) underweight
972 (53) normal weight
432 (24) overweight
101 (6) class I/II/III
Obesity pre-tx and at 1-y post-tx increased patient mortality and graft failure. BMI > 30 had 20%–40%
higher risk for death and graft failure compared to normal BMI patient. Weight gain after tx was also
a predictor for death and graft failure, especially with gains > 5 kg/m2 BMI.
Karabizak22 642 (SUNY Downstate
Medical Center)
77 (12) underweight
215 (33) normal weight
193 (30) overweight
99 (15) class I
61 (10) class II/III
Obese: higher Cr on dismissal, but the difference disappeared by 6 wk. Obesity was not a risk factor
for short- or long-term graft failure, survival, DGF, or acute rejection. No significant differences
between living vs deceased donor or race effect on patient or graft survival.
Bennett11 642 (Portland) 439 (68) BMI < 30
109 (17) class I
55 (8.5) class II
39 (6) class III
Class II/III trended to lower graft and patient survival but was not significant. Class III: Most
significant incidence of surgical wound infections. Obese: trend to more DGF and lower graft
survival, more pre-tx Db. No differences in rates of rejection or causes/rates of death.
Streja30 10,090 (SRTR/DaVita) 886 (9) BMI < 20
4250 (35) normal weight
3246 (32) overweight
1687 (17) class I
820 (8) class II/III
Obese: similar mortality but trend to higher loss of graft. Used serum Cr as marker of muscle mass
(low Cr = lower muscle mass). High BMI and high Cr had lower adjusted death risk, while low BMI
and low Cr trended to higher post-tx mortality.
Ditonno33 563 (Italy) 68 (12) underweight
310 (55) normal weight
143 (25) overweight
32 (6) class I
10 (2) class II/III
Obese: trend to more DGF but not significant. Obese did have significantly higher mean Cr and
worse Cr clearance at 6 mo, 1 y, and 3 y. Obese: increased risk of acute rejection, Cr, and metabolic
complications. Class II/III had more postoperative complications, including wound infections, which
led to longer LOS. No significant difference in patient or graft survival at every time point out 5 y.
Wang35 564 (China) 367 (65) normal weight
125 (22) overweight
72 (13) BMI > 30
Increased BMI was associated with increased incidence of chronic allograft nephropathy (2.046
times greater than normal weight). As BMI increased, so did incidence of hypertension, Db,
Grosso9376 (Italy) 122 (32.5) BMI < 25
190 (50.5) overweight
64 (17) BMI > 30
Obese tended to be older and male. Obese: significantly higher graft loss at 3 y and higher mortality
rate at both 1 and 3 y (mostly due to cardiac causes).
Table 2. (continued)
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Reference Patients BMI Categories, No. (%) Outcomes
Zrim12 508 (Australian and New
Zealand Dialysis and
10 (2) underweight
182 (36) normal weight
194 (38) overweight
93 (18) class I
29 (6) class II/III
Obese were more likely to be male and Db. Weight was associated not with graft failure but with death
with a functioning graft. No association with surgical complications but with wound complication,
need for graft nephrectomy, and DGF. Increased BMI had especially significant effect for
indigenous patients (ethnic effect).
Kuo21 487 (Univ of California–
213 (44) normal weight
153 (31) overweight
99 (20) class I
22 (5) class II
BMI between 30 and 40 kg/m2 had significantly higher risk for developing wound complications,
especially if patients had lost > 10 kg pre-tx (an independent variable).
Patibandla5619,151 (US Renal Data
System / UNOS)
252,789 (41) Db
366,362 (59) non-Db
Db was associated with reduced tx access/listing and Tx; however, this was influenced by increased
BMI and other comorbidities rather than Db per se.
Bardonnaud10 200 (France) 170 (85) BMI < 30
11 (6) class I
8 (4) class II
2 (1) class III
Obese: significantly older, more women, more pre-tx Db. Post-tx, more DGF, which caused longer
LOS but no other significant differences in short-term complications. Patient and graft survival was
not significantly different.
Hatamizadeh27 15,677 (SRTR) All > 65 y Obesity in recipients 65 to 75 y old was associated with lower graft survival. Db was a predictor of
lower patient survival in all age groups and lower graft survival in patient 65 to 70 y old.
Weissenbacher19 1113 deceased donors
367 (33) BMI > 25 BMI > 25: significantly increased incidence of DGF, especially if donor was overweight/obese as well.
BMI > 25: longer surgical time and cold ischemia time, probably the cause of the increased rate of
DGF. DGF also had more acute rejection, worse 1- and 5-y patient and graft survival.
Cannon31 74,983 (UNOS data,
52,668 (70) normal weight
15,010 (20) class I
5744 (8) class II
1561 (2) class III
Pre-tx obesity associated with African American race, more Db, longer wait time, more Db and
hypertension nephropathy, and more women. Recipient BMI was significantly associated with DGF.
Weight class was associated with graft survival, but the actual effect of obesity was small when
corrected for relevant comorbidities. No significant differences in adjusted 5-y patient survival
Kolonko18 513 (Poland) 29 (6) underweight
280 (55) normal weight
166 (32) overweight
38 (7) BMI > 30
Increased BMI was associated with higher renal vascular resistance primarily due to the influence of
obesity on the development of DGF or vice versa.
BMI, body mass index; Cr, creatinine; Db, diabetes; DGF, delayed graft function; LOS, length of stay; SRTR, Scientific Registry of Transplant Recipients; tx, transplantation; UNOS, United Network
for Organ Sharing.
Table 2. (continued)
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176 Nutrition in Clinical Practice 29(2)
They describe a “U-shaped” distribution of the relative risk for
graft loss and patient survival, with higher morbidity and mor-
tality at both the underweight and obese ends of the BMI spec-
trum and with the lowest risk (optimal outcome) in the BMI
range of 22–26 kg/m2. Streja et al reported the same mortality
but with a lower graft survival rates.30 Another group studied
21 obese renal transplant recipients (BMI > 30 kg/m2) and
compared their outcomes to 179 nonobese recipients (BMI <
30 kg/m2) and found a higher rate of lymphatic complications
and DGF, which led to longer hospital stays. This did not, how-
ever, affect long-term results related to graft and/or patient sur-
vival.10 The largest UNOS (United Network for Organ Sharing)
data study of post–renal transplant patients in the modern era
(2004–2010) retrospectively studied 19,983 patients. Those
with BMI > 30 kg/m2 were found to have a significantly
increased risk for DGF, and those with BMI > 35 kg/m2 were
noted to have increased risk for graft failure; however, there
was a minimal effect on adjusted 5-year survival. Investigators
did not conclude that transplant should be denied on the basis
of BMI criteria alone but that aggressive pretransplant risk fac-
tor modifications, which may include bariatric surgery, should
be implemented before transplantation.31
In addition, obesity/weight gain has been linked to an
increased incidence of elevated creatinine, chronic allograft
nephropathy, hypertension, and/or hyperlipidemia.16,32 Perhaps
less controversial is that when an obese recipient dies, it is
more likely to be with a functioning graft and due to either
cardiovascular or infectious causes.3,12,28 Recently, Ditonno
and colleagues studied 563 renal transplant recipients whose
BMI varied from < 18.5 kg/m2 to > 35 kg/m2.33 They noted
higher serum creatinine levels and worse renal function at
6-months, 1-year, and 3-year posttransplant follow-up visits in
those patients with BMI > 30 kg/m2. These patients also had
higher incidences of cardiovascular and metabolic complica-
tions. In addition, those patients with a BMI > 35 kg/m2 were
found to have more surgical complications, yet they did not
find any increase in infection or graft/patient survival among
any of the BMI groups.33 In a correlation study, Streja et al
noted that those obese candidates with higher muscle mass (as
noted by higher serum creatinine, > 14 mg/dL) had improved
(22% better) patient and graft survival after transplant than did
their peers with a low serum creatinine (< 4 mg/dL) before
transplant.30 Conversely, a small study of 37 renal transplant
patients, per an abstract by McCarthy, did not show a correla-
tion between BMI and changes in creatinine prior to transplant
discharge, and no significant differences were found in hospi-
tal length of stay, although this study was short in duration (3
months). The readmission rate was associated with diabetes
and sex).34
Pancreas Transplantation
A paucity of data on the role or impact of obesity on pancreatic
transplant outcomes remains, as most transplant centers have
fairly strict patient selection criteria, which has not allowed
many obese patients to ultimately be transplanted.36 Further
confounding the results is consideration of the type of pancreas
transplant: simultaneous pancreas-kidney transplant vs pan-
creas-after-kidney transplant vs pancreas transplant alone, as
well as a variety of BMI categorization and how obesity was
Table 3 shows the results of research published regarding
weight and obesity in pancreas transplantation. Only 2 studies
looked at the effect of sex on weight and pancreatic transplan-
tation, with both Fridell et al37 and Rogers et al38 noting that
obesity was more common in their male population. Other
studies did not report sex, so it is unclear how significant this
is and if it will remain over time.
Technical failure (leak, thrombosis, and/or infection) is a
common cause of pancreas graft loss and is associated with
increased preservation time, common in both the obese donor
and the recipient. Of the 7 most notable obesity studies, most
show some trend to increased short-term complications, but
there is some variance in what those complications were.
Bumgardner et al found a tendency for increased wound infec-
tions and bleeding in those with BMI > 27 kg/m2.39 Meanwhile,
Afaneh et al found a significantly higher overall complication
rate (63%) in the obese patients as compared to a normal
weight recipient (42%).40 These complications included post-
operative infections, length of stay after readmission, longer
operating room time, and a trend to more DGF. Rogers et al,38
in their review of 88 simultaneous pancreas-kidney transplant
patients, found that obesity increased the rate of anastomotic
pancreatic leaks to 17% (6 of 7 total leaks, with a mean BMI of
27 ± 1.9 kg/m2), compared to just 2% in the nonobese. In the
large University of Minnesota experience,41 in technical fail-
ures that caused pancreatic graft loss, an elevated BMI was the
highest risk factor, with a relative risk of 2.42. An elevated
donor BMI was also significant risk factor (relative risk =
1.66). Hanish et al concurred, finding a significant increase in
the rate of overall complications and postoperative infections
in those with BMI > 30.42 In the largest review of UNOS data
of 5725 simultaneous pancreas-kidney transplant recipients,
Sampaio et al noted a 38% increased risk of overall complica-
tions, especially due to DGF and graft thrombosis in the obese
recipients.43 Fridell et al, in their review of 308 recipients at
Indiana University, did not find a significant difference in post-
operative complications when comparing the obese to over-
weight or normal-weight recipients.37
In regard to long-term outcomes, Bumgardner et al and
Sampaio et al reported a relationship between obesity and long-
term patient and graft survival, with lower trends to both in the
obese patient.39,43 However, Afaneh et al did not see a significant
effect of weight on their patient and graft survivals.37-38,40,42
Heart Transplantation
The initial weight criterion used for heart transplantation (BMI
< 30 kg/m2 or < 140% ideal body weight) was borrowed from
the congestive heart failure population, even though evidence
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DiCecco and Francisco-Ziller 177
Table 3. Pancreas Transplant Weight Studies and Results.37-43
Reference Patients
BMI Categories, No.
(%) Outcomes
Bumgardner39 240 SPK (Ohio State) 212 (88) BMI < 27
28 (12) BMI > 27
Obese: no significant difference in hypertension, lipids,
immunosuppression, creatinine, complications, or acute rejection.
Obese tended to have more wound infections and hemorrhage
complications. While patient survival was comparable,
actuarial pancreas and renal graft survival was lower in the
obese. Posttransplantation deaths were most commonly due to
cardiovascular events and rejection.
Afaneh40 139 (NY Presby)
92 SPK
38 PAK
10 (7) underweight
67 (48) normal weight
35 (25) overweight
27 (20) obese
Obese: had overall higher complication rate (63% obese vs 42%
normal weight). Obese: had 6 times increased risk of developing
new-onset diabetes after transplant; and it occurred sooner than
normal weight, and with poorer control (higher mean A1c at 1 y).
Obese: increased postoperative infections, similar readmission
rate but tended to longer length of stay. Obese: trended to longer
operating room time, more blood products, increased rate of
delayed graft function. No difference was noted in death or graft
loss rates, nonsurgical complications, acute rejection, and length of
stay when compared to normal weight recipients.
Rogers38 88 SPK (Med Univ of
So Carolina)
52 (59) normal weight
17 (19) BMI 25-26.9
13 (15) BMI 27-29.9
6 (7) BMI > 30
Obese had increased rate of pancreatic anastomotic leak, male sex.
Similar rates of cumulative kidney and/or pancreas rejection. No
other significant effect on complications or patient/graft survival.
Obese tended to have lower 5-y pancreas graft survival with
similar kidney graft survival.
Humar41 937 (Univ of Minn)
327 SPK
399 PAK
211 PTA
BMI < 30 vs BMI > 30 13% technical failure rate caused graft loss in all patients. BMI > 30
was the highest risk factor (relative risk = 2.42). Donor BMI > 30
also significant (relative risk = 1.66)
Hanish42 145 (Duke)
110 SPK
34 PAK
112 (77) BMI < 30
33 (23) BMI >30
Obesity increased risk of overall complications of 81% vs 40% in
those with BMI < 30; same for postoperative infection rates (45%
obese vs 18% nonobese). Complications include dehiscence,
ventral hernia, abdominal infection, gangrene, and necrotizing
fasciitis. No significant difference in patient or graft loss. Trend to
increase in pancreatitis, leak, and postoperative insulin resistance.
Sampaio43 5725 (United Network
for Organ Sharing)
3201 (56) normal weight
1911 (33) overweight
549 (10) class I/II
64 (1) class III
Overweight and obese tended to be older and have more
cardiovascular disease. Obese had increased overall complication
rate (38%) risk due to delayed graft function, increased 1-y
kidney rejection rate and pancreatic graft thrombosis, which was
associated with increased death rate, pancreatic graft loss, and
kidney graft loss at 3 y. Other complication rates were not different
between normal weight and overweight patients.
Fridell37 308 (Indiana) 166 (54) normal weight
< 25
100 (32) overweight
42 (14) BMI > 30
Obese tended to be male and older. No significant differences were
noted on postoperative complications (technical, immunologic,
or infectious complications except for more cytomegalovirus) in
carefully selected patients.
BMI, body mass index; PAK, pancreas after kidney transplantation; PTA, pancreas transplantation alone; SPK, simultaneous pancreas-kidney
has been at level C.44 Therefore, the data are quite limited for
those with obesity, especially more than class I (BMI > 30).
Demographics of obese heart candidates suggest that they tend
to be diabetic, hypertensive, and/or African American, similar
to other transplant populations.45 See Table 4 for a summary of
heart transplant and weight research.
Several groups have looked at the effect of obesity on wait-
list survival and posttransplant effect. Amarelli and colleagues
conclude that the number of heart transplant patients listed
with BMI > 30 kg/m2 have increased significantly in recent
years and that these patients wait longer for their organs.46
Weiss et al, looking at nearly 27,000 patients within the UNOS
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178 Nutrition in Clinical Practice 29(2)
database, noted that the obese patients at transplant waited a
significantly longer time than nonobese such that for each 1 kg/
m2 in BMI, the chance of receiving a transplant decreased by
4% or a mean of 200 days longer on the waitlist.45 Those with
BMI > 30 also had increased waitlist mortality if they became
status 1, had a 6% lower 5-year mortality than their nontrans-
planted peers, yet had similar posttransplant outcomes. From
their data, Weiss et al calculated a 16% higher survival benefit
between an obese transplant recipient and a waitlisted peer.
Komoda et al, looking at the German experience of 558
patients, found that most patients stayed in the same weight
class while listed for transplant, with the overweight patients
having the best waitlist survival, even when they became criti-
cally ill or required a ventricular assist device. However, the
class I obese patients had the worst survival when they became
critically ill.47
Then, looking at peritransplant complications, Kashem et
al, in reviewing the Temple experience in 2008, found no effect
of obesity on mortality, reoperations, or infection rates; how-
ever, the recipients with BMI > 36 at transplant trended to have
a lower survival at all time points out to 5 years.48 Sareyyupoglu
et al49 did not find a significant effect of obesity on hospital
Table 4. Heart Transplantation Weight Studies and Results.45,47-52
Reference Patients BMI Categories, No. (%) Outcomes
Grady52 3540 (Cardiac
Transplant Research
Database, 33 centers)
123 (3) underweight
1497 (42) normal weight
1309 (37) overweight
499 (14) class I
101 (3) class II
11 (<1) class III
Obesity and underweight correlated with increased risk of
rejection at 1-y post-tx.
Kashem48 430 (Temple) 367 (85) BMI < 30
52 (12) BMI 31-35
11 (3) BMI > 36
BMI did not significantly predict mortality, need for
reoperation, or infection rates. BMI > 36 did trend to lower
survival at all-time points to 5 y.
Weiss45 26,962 listed (UNOS
Standard Transplant
Analysis and
9712 (36) normal weight
10,051 (37) overweight
5496 (20) class I
1703 (6) class II/III
Obese more likely to be diabetic, hypertensive, African
American. Obese waited longer than nonobese candidates
(mean of 200 more d). Each BMI increase of 1 kg/m2
decreased likelihood of tx by 4%. BMI > 30 was 35% and
BMI > 35 was 46% less likely to get a tx. BMI did not
influence overall increased risk of death on waitlist; however,
BMI > 35 + status 1 had higher waitlist mortality (39% at 3
y). Obese: similar short-term post-tx mortality rate but had 6%
lower 5-y survival. Obese survival was 16% higher if received
tx vs comparable waitlisted patients.
Sareyyupoglu49 484 (Pittsburgh) 159 (33) normal weight
185 (38) overweight
92 (19) class I
22 (4) class II
8 (2) class III
Mortality similar at all-time points out 5 y for each weight
class. BMI did not predict length of stay or vasculopathy or
increased risk of infection but trended to be more in class II
and III obesity.
Barten50 1007 (3 multicenter
BMI < 30 vs BMI >30 Obese had 21% risk of surgical wound complication compared
to 8.3% in those with BMI < 30. For every BMI increase of 1
kg/m2, the risk of surgical wound complication was increased
by 13.5%. Males also had increased risk of surgical wound
Russo51 19,593 (UNOS) 741 (4) underweight
7883 (40) normal weight
7280 (37) overweight
3005 (15) class I
684 (4) class II/III
Obesity associated with increased need for dialysis, more
new-onset diabetes, more rejection, increased risk of serious
infections, and coronary artery disease after tx. Class II/III
trended to higher morbidity/mortality over long-term through
10 y.
Komoda47 558 (Germany) 23 (4) underweight
237 (42) normal weight
204 (37) overweight
81 (15) class I
12 (2) class II
1 (<1) class III
83.2% of patients stayed in same class from listing to critical
illness. Overweight had best waitlist survival compared
to obese or normal weight, including when on ventricular
assist device or critically ill. Class I obesity patients had
significantly higher mortality than overweight on waitlist
when they progressed to critically ill status / ventricular assist
device placement
BMI, body mass index; tx, transplantation; UNOS, United Network for Organ Sharing.
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DiCecco and Francisco-Ziller 179
length of stay or the development of vasculopathy. Class II and
III obese patients did tend to have increased risk of infections,
but this was not significant. Meanwhile, Barten et al, looking at
data pooled from 3 centers, found a significant increased risk
of surgical wound infections in those with BMI > 30 such that
for every BMI increase of 1 kg/m2, the risk of surgical wound
complications increased by 13.5%. They noted that men over-
all tended to have more surgical wound complications as
well.50 Weiss et al saw a similar short-term mortality between
obese and nonobese patients.45 Last, Russo et al, while looking
at long-term UNOS data, found that the class II and III obese
patients tended to have significantly higher posttransplant
complications (dialysis, NODAT, rejection, infection, and cor-
onary artery disease) as well as higher overall mortality.51
Long-term data show a mixed picture of effect of obesity on
transplant outcomes, with some groups showing decreased
long-term morbidity and mortality.45,48,51 Kashem et al48 found
a trend to decreased survival in patients with BMI > 36 at all
time points out 5 years; Weiss et al45 calculated a 6% lower
5-year survival for obese recipients; and Russo et al51 found
similar results at 10 years. Meanwhile, others have shown little
or no effect on excess weight on long-term posttransplant out-
comes.49,52 Grady et al did note that while obese patients (and
the underweight) had an increased risk of rejection at 1-year
posttransplant, their long-term survival was not significantly
different.52 No significant difference was found in 5 year sur-
vival data by Sareyyupoglu as well.49
Lung Transplantation
With the advent of successful lung transplantation starting in
the early 1980s, strict criteria were developed due to the signifi-
cant imbalance between supply and demand as well as the
potential effect of obesity or low body weight on transplant suc-
cess. Borrowing from the cardiothoracic surgery and heart
transplant data available at the time, common weight criteria
have been to maintain a weight within 70%–130% of ones’
ideal body weight, with goals for weight gain or loss to meet
these criteria.53 Beginning in 2001 with Madill’s group, data
began to become available regarding the incidence and effect of
obesity on outcomes for lung transplantation.54 As with other
organs, the literature becomes more challenging to compare due
to practice changes, immunosuppression changes, single- vs
double-lung transplant, and different weight/obesity criteria, as
well as comparing listing vs weight at transplantation.
Table 5 reports research published in lung transplantation.
In descriptive terms, overweight and/or obese candidates as a
group have tended to have restrictive lung disease and hence
receive single-lung grafts, be older, be of male sex, and have a
higher lung allocation score.55-58 Importantly, Culver et al59
compared the traditional use of percentage body weight vs
BMI to determine the incidence of obesity in this population,
as well as determining if one measurement would be a more
reliable predictor of outcomes than another. This group found
that percentage body weight and BMI did not correlate and that
percentage body weight was not useful in predicting outcomes
When looking at the effect of obesity on immediate post-
lung transplantation, 7 studies showed that obesity did increase
90-day mortality and the incidence of grade 3 primary graft
dysfunction, which is an acute form of lung injury within 48–
72 hours and is the leading cause of morbidity and mortality
through 1 year posttransplant.60 This increase in risk seems to
develop around a BMI > 2754,56,60-62 and definitely by a BMI >
30.55,59 In addition, Madill et al noted an increase in intensive
care unit length of stay for those with BMI > 25 and a trend to
higher mortality for those receiving a double-lung transplant.54
In addition, Ye et al found a strong relationship between the
development of NODAT and those with a BMI > 30.63
Two groups have looked at the relationship among weight,
physical function, and quality of life. Hoy et al64 noted that,
based on the Short Form 36 Health Survey completed by
patients at a mean of 41 months posttransplant (range, 1–127
months), being overweight or obese pretransplant had a nega-
tive correlation with posttransplant physical function scale;
that is, an increased BMI before transplant correlated to
reduced posttransplant quality of life. However, they did not
quantify or describe what the weight histories were after trans-
plant, as this could have affected their functional status as well.
Sager et al used the 6-minute walk (a standard measure of
functional status in lung and cardiac disease where faster and
longer is better) to define functional status both pre- and post-
transplant. They found that a pretransplant BMI > 27 was asso-
ciated with decreased functional status pretransplant, which
carried over to posttransplantation. Being female and having
shorter pretransplant 6-minute walk results also correlated
with a decreased functional status at 1 year.65
The effect of obesity on long-term patient and graft survival
is less clear. Several groups have reported data indicating that
higher pretransplant BMI (> 30) correlates with decreased 3-
and 5-year survival.55 Lederer et al found that obesity (BMI >
30) functioned as an independent risk factor (increased risk of
12%) for death at 1 year and with an adjusted overall mortality
rate of 15% for overweight recipients and 22% for obese recip-
ients.56 Allen et al also found a higher mortality rate among the
obese (BMI > 30) compared to the other weight groups at 1 and
5 years.58 Conversely, Culver et al reported that pretransplant
obesity did not predict long-term outcome.59 Additionally,
Hadjiliadis et al57 and Kaplan et al66 both reported that their
obese patients (BMI > 30), despite trends in being older and
having a higher lung allocation score, had similar survival rates
as compared to their nonobese peers.
Liver Transplantation
Table 6 contains a summary of relevant studies and out-
comes regarding the role of obesity and weight in liver
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180 Nutrition in Clinical Practice 29(2)
Table 5. Lung Transplantation Weight Studies and Results.54-66
Reference Patients BMI Categories, No. (%) Outcomes
Madill54 229 total (Toronto)
62 single lung
184 double lung
23 (10) BMI < 17
62 (27) BMI 17 to < 20
82 (36) BMI 20-25
19 (8) BMI 25-27
43 (19) BMI > 27
32 (14%) died within 90 d of tx. Odds ratio significantly higher for
death within 90 d of tx in patients with BMI > 27 or male. Double
lung also trended to higher mortality. BMI > 25 had increased
intensive care unit length of stay but less death from sepsis.
Kanasky55 85 total (Univ of
19 (22) underweight
37 (44) normal weight
19 (22) overweight
10 (12) BMI > 30
Overweight and obese were more likely to have restrictive disease
while, normal weight and underweight were more likely to have
obstructive disease. BMI > 30 increased mortality rate 3 times
compared to normal weight. Each 1 kg/m2 increase in pre-tx
BMI increased risk of death by 7% post-tx and development of
obliterative bronchiolitis. Being overweight did not affect survival.
Culver59 283 total (Cleveland
177 single
106 double or heart/
43 (15) underweight
120 (42) normal weight
74 (16) overweight
46 (16) BMI > 30
Compared use of percentage ideal body weight to BMI for
predicting post-tx mortality. Percentage ideal body weight and
BMI were inconsistent and did not correlate with each other.
Pre-tx percentage ideal body weight did not have any utility
to predict post-tx mortality. BMI >30 patients had higher 90-d
mortality but this resolved by 1-y post-tx. Male and single-lung
tx also had increased risk of mortality.
Sager65 227 (Univ of Penn) No raw data Pre-tx BMI > 27 was associated with decreased functional status as
measured by 6-min walk. Females and shorter 6-min walk time
before tx were also associated with decreased functional status at 1 y.
Hadjiliadis57 181 total (Univ of
45 (25) BMI > 30 Obese tended to older and higher lung allocation score. Weight did
not affect survival in multivariate analysis.
Lederer62,56 5978 total (UNOS/
3671 single
2307 double
862 (14.5) underweight
2864 (48) normal weight
1644 (27.5) overweight
608 (10) BMI > 30
Overweight and obese were more likely to have diffuse
parenchymal lung disease and get single lung. Adjusted overall
mortality rate was increased by 15% for overweight and 22% for
obese compared to normal weight. At 1-y post-tx, obesity and
underweight together accounted for 12% of the deaths. Causes of
death trended to infection, coronary artery disease, and cancer.
Overweight had increased risk of death from PGD. Obese had
increased risk of death from respiratory failure
Kaplan66 154 total (Univ of
44 (29) BMI > 30 1- and 3-y survival rates were not statistically significant between
obese and nonobese, despite being older and having higher lung
allocation scores.
Allen58 11,411 (UNOS/
1355 (12) underweight
4998 (44) normal weight
3662 (62) overweight
1396 (12) BMI > 30
Overweight and obese were more likely to be older, male,
nonwhite, more idiopathic pulmonary fibrosis, shorter wait time,
more single-lung tx, less educated. Increased weight correlated
with hypertension and Db type II. Obese: decreased survival at
most time points and even when compared to normal weight
once corrected after 1 y and trended to more rejection. BMI did
not have effect on survival in Db lung recipients. The more obese
had lower 5-y survival than less obese.
Winterbottom61 232 (10 centers,
43% overweight
21% BMI > 30
Both overweight and obese had increased risk of grade 3 PGD within
72 h compared to normal weight and underweight, especially for
ILD but overall was independent of usual risk factors.
Lederer62 512 with chronic
pulmonary disease
224 (44) normal weight
197 (38) overweight
91 (18) BMI > 30
Overweight or obese more likely to have ILD, need
cardiopulmonary bypass, and have increased ischemia time.
Higher BMI increased risk of grade 3 PGD. Obesity had 2-fold
greater risk vs normal weight such that a 5-kg increase in BMI
caused a 40% increase in risk of stage 3 PGD at 72 h.
Ye63 2991 non-Db (UNOS) 212 (7) underweight
1347 (45) normal weight
1044 (35) overweight
388 (13) BMI > 30
BMI > 30 had 51% increased risk of developing new-onset
diabetes after transplant compared to normal weight.
Hoy64 92 (Vanderbilt) 5 (5) underweight
32 (35) normal weight
38 (41) overweight
17(19) BMI > 30
Overweight and obesity were associated with decreased physical
quality of life after lung tx.
Diamond60 1255 (LTOG, 10
119 (9) underweight
509 (41) normal weight
439 (35) overweight
188 (15) BMI > 30
Both overweight (odds ratio, 1.8) and obesity (odds ratio, 2.3) had
increased risk of grade 3 PGD at 48 or 72 h.
BMI, body mass index; Db, diabetes; ILD, interstitial lung disease; LTOG, Lung Transplant Outcomes Group; OB, obliterative bronchiolitis; PGD,
primary graft dysfunction; STAR, Standard Transplant Analysis and Research; tx, transplantation; UNOS, United Network for Organ Sharing.
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Table 6. Liver Transplantation-Selected Weight Studies and Results.67-73,76-86
Reference Patients BMI Categories, No. (%) Outcomes
Keefe77 276 total (Cal Pacific Med
18 (7) BMI > 33.2
5 (2) BMI 33.2-34.6
13 (5) BMI 36-48
Tx of obese was feasible with some increase in morbidity (wound infections, Db, HTN),
which was manageable. Pattern of weight gain or loss was unpredictable.
Braunfield83 40 with 61 matched controls
Control: mean BMI 23.5
Obese: mean BMI 36.3
Well-selected obese patients without coronary artery disease did not have increased risks or
complications compared to normal-weight controls. Obesity did not have any effect on
patient survival.
Sawyer78 277 (302 tx) (Univ of Virginia) 202 (73) BMI < 30
49 (18) class I
26 (9) class II/III
Severe obesity was associated with increased wound infections and early death from
multisystem organ failure but had similar long-term outcomes. Obese had similar results
and complication rates to normal weight; 1-y patient and graft survival was decreased but
not significantly and not at 3 y.
Nair76 121 (Johns Hopkins) 64 (53) nonobese (BMI < 27.3
women / < 27.8 men)
36 (30) obese
21 (17) severely obese (BMI > 32
women / BMI > 31.1 men)
Severely obese had increased wound infections, increased sepsis episodes, and longer
ventilation dependency and LOS but comparable long-term survival.
Nair69 18,172 (UNOS) 8382 (46) normal weight
5913 (33) overweight
2611 (14) class I
911 (5) class II
355 (2) class III
Class III: tended to be more women, more cryptogenic, have higher creatinine, and more
Db. Class II: higher 5-y mortality with primary cause due to cardiovascular events. Class
III: more primary graft failure (10%) and worse patient mortality at all periods but no
difference in graft survival. No significant differences in infection rates.
Rustgi85 26,920 (UNOS) 2991 (11) underweight
9056 (34) normal weight
8289 (31) overweight
3961 (15) class I
1585 (6) class II
738 (3) class III
Risk of death was increased in those underweight or BMI > 40. BMI did not significantly
affect graft failure rates.
Fujikawa84 700 (Univ of Florida) 288 (41) normal weight
245 (35) overweight
130 (19) class I
33 (5) class II
4 (<1) class III
No significant differences between groups in any clinical outcomes, graft or patient survival,
or financial outcomes.
Segev70 29,136 (UNOS Standard
Transplant Analysis and
25,448 (87) reference group BMI
< 35
2619 (9) class II
1069 (4) class III
Obese: more likely to be female, Db, have HTN, have severe ascites, higher MELD, and
more cryptogenic cirrhosis. Class II and III patients received significantly fewer MELD
exceptions and had more organ turndowns causing a lower tx rate for class II (11%) and
class III (29%).
Leonard67 704 (National Institute of
Diabetes and Digestive and
609 (Mayo Clinic Rochester)
67 (5) underweight
561 (43) normal weight
405 (35) overweight
178 (14) class I
69 (5) class II
33 (3) class III
Increasing trend in number of obese patients over the time of the data from 15% in early
1990s to >25% in 2002, mirroring society. Ascites/fluid overload was not equal between
groups; 11%–20% of patients with BMI > 25 had a lower BMI class when weight was
corrected for ascites. Each liter of ascites removed at tx increased the relative risk for post-
tx mortality by 7% and graft failure by 6%. No difference in patient or graft survival, but
class III did trend to longer LOS. Selected obese do well with comparable outcomes
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Reference Patients BMI Categories, No. (%) Outcomes
Dick71 71,466 (UNOS) 1847 (3) BMI < 18
68,172 (95) BMI 18-40 (control)
1447 (2) class III
Class III: higher MELD, were younger, more females, Caucasian, more likely to be in
ICU and had longer LOS, hepatitis C virus or cryptogenic disease, severe ascites. At tx,
obese had longer ischemia times from older donors who had a higher BMI. Class III had
increased risk of death due to infection and cancer. Class III obesity was an independent
variable for death in the multivariate analysis.
LeMattina72 813 (Univ of Wisconsin) 25 (3) underweight
216 (27) normal weight
266 (33) overweight
176 (22) class I
83 (10) class II
47 (6) class III
Obese: longer waiting time with comparable MELD, more nonalcoholic steatohepatitis,
longer operating room times and blood use, more infections, wound complications, and
intraoperative complications. Class II: had the most complications overall (decreased
patient and graft survival, longer ICU stay, more reoperations). Class III had more deep
vein thromboses and trend to more hernias. No significant differences in causes or overall
in graft and patient survival except in class II.
Mathur80 159 with hepatocellular
carcinoma (Univ of So
47 (30) normal weight
54 (34) overweight
58 (35) BMI >30
Overweight and obese had significantly more severe complications and longer LOS.
Hepatocellular carcinoma recurred sooner and in greater frequency in both overweight and
Taner82 73 (Mayo Clinic Florida) All BMI > 40 6 of 73 (8.2%) “superobese” required re-tx (40.2-61.1 BMI kg/m2). All had complications
including 2 perioperative deaths.
Orci73 38,194 (Scientific Registry of
Transplant Recipients)
952 (2.5) underweight
11,430 (30) normal weight
13,354 (35) overweight
7797 (20) class I
3348 (9) class II
954 (2.5) class III
359 (1) BMI > 45
At waitlisting, 37.6% had BMI > 30, which was associated with Db, HTN, coronary artery
disease, and drug-treated chronic obstructive pulmonary disease. Overweight and obese
males had lowest mortality rates, while underweight had highest. In women, only being
underweight increased risk of death. Underweight and normal weight tended to gain weight
while listed, while overweight and obese tended to lose weight. Being overweight seemed
to have a protective effect, especially in males.
Schoening86 313 (Germany) BMI < 25 vs BMI > 25 Men tended to have higher BMI after tx; 81.3% of cardiovascular deaths occurred beyond 5
y after tx, with more in men especially after 10 y. While increased BMI, HTN, and Db did
not significantly affect survival, they did occur more in males who had lower survival rates.
Hakeem79 1325 (UK Leeds) 47 (3) underweight
643 (49) normal weight
417 (31) overweight
145 (11) class I
73 (6) class II/III
Overweight and obese had significantly increased rates of infection that cause a trend in
increased ICU days and LOS. No difference in graft or patient survival between any weight
230 (Cleveland Clinic) 183 (80) normal weight
47 (19)
BMI > 38 (mean 41.6 kg/m2)
Used BMI 38 kg/m2 to help correct for fluid retention. No significant difference in patient or
graft survival, ICU or hospital LOS, but selective group with relatively low MELD. Obese
did have higher incidence of metabolic syndrome after tx. Follow-up > 3 y may be needed
to discern true cardiac effect on survival.
Vater68 206 (Univ of Washington) 141 (65) BMI < 30
65 (32) BMI class I/II/II
Nonobese patients had significantly more ascites at tx than obese, 17 of 65 (26%) obese
became non-obese when wt was corrected for ascites. Ascites at tx, not obesity, influenced
perioperative factors.
BMI, body mass index; Db, diabetes; HTN, hypertension; ICU, intensive care unit; LOS, length of stay; MELD, model for end-stage liver disease; tx, transplantation; UNOS, United Network for
Organ Sharing.
Table 6. (continued)
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DiCecco and Francisco-Ziller 183
While heart, kidney, and, to some extent, lung transplant
candidates may have enough fluid retention to affect their
BMI, it is not comparable to the amount of ascites and edema
that many liver transplant candidates may have. Therefore, it is
critical in this portion of the literature—to accurately compare
results—to be clear about which weight is used: listing, at
transplant, corrected or not corrected for ascites. For example,
Leonard et al67 and Vater et al68 both reviewed the importance
of ascites and its effect on weight and BMI. Leonard et al found
that ascites itself increased the relative risk for posttransplant
mortality (each liter of ascites increased mortality by 7% and
graft loss by 6%) as well as drove BMI up so that when weight
was corrected for ascites drainage at transplantation, 11%–20%
of patients with BMI > 25 actually had a lower BMI classifica-
tion. Vater et al found comparable results, with 26% of their
patients becoming “nonobese” or having a BMI < 30 after their
weight was corrected for ascites.68
In determining who the obese liver failure/potential trans-
plant candidate is, several groups have sought to describe this
population. Fairly consistently, it seems to be women, those
with diabetes or cryptogenic cirrhosis (presumably nonalco-
holic fatty liver disease or nonalcoholic steatohepatitis
[NASH]), those with higher Model for End-Stage Liver
Disease (MELD) scores, those of younger age, and those who
are more ill (increased creatinine, more ascites, hypertension,
coronary artery disease, and chronic obstructive pulmonary
disease).69-73 Specific liver diseases are related to obesity as
well, such as NASH. Patients with NASH tend to have a higher
BMI than patients with other liver diseases. Charlton and his
group74 demonstrated that 63% of NASH patients had BMI >
30 kg/m2, as compared to patients with other types of liver dis-
ease, of which 32% had BMI > 30 kg/m2. In addition, NASH is
on a predicted path to be the most common indication for liver
transplantation with the next 1–2 decades.75 Important though,
is that while the obese population may qualify as sick enough
for transplant, Segev et al70 and LeMattina et al72 found that
this population often waits a significantly longer time for liver
transplant. In addition, Segev et al found that those with BMI
> 35 received significantly less MELD exceptions and had a
higher rate of organ turndowns, leading to a much lower rate of
transplantation (class II at 11% less often and class III at 29%
less often) than those with BMI < 35.70 They begin the discus-
sion regarding list bias against the obese liver transplant candi-
date and wonder if is it justified. Whether true or not, it is likely
that some patients have been bypassed in hopes that they would
lose more weight. What is unclear is whether this delay is
worth the risk of catastrophic events in the meantime and/or
the patient is missing one’s opportunity for transplantation.
In terms of immediate or perioperative complications, most
data suggest that those with BMI > 30 are at an increased risk
for wound infections,76-78 more overall infection and sep-
sis,71,76,79 as well as other potential complications, such as lon-
ger ischemia times,71 longer vent/intensive care unit stays,76,79
longer hospital length of stay,67,76,79,80 and perhaps more
metabolic syndrome/diabetes and hypertension.77,81 All of
these potential complications lead to some increased risk of
early posttransplant mortality.71,78 Nair et al also reported an
increased rate of primary graft failure (10%) in their class III
obese patients.69 Only Perez-Protto et al did not see trends or
significant differences among the obesity groups’ short-term
posttransplant; however, the authors recognized that their very
obese patients were a relatively select group with low MELD
scores.81 Yet, Taner et al reported their experience in retrans-
planting 73 “super” obese patients (BMI > 40).82 While all
patients had complications and were challenging to manage
(including 2 perioperative deaths), they still felt that it was
worth the effort.
Long-term effect of obesity on liver transplantation is not
quite as clear, as the data do not reflect consistent results in the
obese patient. Groups have reported no significant effect of
obesity on patient or graft survival.76,78,79,83,84 Meanwhile, those
groups that have seen the influence of obesity on transplant
outcomes have reported decreased survival,71 more complica-
tions but less effect on survival,72 increased mortality but no
effect on graft failure,85 and more death from cardiovascular
complication in class II obesity69 and in the obese, especially
men.86 Mathur et al found a correlation between overweight
and obese patients and the rapidity of recurrent hepatocellular
carcinoma.80 Siegel et al also looked at outcomes of hepatocel-
lular carcinoma in obese patients after transplantation and
found that those with a BMI > 30 km/m2 had significantly
decreased overall survival and a trend toward predicting hepa-
tocellular carcinoma recurrence.87 Elevated BMI was related to
increased microvascular invasion within hepatocellular carci-
noma tumors. Given these data, Dick et al, instead of avoiding
transplantation of the obese, suggest that we should not wait
for them to lose weight but that they should be transplanted
earlier (at a lower MELD score) to decrease their complica-
tions and improve survival.71
When Do Transplant Patients Gain
Posttransplant weight gain is prevalent to some degree in all
organ types and occurs for a variety of reasons. General
thoughts regarding why posttransplant weight gain occurs
include the potential for metabolic changes that may result in
better nutrient absorption and/or reduced energy expenditure
with improved organ function after transplant. Furthermore,
during the immediate posttransplant period, patients are less
active as they recover from surgery, and returning to an active
lifestyle can be a slow process. Another contributing factor
may be that many patients are enjoying a less restricted diet
and an improved appetite, which can lead to “celebratory eat-
ing” on a regular basis.88-90 Steroid-induced hyperphagia is
often blamed for the weight gain; however, this can falsely
absolve the transplant recipient from taking responsibility to
try to control his or her intake and weight.
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184 Nutrition in Clinical Practice 29(2)
In a small study of renal transplant patients by Stanfill and
others, the patients expressed their personal thoughts on why
they gained weight. The most prevalent reasons included medi-
cation effect on appetite, enjoyment of a nonrestricted diet,
lack of knowledge regarding exercise and nutrition, and a fear
that exercise could injure their new kidney.89 Metabolic data by
Schütz et al (42 liver transplant, 39 cirrhotic, 30 kidney trans-
plant, and 10 hemodialysis patients) revealed, as expected, an
increase in metabolic rate of transplant patients compared to
that predicted in the cirrhotic and dialysis patients.91 However,
the posttransplant patients were comparable to their predicted
resting energy expenditure. Dietary recall indicated that the
patients were not exceeding their calorie intake goal. Liver
recipients all had increased weight, fat mass, body cell mass,
and muscle mass compared to the cirrhotic patients, with simi-
lar but not statistically significant trends in the kidney popula-
tion (presumably due to lower numbers). This led the authors
to conclude that long-term posttransplant patients are not just
overweight but also sarcopenic (increased weight and body fat
with decreased muscle mass). Those patients who were obese
at the time of transplant gained more weight after transplant
than did normal-weight patients.16 Cupples et al, when com-
paring weight gain with food intake and exercise levels, found
that their group of patients had a mean weight gain of 6% (9.6
lb) at 6 months, with a 7% increase in BMI. Food records indi-
cated that their nutrient intake was stable from transplant
through 6 months: lower total calories but higher fat intake.
Activity records showed a decrease in mean hours of sleep and
no significant increase in their daily activity levels. This infor-
mation is important as we try to design programs and monitor-
ing systems to for better posttransplant weight management.92
In early research during the cyclosporine era, Merion et al
found that obese recipients (defined as > 120% ideal body
weight) gained more weight (mean 14.2 ± 2.2 kg) than the non-
obese (weight < 120% ideal weight; mean 8.9 ± 0.6 kg).13
Torres et al, in their review of 152 Brazilian patients, found the
incidence of being overweight and obese increased from 22%
before transplant to 60% at 10 years posttransplant, then
decreased to 36% between 15 and 20 years.32 They noted a
mean gain of 12.4% during year 1 and 16.6% by year 5 after
transplantation. In addition, there was a significant positive
association between having gained weight and having a better
creatinine clearance.32 In a review of weight gain rates in 100
kidney transplant patients, Nazemian et al found that their
patients tended to lose weight in the first month after trans-
plant, then progressively gain over the following year (men
gained a mean of 5.9 kg and women, 9.7 kg).93 This weight
gain was also associated with being older, being female, and
having increased lipid levels. It did not correlate with socio-
economic status or acute rejection events. El-Agroudy et al fol-
lowed 650 kidney recipients who had a normal BMI at
transplant; 188 (29%) went on to become overweight, and 86
(13%) became obese at 6 months. While the obese patients had
significantly more hypertension, NODAT, coronary artery
disease, and increased lipids, they did not experience any
increase in other complications, including infection. In addi-
tion, the authors noted that the obese patients were more likely
to die due to cardiac events, while the normal-weight and over-
weight patients’ most common cause of death was infection.94
Hoogeveen et al found that continued weight gain after 1 year
posttransplant, irrespective of pretransplant weight, also
increased risk of death by 22% and graft failure by 18% for
every 5-kg/m2 increase in BMI.26 Torres et al, in a long-term
analysis of weight changes after transplant, found that weight
gain was progressive and significant over 20 years posttrans-
plant, with a maximum of 60% of patients being overweight or
obese at 10 years and then a decline in prevalence to 36% at 20
years posttransplant. The authors also found an association
between posttransplant weight gain and improvement in creati-
nine clearance.32
In a study of 139 pancreas transplants, researchers found
that underweight pancreas transplant recipients had significant
weight gain by 6 months posttransplant and through 36 months
posttransplant. The group with a “normal” BMI did not have
significant weight gain until 18 months and after. The over-
weight and obese groups were not found to have significant
increases in weight during these time frames. In fact, the BMI
in the obese group had significantly decreased at 6 months
posttransplant but became similar to their pretransplant BMIs
by 18 months out.40 In addition, Bumgardner et al found that
men gained more total weight in the year after transplantation,
gaining an average of 11.1 kg while women gained an average
of 7.3 kg.39 The authors also noted that 25% of the patients who
were not obese before transplant became obese by 1 year after-
ward due to their significant weight gain.
Williams et al compared weight at transplant in 158 heart
transplant patients and 128 renal transplant patients to their
weight at 1 year posttransplant.95 The study shows signifi-
cantly more weight gain in the heart transplant recipients
(mean of 10.3 kg in the first year) as compared to the renal
transplant patients, whose weight increased by 3.6 kg during
the same time frame. Prednisone dose did not correlate to the
degree of weight gain in either of the 2 groups studied.95 Grady
et al found that 79% of patients gained weight after heart trans-
plantation, including an increase in the numbers who had a
BMI > 30 kg/m2, from 17% at transplant to 38% at 5 years
posttransplant. Both African American men and women tended
to gain more weight than Caucasian men and women.52
In a recent study of 42 lung transplant patients in 2011,
Bossenbroek and colleagues found that overweight and obese
recipients had lower physical activity levels based on pedom-
eter steps, lower fat-free body mass, and lower resting energy
expenditures based on ventilated-hood measurement.
Interestingly, there was no difference in the daily calorie intake
between the 2 groups, with the overweight/obese trending to a
slightly lower intake. This led the authors to believe that the
posttransplant weight and body fat mass gains were not due to
increased intake but rather a decreased activity level.96 In a
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DiCecco and Francisco-Ziller 185
study of 579 lung transplant recipients in 2003, investigators
noted an increased posttransplant 1-year survival in those
patients who gained weight in the first year. The group saw a
10% average weight gain after lung transplant, and patients
with obstructive and interstitial lung diseases tended to gain
more weight than those with other types of lung diseases.97
Weight gain after liver transplantation tends to occur in the
initial 6- to 12-month period after transplant. While some
patients need to gain weight and/or muscle mass, those who are
overweight or obese at the time of transplant tended to remain
in those weight categories after transplant or not gain signifi-
cant amounts.88 In a review of 80 liver transplant patients, out-
comes indicate that patients who lost weight before transplant
due to liver disease tended to regain that weight within 1 year
after transplant. The average weight gain in the first year after
transplant in this study was 9.1 kg, and at 3 years after liver
transplant, the average patient had gained 11.6 kg. More than
half these patients were either overweight or obese by 3 years
post–liver transplant. Factors related to the incidence of post-
transplant weight gain included having an elevated BMI pre-
transplant and a family history of obesity, among other
Can Transplant Candidates and/or
Recipients Lose Weight?
Most centers agree that obese patients listed for solid organ
transplant should be actively making an effort to improve their
nutrition status. For some, this may mean gradual controlled
weight loss and, for others, simply making healthful dietary
changes and/or increasing physical activity as able. It is gener-
ally not advised that patients pursue rapid weight loss through
fad diets or fasting, as this can compromise organ function and
nutrition status. Caregivers need to also be aware that while
many patients have an elevated BMI, they may also have ele-
ments of malnutrition. Their end-stage disease, various symp-
toms of organ failure, as well as the element of fatigue certainly
make controlled successful weight loss a daunting task in the
transplant population.37
In addition to general health issues, being overweight or
obese can affect organ function. Research has shown that obe-
sity increases the risk of developing renal disease,99 cardiac
disease, and nonalcoholic steatohepatitis.74
In those patients with BMI > 30 kg/m2, weight loss has been
shown to reduce the progression of focal segmental glomerulo-
sclerosis.100 Morales and colleagues have shown that patients
with chronic proteinuric renal disease who followed a 500-cal-
orie-per-day deficit diet and successfully lost a moderate
amount of weight reduced their degree of proteinuria.101 Wang
et al studied 38 obese patients with chronic kidney disease for
2 months while they attempted to make healthful diet and exer-
cise changes. The authors found that those who successfully
lost at least 3% of their body weight had significant improve-
ment in their lipid profile, estimated glomerular filtration rate,
and blood pressure measurements.102 In a study of 1229 kidney
transplant patients, 10% of the patients with a BMI > 30kg/m2
successfully lost weight before transplant, with only 5% losing
enough to reduce their BMI to < 30 mg/k2.29
Pancreas transplant recipients are also being studied in
regard to obesity. Despite finding increased risk of posttrans-
plant complications as well as early increased rates of graft
failure and patient death in those with a BMI > 30 kg/m2,
Sampaio and his group did not advocate avoiding transplanting
these patients. They encouraged gradual weight loss before
transplant but felt that weight alone should not postpone trans-
plant timing, as it may further compromise outcomes because
renal and diabetic issues can worsen.43 Humar and colleagues
also suggest that pancreas transplant recipients make an effort
to lose weight before transplant surgery due to the finding that
recipient BMI > 30 kg/m2 was a relative risk in technical fail-
ure of pancreas grafts.41
However, research indicates that an “obesity paradox”
exists in renal dialysis patients and has been shown in patients
with congestive heart failure as well. Some studies have sug-
gested that patients on dialysis tend to have improved survival
with higher BMI.2 This phenomenon deserves further study
toward whether or not BMI is the best measurement of obesity
in this patient population and if different lifestyle recommen-
dations should be provided to those who will remain on dialy-
sis vs those waiting for renal transplant.103 In research of heart
failure patients, Russo et al note that malnutrition/underweight
has been related to poorer overall prognosis with or without
transplant. Looking at posttransplant outcome of underweight
heart transplant patients, they found increased risk of early
infection and decreased 1- and 10-year survival.51
In a study of 344 patients with advanced heart failure, Clark
et al found that increased waist circumference and increased
BMI were associated with improved survival outcomes in end-
stage heart disease.104 Per guidelines developed by the
European Society of Cardiology, Dickstein et al concluded
(class 1 evidence) that “weight reduction in patients with heart
failure should be considered to prevent the progression of heart
failure, decrease symptoms and improve well-being.”105 A
small study of 19 obese heart failure patients receiving left
ventricular assist device placement found that those postinser-
tion lost weight and reduced their BMI from a mean of 36.1 kg/
m2 to 31.8 kg/m2 in 6 months as compared to no weight change
in those patients who did not receive the device.106 Russo et al
considered nutrition status a “potentially modifiable risk fac-
tor” in reducing posttransplant risks, highlighting the need to
closely monitor the nutrition status of patients while they are
waiting for heart transplantation, in hopes of avoiding severe
malnutrition or increasing weight.51
Landmark research by Madill et al set the stage for an
increased awareness of the effect of both malnutrition and obe-
sity in the lung transplant population. Patients with emphysema,
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186 Nutrition in Clinical Practice 29(2)
cystic fibrosis, and other bronchiectasis tended to be malnour-
ished pretransplant and were found to be able to regain nutrition
status posttransplant.107
Diffusing the metabolic abnormalities that can occur after
transplantation through close patient monitoring is essential.
Both the Fridell37 and Hanish42 groups, while finding a poten-
tial increase in complications in obese post–pancreas trans-
plant patients, conclude that careful postoperative monitoring
of obese patients is needed and that encouraging weight loss as
organ function normalizes may be helpful in minimizing long-
term obesity-related complications. Sager and colleagues con-
clude that overweight patients waiting for lung transplant
should be advised to work toward an appropriate weight goal.65
In a study of 23 patients regarding weight gain, resting
energy expenditure, and body composition after liver trans-
plantation, Richardson et al found a common pattern of increas-
ing total calorie and fat intake, as well as total weight and body
fat, yet a significantly decreasing resting energy expenditure.
Changes in body composition did not correlate with immuno-
suppressive drug doses. The authors speculate that the liver
denervation’s effect on thermogenesis, as well as changes in
metabolic hormones, contributes to the altered metabolism and
weight gain, rather than dietary intake alone.108 Another group
studied the body composition of 143 patients who were at least
1 year out from liver transplant, using bioimpedance, BMI
measurements, and waist circumference. It noted that bio-
impedance and waist circumference measurements resulted in
higher percentages of overweight/obese patients than if BMI
was used. Dietary surveys done with these patients indicate
that a lower intake of calcium was associated with obesity.109 A
recent study by Sprinzel et al looked at 170 post–liver trans-
plant patients and found a 32.9% rate of new-onset metabolic
syndrome after transplant. Interestingly, pretransplant risk fac-
tors identified as affecting the development of new-onset meta-
bolic syndrome posttransplant include glycosylated
hemoglobin > 5%, diabetes mellitus, and arterial hypertension.
Due to the potential morbidity and/or mortality issues related
to metabolic syndrome, the authors recommend lifestyle inter-
ventions, including counseling on weight and lipid manage-
ment. The patients may need specific advice regarding physical
activity goals and, possibly, medical treatment of persistent
Ongoing Weight Management Efforts
In a small study done recently in 35 renal transplant recipients,
the authors noted a mean posttransplant weight gain of 17 lb by
12 months and that those patients with a lower BMI posttrans-
plant tended to have a higher intake of vegetables. Their veg-
etable intake was only between 2.07 ± 2.71 servings per day,
suggesting that a relatively small change may help control
weight.111 Focus group data gathered by Stanfill et al found
that kidney transplant recipients did desire education and sup-
port regarding how to deal with barriers to healthy eating, bar-
riers to physical activity, perceived effects of weight gain, as
well as intervention ideas. This might include healthy cooking
classes, support groups, written physical therapy recommenda-
tions, and meal plans.89 Intervention by a transplant dietitian
can contribute to healthier overall eating habits and a trend for
weight loss in overweight patients who have had a renal trans-
plant as shown in research by Orazio and colleagues. The study
included 102 patients and did result in lowering the total and
saturated fat intake in the group given dietary advice.112 In a
review of nutrition management of renal transplant recipients,
Chan et al offered suggestions for clinical care, including
restricting dietary sodium intake, weight reduction if needed,
and providing calcium and vitamin D supplementation.113
Grady and her group recommend providing obese patients
with specific weight loss guidelines after heart transplant with a
plan for follow-up in the outpatient area for nutrition education,
exercise goals, and psychological interventions to aid in weight
loss success. Providing individualized advice to those with
varying cultural backgrounds, those at risk for weight gain and
those with other comorbidities may also help these patients
achieve weight loss success and improved quality of life.52
Some transplant centers have implemented a dedicated
treatment plan to manage obese patients who may benefit from
gradual controlled weight loss before transplant surgery. This
may include more frequent follow-up visits with a transplant
dietitian, implementation of a calorie-restricted meal plan, spe-
cific weight goals (BMI < 35), encouragement to attend weight
loss support groups, completion of food and weight records,
and the use of a pedometer to track activity. Success includes
enabling about 75% (46 of 75 patients) to lose weight (mean of
10.6 kg). In addition, 14 patients lost to their BMI < 35 and
have undergone transplantation. This shows that the team
approach, while labor-intensive, can be effective, including
physical therapy, nutrition, psychiatry, and surgeon and hepa-
tologist support. Further study is warranted to determine if
patients can maintain their weight loss posttransplantation and
if will reduce their risk for long-term complications.114
Should There Be Criteria or Exclusion for
Transplantation Based on Weight?
Whether or not transplant centers should impose a BMI cutoff
for transplant candidacy remains controversial. Most transplant
programs consider weight as one of many other factors when
considering the appropriateness of transplant for individual
patients. Research has shown variable results in transplant/graft
outcomes related to obesity. BMI is typically used to determine
appropriateness of weight despite its obvious flaws, including
being unable to differentiate fluid vs fat mass or muscle mass.
BMI also does not indicate distribution of the fat mass (ie, apple
vs pear shape), which may affect the surgical technicality.
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DiCecco and Francisco-Ziller 187
Table 7. Common BMI Guidelines for Transplant Weight
BMI, kg/m2
Organ Optimal Considered
Relative Contraindication
Dependent on Other
Heart <30 30-35 >35
Lung 19-27 27-30 >30
Pancreas <27 28-30 >30a
Kidney <35 35-40 >40a
Liver <30 30-40 >40a,b
BMI, body mass index.
aBMI where many consider bariatric surgery.
bUnless bariatric surgery concomitant with transplantation.
Many centers follow guidelines similar to those in Table 7,
although more research is needed regarding long-term follow-
up outcomes for obese solid organ transplant recipients. Factors
including patient age, cardiac status, exercise tolerance, and
overall physical well-being are all parts of the equation as well.
The BMI categories may be useful in identifying higher-risk
groups of patients.
Future Opportunities
Genomics and other metabolic research may play an exciting
role in the diagnosis, prevention, and management of obesity
and its related comorbidities for the transplant population. For
example, Cashion et al, in their genomic research on post–kid-
ney transplant weight gain, were able to preliminarily identify
several genes that were both positively and negatively corre-
lated with weight gain at 6 months after transplant.118 Watt et al
have reported that 2 of the 3 PNPLA-3 genotypes (GG and
CG)—which are associated with nonalcoholic fatty liver dis-
ease, obesity, liver fibrosis, and insulin resistance—are also
associated with obesity both before and after transplant through
3 years. This included even those who were not obese before
transplantation. Meanwhile, those with the CC genotype were
much less likely to become obese at 3 years after transplant.119
This may become valuable genomic information to allow
determination of a nutrition plan for those patients as well as
explain why some struggle with weight loss more than others.
Forli et al noted a disruption in energy metabolism in 35
patients studied after heart and lung transplantation. His group
measured serum leptin levels and compared these to metabolic
syndrome and weight gain. Leptin is a satiety hormone, and
higher leptin levels may represent leptin resistance. In this
study, patients with higher serum levels of leptin had increased
incidence of both metabolic syndrome and degree of weight
gain at 12 months posttransplant. This effect was more preva-
lent in the lung patients. This area deserves further investigation
into other solid organ transplant recipients and with larger
patient numbers.120
Bariatric Surgery in Pre– and Post–Organ
As a method of more permanent weight loss, obese transplant
candidates and recipients are now being considered for bariat-
ric surgery.121,122 Knowledge is only in its infancy regarding
the optimal procedure and timing for bariatric surgery pre-
transplant, concurrent with transplant or posttransplant. In
addition to the usual bariatric cares, these patients need to be
monitored closely for fluid management, prevention of nutri-
tion deficiencies, and effect on immunosuppressive medication
levels.123-125 The importance of avoiding those bariatric proce-
dures that induce an element of malabsorption, to prevent med-
ication malabsorption posttransplant, is still unknown.
Before transplant, the largest published bariatric experience
in those with kidney failure is by the Wesley Alexander and
Cincinnati group.126 The advantage of pretransplant bariatric
surgery is the potential benefit to ease the obesity-induced
“workload,” which may postpone the need for transplantation
and/or enable enough weight loss to allow transplantation.127,128
One of the concerns, however, is the increased risk for the
development of oxalate nephropathy and its effect on renal
Select transplant centers are performing bariatric surgery in
obese renal and liver patients before transplant, at the time of
transplant, or after recovery from transplantation. Lin and col-
leagues recently studied 26 renal and liver transplant candi-
dates and found that laparoscopic sleeve gastrectomy was safe
and the patients lost enough weight to meet their center’s BMI
criteria within 12 months after surgery. Eight of these patients
eventually underwent transplant and sustained their weight
loss for the first year based of study duration.130 Additional
case reports of various bariatric procedures used (laparoscopic
band, gastric sleeve and Roux-en-Y-gastric bypass) have been
published by several programs, all reporting successful recov-
ery and weight loss, as well as enabling patients to qualify for
The Mayo Clinic Rochester group has initiated a protocol
to determine the effectiveness and safety of combining liver
transplantation with a gastric-sleeve procedure in those
patients unable to successfully lose weight before transplant.
In an initial review of their first 8 patients, significant weight
loss was achieved, and none of the patients developed NODAT.
Complications did occur, with the primary one a gastric staple
line leak, which required reoperation, and with 1 patient hav-
ing excess weight loss, which was stabilized with dietary
counseling. This type of procedure requires close monitoring
and encouragement of hourly fluid intake and a focus on
intake of protein sources.134 In addition, several other groups
have reported their experience with bariatric surgery after
transplantation, again with reported good initial success with
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188 Nutrition in Clinical Practice 29(2)
weight loss, reversal of comorbidities, and minimal effect on
Bariatric surgery, within the field of transplantation, has
challenging and exciting potential. We encourage the follow-
ing of a specific protocol designed to meet the combined
needs of bariatric surgery patients as well as those with special
needs because of their organ failure or posttransplant issues.
This will be key to a program’s success for optimizing patient
outcomes. Further research with larger patient numbers and
long-term results is needed to determine the most appropriate
timing, to identify if special needs exist, and to guide long-
term management.114
Perhaps the conflicting results in the literature reflect the conun-
drum of obesity itself: is obesity a complicating factor, or is it
the obesity-related comorbidities that really contribute to differ-
ences in outcomes? Many have shown that in carefully selected
obese patients, the short- and long-term transplant outcomes are
very similar as those of normal-weight recipients. Perhaps these
obesity-related comorbidities should really be the important
screening criteria and selection points and not weight based on
the absolute BMI.85 This may be especially true considering
that many patients would be in a different BMI classification if
their weight was corrected for fluid retention.67,135
There is no doubt that present research available in obesity
and transplant can be difficult to interpret due to differences in
weights used (ie, listing weight vs weight at the time of trans-
plant) and a lack of consideration of weight change while wait-
ing for transplant.79 From an outcomes perspective, it may be
relevant to find out if weight loss pretransplant was intentional
or unintentional, rapid or gradual. Some studies group obese
patients as having a BMI > 30 kg/m2 rather than comparing
differences among the classes of obesity (I, II, and III). Yet
another confounding factor is simply change of practice in the
field of transplantation over the years. The effect of various
eras of transplant with respect to improvements in immunosup-
pression, surgical expertise/experience, and general differ-
ences in program protocols may affect results/outcomes.17
Researchers need to continue to look at other markers or
criteria, such as waist circumference or the measurement of
lean and fat body mass, to use as refined parameters rather than
absolute BMI alone to better assess a patient’s risk.136
Furthermore, transplant clinicians need to see past the BMI and
be attentive to elements of malnutrition present not only in
underweight and normal-weight patients but in the obese as
well. This may be obvious sarcopenia, cardiac cachexia, or sig-
nificant debility or the more subtle temporal muscle wasting or
ongoing decline in protein intake. With no potential benefit and
opportunity for harm, waiting for patients to lose weight before
listing or transplant may not be worth the risk.
In general, the transplant team agrees that weight is just one
of many factors to consider when selecting appropriate
transplant candidates. While weight loss before transplantation
may or may not change outcome, Lentine et al suggest that all
transplant candidates be encouraged to develop healthy behav-
iors before transplant. These positive lifestyle changes may
minimize posttransplant weight gain and optimize posttrans-
plant outcomes.137 Transplant programs need to be proactive in
caring for obese patients, both before and after transplant.
Providing appropriate nutrition education, exercise advice, and
psychiatric care as well as close follow-up of weight, blood
pressure, and lipids allows the patient the opportunity to take
good care of his or her new organ. Managing obesity and its
comorbidities likely will effect issues such as program cost and
outcome statistics. Patients also need to be aware that changes
in these comorbidities could affect their transplant candidacy,
as well as improve their posttransplant quality of life.
Ultimately, we all want to make ethical decisions and pro-
vide patients with a chance at a healthy future. We need further
guidance in the development of recommendations in regard to
weight appropriateness for specific transplant types, as well as
the presence of comorbidities considered safe for successful
transplant and the years following. Since nutrition and weight
issues are potentially modifiable, it is an area of study worthy
of future research.
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... These interventions are often designed to have an impact on diet and/or physical activity patterns, and increasingly involve cognitive behavioural therapy components such as goal-setting, self-monitoring, and problem-solving [4,5]. In SOT recipients, excess weight gain and obesity are associated with adverse outcomes including cardiovascular disease, graft failure, and increased mortality [6][7][8], and are consequently recognised as important considerations in the design of lifestyle interventions for these patients [6,9,10]. Although recent research suggests that effective lifestyle interventions for weight management in SOT recipients must be tailored to the unique physical and psychosocial requirements of this population [11][12][13][14][15], evidence on how to best meet these needs in delivering post-transplant lifestyle advice is scarce. ...
... These interventions are often designed to have an impact on diet and/or physical activity patterns, and increasingly involve cognitive behavioural therapy components such as goal-setting, self-monitoring, and problem-solving [4,5]. In SOT recipients, excess weight gain and obesity are associated with adverse outcomes including cardiovascular disease, graft failure, and increased mortality [6][7][8], and are consequently recognised as important considerations in the design of lifestyle interventions for these patients [6,9,10]. Although recent research suggests that effective lifestyle interventions for weight management in SOT recipients must be tailored to the unique physical and psychosocial requirements of this population [11][12][13][14][15], evidence on how to best meet these needs in delivering post-transplant lifestyle advice is scarce. ...
Full-text available
Previous research suggests that effective lifestyle interventions for solid organ transplant (SOT) recipients must be tailored to address the unique life circumstances of this population. As few studies have investigated this design consideration, this study aimed to explore the perspectives and experiences of SOT recipients after completing a Group Lifestyle Balance™ [GLB]-based intervention incorporating either (a) standard population-based nutrition guidance or (b) nutrigenomics-based nutrition guidance. All active participants in the Nutrigenomics, Overweight/Obesity, and Weight Management-Transplant (NOW-Tx) pilot study were invited to participate. Data were collected through focus groups and individual interviews. Ninety-five percent (n = 18) of the NOW-Tx pilot study participants enrolled in the current study: 15 participated in 3 focus groups; 3 were interviewed individually. Three themes were common to both intervention groups: (1) the post-transplant experience; (2) beneficial program components; (3) suggestions for improvement. A unique theme was identified for the nutrigenomics-based intervention, comprising the sub-themes of intervention-specific advantages, challenges, and problem-solving. The readily available and adaptable GLB curriculum demonstrated both feasibility and acceptability and was aligned with participants’ needs and existing health self-management skills. The addition of nutrigenomics-based guidance to the GLB curriculum may enhance motivation for behaviour change in this patient population.
... As mentioned earlier in this review, many institutions adopt a BMI cut-off for access to transplantation, therefore, propose to the patient to lose weight in the pretransplant setting with medical and/or surgical treatment [103]. Medical weight loss techniques, nutritional and pharmacological could potentially be effective but are resource intensive and have a modest long-term success rate [104]. ...
... Medical weight loss techniques, nutritional and pharmacological could potentially be effective but are resource intensive and have a modest long-term success rate [104]. While medical management has a very limited role in the CKD population [103], surgery has proven to be highly effective for weight reduction [105]. Bariatric surgery which was considered, no longer than a decade ago, high risk among kidney transplant candidates [106], has shown in recent reports acceptable morbidity and mortality rates in CKD [105,107] and ESRD patients [108,109]. ...
The prevalence of obesity among patients with chronic kidney disease continues to increase as a reflection of the trend observed in the general population. Factors affecting the access to the waiting list and the transplantability of this specific population will be analyzed. From observational studies, kidney transplantation in obese patients carries an increased risk of surgical complications compared to the non‐obese population; therefore many centers have been reluctant to proceed with transplantation, despite this treatment modality confers a survival advantage over dialysis. As a consequence, obese patients continue to face decreased access to the waiting list, with a lower likelihood of being transplanted and higher waiting times when compared to the non‐obese candidates. In this review will be described the current strategies for treatment of obesity in different settings (pre‐transplant, at transplant and post‐transplant)Obesity represents a risk factor for surgical complications but not a contraindication for kidney transplantation; outcomes could be greatly improved with its multidisciplinary and multimodal treatment. The modern technology with minimally invasive techniques, mainly using robotic platform, allows a reduction in the surgical complications rate, with graft and patient survival rates comparable to the non‐obese counterpart.
... Obesity is a factor that affects surgery and overall health due to its comorbidities and complications worldwide [30]. On the other hand, today it is accepted in the malnutrition class due to the negative results it creates in the organism [31]. ...
... However, the obesity paradox should not be a barrier in advising weight loss to patients suffering from severe obesity. These benefits of obesity mainly span in the overweight to mildly obese range, whereas there is enough evidence on adverse outcomes in patients suffering from severe obesity with a BMI > 40 kg/m 2 to refute using the obesity paradox as an excuse to prevent weight loss, either before or after transplant [19][20][21]. ...
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PurposeSevere obesity can increase risk of complications after kidney transplantation. There is a paucity of literature on bariatric surgery outcomes in renal transplant candidates. The objective of this study was to analyze outcomes of bariatric surgery as a weight reduction strategy for patients with kidney failure to enhance eligibility for kidney transplantation.Materials and Methods We performed a retrospective analysis of the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program database at a single institution for patients with chronic kidney disease receiving hemodialysis therapy (CKD G5D) undergoing bariatric surgery between 2011 and 2018.ResultsOf 2363 patients who underwent bariatric surgery, 38 (1.6%) had CKD G5D; median age (range) was 49 years (33; 69), 52.6% were female, and mean BMI was 44.2 kg/m2. Twenty-four patients underwent laparoscopic Roux-en-Y gastric bypass (LRYGB), and 14 patients underwent laparoscopic sleeve gastrectomy. Seventeen patients (46%, n=37) had a BMI≤35 at 6 months, while 25 patients (75.8%, n=33) achieved a BMI≤35 at 12 months. Of these, 18 patients (47%) were listed for kidney transplant, and 8 patients (21%) received kidney transplant. There was no statistically significant difference between sleeve and LRYGB procedures in patients who reached BMI of 35 at 12 months (P=0.58). Median length of stay was 2.3 days. Thirty-day readmission rate was 2 patients (5.3%), and 2 patients (5.3%) required reoperation (one for bleeding, one for acute recurrent hiatal hernia). No mortality occurred.Conclusion Laparoscopic bariatric surgery offers effective weight loss for CKD G5D patients to achieve transplant eligibility with acceptable outcomes.Graphical abstract
... As a method of permanent weight loss, obese transplantation candidates and recipients are now being considered for bariatric surgery [13,14]. Before transplantation, the largest published bariatric experience in patients with kidney failure is by Alexander et al [15]. ...
During the last century, obesity has become a global epidemic. The effect of obesity on renal transplantation may occur in perioperative complications and impairment of organ function. Obese patients have metabolic derangements that can be exacerbated after transplantation and obesity directly impacts most transplantation outcomes. These recipients are more likely to develop adverse graft events, such as delayed graft function and early graft loss. Furthermore, obesity is synergic to some immunosuppressive agents in triggering diabetes and hypertension. As behavioral weight loss programs show disappointing results in these patients, bariatric surgery has been considered as a means to achieve rapid and long-term weight loss. Up-to-date literature shows laparoscopic bariatric surgery is feasible and safe in transplantation candidates and increases the rate of transplantation eligibility in obese patients with end-stage organ disease. There is no evidence that restrictive procedures modify the absorption of immunosuppressive medications. From 2013 to 2016 we performed six bariatric procedures (sleeve gastrectomy) on obese patients with renal transplantation; mean preoperative body mass index (BMI) was 39.8 kg/m². No postoperative complication was observed and no change in the immunosuppressive medications regimen was needed. Mean observed estimated weight loss was 27.6%, 44.1%, 74.2%, and 75.9% at 1, 3, 6, and 12 months follow-up, respectively. Our recommendation is to consider patients with BMI >30 kg/m² as temporarily ineligible for transplantation and as candidates to bariatric surgery if BMI >35 kg/m². We consider laparoscopic sleeve gastrectomy as a feasible, first-choice procedure in this specific population.
The increasing obesity epidemic has major implications in the realm of transplantation. Patients with obesity face barriers in access to transplantation as well as unique challenges in perioperative and postoperative outcomes. Due to comorbidities associated with obesity along with the underlying end‐stage organ disease leading to transplantation candidacy, these patients may not even be referred for transplant evaluation, much less be waitlisted or actually undergo transplantation. However, the utilization of bariatric surgery in this population can help optimize the transplant candidacy of patients with obesity and end‐stage organ disease as well as improve perioperative and postoperative outcomes. In this paper, we will review the impact of obesity on kidney, liver, and cardiothoracic transplant candidates and recipients, as well as explore potential interventions to address obesity in these populations.
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Background: International guidelines recommend dysplasia surveillance in IBD. Aim: To compare endoscopic techniques for dysplasia surveillance METHODS: We searched MEDLINE, Embase, CENTRAL for randomised trials through May 2019. We estimated odds ratios (ORs) for binary and mean differences (MDs) for continuous outcomes, using frequentist random-effects network meta-analysis. We assessed study risk of bias and appraised evidence certainty using GRADE. Results: Eighteen trials (2638 participants) were included. Standard definition white-light endoscopy (OR 0.44, 95% CI 0.26-0.73; high certainty) and i-SCAN (OR 0.47, 95% CI 0.25-0.90; moderate certainty) had lower odds of detecting neoplasia than chromoendoscopy. Fujinon intelligent colour enhancement (FICE), standard definition white-light endoscopy and i-SCAN had lower odds for this outcome than full spectrum high definition white-light endoscopy (ORs 0.02 to 0.15; low certainty). Standard definition white-light endoscopy had lower odds of detecting nonpolypoid neoplasia than full spectrum high definition white-light endoscopy, narrow band imaging, chromoendoscopy and high definition white-light endoscopy (ORs 0.01-0.14; moderate certainty). Full spectrum high definition white-light endoscopy ranked as the best technique for both outcomes (moderate certainty). Standard definition white-light endoscopy had lower odds of detecting neoplasia by target biopsy (OR 0.27, 95% CI 0.08-0.91) and had shorter procedure time (MD -14.81 minutes, 95% CI -25.03, -4.06) than chromoendoscopy (moderate certainty). Conclusions: Chromoendoscopy, high definition white-light endoscopy, narrow band imaging, autofluorescence, FICE and full spectrum high definition white-light endoscopy may be comparable for dysplasia surveillance. Standard definition white-light endoscopy and i-SCAN probably provide lower yields for neoplasia identification. Full spectrum high definition white-light endoscopy may represent the first-line approach.
Background: International guidelines rate class III (morbid) obesity (body mass index [BMI]≥40 kg/m(2) ) as a relative contraindication for liver transplantation (LT) requiring further research. Moreover, data on the mortality risk in candidates with a BMI: 30-34.9 and 35-39.9 kg/m(2) (class I and class II obesity, respectively) are weak. Aim: Herein, we compared post-operative complications and mortality risks in all obese candidates vs candidates with a BMI: 18.5-29.9 (normal/overweight) assumed as controls. Methods: We searched the Cochrane library, PubMed, Scopus, Web-of-Science and article reference lists, restricted to the English language, and selected cohort studies analysing the following outcomes: all-causes mortality (at 30 days, 1-2-3-5 years), post-operative and cardiopulmonary complications, hospital and intensive care unit (ICU) length of stay. Two reviewers independently extracted the studies data and a third one resolved discrepancies. Results: Twenty-four studies comprising 132 162 patients met the inclusion criteria. As compared to controls, mortality risk was increased at all time-periods (except at 3 years) for a BMI≥40, at 30 days for a BMI: 30-34.9 and in none of the considered time-periods for a BMI: 35-39.9. Post-operative complications were significantly higher for a BMI>30 and 30-34.9. Due to the shortage/absence of data, we evaluated cardiopulmonary complications, hospital and ICU length of stay only in the BMI≥30 category. In these patients, only cardiopulmonary complications were increased as compared to controls. Conclusions: Morbid obesity has an impact on patients' survival after LT. However, since even a BMI>30 increases post-transplant complications, new strategies should be included in the LT programme to favour weight loss in all obese candidates.
Obesity and weight gain are serious concerns after solid organ transplantation (Tx); however, no unbiased comparison regarding body weight parameter evolution across organ groups has yet been performed. Using data from the prospective nationwide Swiss Transplant Cohort Study, we compared the evolution of weight parameters up to 3 years post-Tx in 1359 adult kidney (58.3%), liver (21.7%), lung (11.6%), and heart (8.4%) recipients transplanted between May 2008 and May 2012. Changes in mean weight and body mass index (BMI) category were compared to reference values from 6 months post-Tx. At 3 years post-Tx, compared to other organ groups, liver Tx recipients showed the greatest weight gain (mean 4.8 ± 10.4 kg), 57.4% gained >5% body weight, and they had the highest incidence of obesity (38.1%). After 3 years, based on their BMI categories at 6 months, normal weight and obese liver Tx patients, as well as underweight kidney, lung and heart Tx patients had the highest weight gains. Judged against international Tx patient data, the majority of our Swiss Tx recipients' experienced lower post-Tx weight gain. However, our findings show weight gain pattern differences, both within and across organ Tx groups that call for preventive measures. This article is protected by copyright. All rights reserved.
The transjugular intrahepatic portosystemic shunt (TIPS) is a non-selective portosystemic shunt created using endovascular techniques. The first TIPS was performed in Germany in 1988. The VIATORR self-expandable PTFE covered stent-graft (WL Gore, Flagstaff AZ) was approved by the FDA for a TIPS application in December of 2004. This stent-graft offers excellent shunt patency rates and it is possible that it has a beneficial effect on patient survival. Patient surveillance and post-procedural management have changed after the introduction of this stent-graft. This article presents the current management strategies that are followed at our Institution for patients who have undergone a TIPS procedure with a VIATORR stent graft including imaging follow-up, management of encephalopathy, medical management and nutritional aspects.
The influence of body mass index (BMI) on outcome of simultaneous pancreas-kidney transplantation (SPK) has not been well described. We retrospectively reviewed 88 consecutive primary SPKs performed at our institution between March 15, 1995 and August 28, 2001. All patients received antibody induction and maintenance immunosuppression with tacrolimus, mycophenolate mofetil, and steroids. Systemic-enteric implantation was performed in all patients. Primary end points were patient, pancreas, and kidney survival. Secondary end points were rates of anastomotic leakage, pancreas thrombosis, major infection, rejection, repeat laparotomy, and length of hospital stay. Values are shown as mean±standard deviation, range, or percentage. Fifty-two patients (59.1%) were nonobese with a BMI ⩽24.9 (mean 21.7±2.2, range 15.4 to 24.9). Thirty-six patients were mild to moderately obese with a BMI ⩾25 (mean 27.7±2.2, range 25 to 35.1). Distribution of recipient age, sex, and ethnicity was similar between groups. Kidney and pancreas preservation times were similar between nonobese and obese patients. One-, three-, and five-year actuarial patient (nonobese: 95%, 95%, 95% vs. obese: 95%, 95%, 89%), kidney graft (nonobese: 91%, 91%, 87% vs. obese: 97%, 91%, 85%), and pancreas graft (nonobese: 78%, 78%, 73% vs. obese: 70%, 62%, 62%) survival were comparable between nonobese and obese (P = NS). The mean rates of pancreas thrombosis, major infection, pancreas rejection, kidney rejection, relaparotomy, and length of hospital stay were similar in the two groups. The overall duodenojejunal anastomotic leakage rate was 8%. Obese patients had a 17% incidence of leakage (6 of 36) compared to a 2% incidence of leakage in nonobese patients (P = 0.012). Six of seven leaks occurred in obese patients. Mean BMI in the seven patients with a leak (27±1.9) was significantly higher than in patients who did not develop a leak (24±3.7; P = 0.05). Although obesity had no effect on patient or graft survival, it was associated with a significantly higher leakage rate. There should therefore be a higher degree of suspicion for the presence of duodenojejunal anastomotic leaks in obese SPK recipients.