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Effect of Body Mass Index at Time of Transplantation and Weight

Gain After Transplantation on Allograft Function in Kidney Transplant


Recipients in Shiraz
G. A. Raiss-Jalali, A. R. Mehdizadeh, A. Razmkon, J. Rouzbeh, S. Behzadi, H. Memari, and S. A.
Malek-Hosseini

ABSTRACT
Chronic renal allograft dysfunction is the most common cause of graft loss, for which there
are multiple risk factors, including obesity before transplantation, which is believed to
lower long-term renal allograft survival. One hundred eighty-two kidney transplant
recipients were studied. Body mass index (BMI) at the date of transplantation was
calculated. BMI values were classified into 4 categories: (1) patients with BMI ⬍20, (2)
BMI between 20 and ⬍25, (3) BMI between 25 and ⬍30, and (4) BMI ⱖ30. The minimum
follow-up period in this study was 3 years after transplantation. The link between
categorized BMI and the presence of renal allograft dysfunction and mortality within 3
years posttransplantation was investigated using independent sample t test. BMI at the
date of transplantation showed statistically significant association with presence of renal
allograft dysfunction and mortality within 3 years posttransplantation (P ⫽ .008, P ⫽ .01,
respectively). BMI at the date of transplantation has a strong association with outcomes
after renal transplantation. The extremes of very high and very low BMI are important risk
factors for chronic renal allograft dysfunction; therefore, weight adjustment before kidney
transplantation can be useful in improving the function of a transplanted kidney and
increasing patient’s survival.

A DVANCEMENTS in renal transplantation (Tx) have


dramatically improved outcome, especially 1-year graft
survival rates for recipients with end-stage renal disease
that obese patients should be excluded as candidates for
transplantation.5,11,12 The purpose of this study was to
assess the relationship between BMI and between WG after
(ESRD).1,2 Recent studies indicate that pre-Tx obesity and Tx and renal allograft function in recipients of renal grafts
increased body mass index (BMI) in adults are associated with in a single center.
decreased long-term renal allograft survival.3–5
Increased BMI is an important risk factor for death in the MATERIALS AND METHODS
general population and has also been linked to specific
causes of mortality, such as cardiovascular death.6,7 Simi- This is a retrospective review of medical records from 182 renal
allograft recipients at Shiraz Transplant Center between 1987 and
larly, in patients with ESRD who have undergone renal Tx,
1999. Patients’ files in addition to Persian Network for Organ
higher BMI has been associated with a significantly in-
Transplant (PNOT) were used to collect data such as age, gender,
creased patient mortality.3,8 However, available data sug- BMI at the time of operation, source of organ, amount of WG after
gest that being overweight or obese at the time of kidney 3 years, and cause of ESRD in recipients. Regular follow-up was
transplantation has a detrimental effect on both the patient performed at the time of operation, every 3 months in the first year
and allograft outcomes.5,7 Furthermore, kidney transplant after the operation, and every 6 months in the following years. The
recipients are at risk for even further significant weight gain normal levels of creatinine and blood urea nitrogen (BUN) were
(WG) post-Tx.9,10 Thus, the impact of the obesity epidemic defined as ⬍1.8 mg/dL and 15– 45 mg/dL, respectively.
may have far-reaching consequences in this high-risk
group.9 From the Southern Organ Transplant Center, Shiraz, Iran
Because of the reported poorer outcomes of renal trans- Address reprint requests to Ghanbar Ali Raiss-Jalali, MD, PO
plantation in obese patients, some investigators suggested Box 71455-166, Shiraz, Iran. E-mail: ali_ra@yahoo.com

0041-1345/05/$–see front matter © 2005 by Elsevier Inc. All rights reserved.


doi:10.1016/j.transproceed.2005.08.036 360 Park Avenue South, New York, NY 10010-1710

2998 Transplantation Proceedings, 37, 2998 –3000 (2005)


EFFECT OF BMI AND WEIGHT GAIN 2999

Table 1. Demographic and Risk Factors Among 4 Groups


BMI

Group 1 Group 2 Group 3 Group 4

No. (%) 56 (31%) 86 (47%) 28 (15%) 12 (7%)


Age (mean ⫾ SD) 33.9 ⫾ 11.2 34.3 ⫾ 10.3 33.0 ⫾ 12.4 34.7 ⫾ 14.7
Male/female 3 (42/14) 2.44 (61/25) 3 (21/7) 2 (8/4)
Source of organ
Cadaveric 3 (5.3%) 4 (4.6%) 2 (7.1%) 1 (8.3%)
Living 53 (94.7%) 82 (95.4%) 26 (92.9%) 11 (91.7%)
Primary cause of ESRD
GN 16 (28.6%) 30 (34.9%) 9 (32.1%) 4 (33.3%)
DM 14 (25%) 22 (25.6%) 9 (32.1%) 5 (41.7%)
HTN 8 (14.3%) 14 (16.3%) 4 (14.3%) 1 (8.3%)
AI 4 (7.1%) 6 (6.9%) 3 (10.7%) 2 (16.7%)
Abbreviations: GN, glumeronephritis; DM, diabetes mellitus; HTN, hypertension; AI, autoimmune disease.

BMI was calculated based on the formula: BMI ⫽ weight .007), allograft dysfunction (P ⫽ .008), and mortality rate
(kg)/[height (m)2] at the time of operation and was documented by during the 3 years after Tx (P ⫽ .01); however, there was no
the transplant coordinator. Patients were divided into 4 groups: (1) statistical significant relationship between WG and BMI at
patients who had BMI ⬍20; (2) BMI between 20 and ⬍25; (3) BMI the time of Tx (P ⫽ .645), serum BUN (P ⫽ .28), serum
between 25 and ⬍30; and (4) BMI ⱖ30.
creatinine (P ⫽ .612), allograft dysfunction (P ⫽ .993), and
WG was calculated based on the formula: WG ⫽ [weight at third
mortality rate after Tx (P ⫽ .361).
year after Tx (kg)]-[weight at the time of Tx]. Patients were divided
into 4 groups: (A) patients with WG ⬍5; (B) WG between 5 and The distribution of patients and also the mean BUN,
⬍15; (C) WG between 15 and ⬍25; and (D) WG ⱖ25. creatinine, mortality rate, and frequency of allograft dys-
Allograft dysfunction was defined as the following: serum creat- function in different groups are shown in Table 2.
inine level ⬎1.8 mg/dL, pathological diagnosis of renal allograft
rejection, need to administer steroid pulse therapy, and need for DISCUSSION
admission due to allograft dysfunction.
The chi-square test and independent samples t test were used to BMI is a strong independent risk factor for patient mortal-
evaluate the relationship between the groups. P ⬍ .05 was defined ity and graft failure independent of patient death after renal
as statistical significance. transplantation.7 Evidence is emerging demonstrating a
negative role of obesity on outcome of renal Tx in adults.
RESULTS
Most reports agree that renal Tx in obese adult patients is
Of 182 patients, 50 were female and 132 were male associated with increased patient mortality, diminished
(male/female ratio ⫽ 2.64). The mean age of recipients was short-term and long-term graft survival, and increased
34.0 ⫾ 9.9 (14 –58) years. Ten patients received organs from surgical and medical complications. Moreso et al4 showed
cadavers, 76 from live-related donors (LRD), 24 from that obese kidney transplant recipients had a reduced
live-unrelated donors (LURD), and 22 from spouses. De- short-term graft function. Modlin et al5 and Halme et al8
mographics and major risk factors among 4 groups are showed that BMI ⬎30 was associated with increased patient
shown in Table 1. Mean patient BMI was 22.2 ⫾ 4.6 kg/m2 mortality. Recently, Meier-Kriesche et al3 demonstrated
(12.3–50.7) and mean patient WG was 11.3 ⫾ 7.4 (0 –35) kg. that even mild obesity (BMI ⬎25) was an independent risk
The mean average BUN during the first 3 years after Tx factor for both decreased graft survival and patient survival.
was 21.6 ⫾ 6.2 mg/dL (12– 62). BUN was significantly In contrast, Drafts et al13 showed no correlation between
higher in patients with higher BMIs (P ⫽ .03). mild obesity and graft survival for either cadaveric or
The mean average serum creatinine level during the first live-donor Tx. In addition, no difference in graft survival
3 years after Tx was 1.4 ⫾ 0.5 mg/dL (0.7– 4). There was no between obese and age-matched non-obese patients was
significant difference between groups 1 and 2, but in reported by Merion et al.14 In our study, the rate of
patients with BMI ⱖ 25 kg/m, the creatinine level increased allograft dysfunction and the mortality rate were higher in
with increasing BMI (P ⫽ .01). patients with obesity (BMI ⱖ30). Also, in underweight
Mean BMI in patients with allograft dysfunction was 21.6 patients, these rates were higher compared with patients
⫾ 3.8 kg/m2 and in patients without allograft dysfunction with normal weight. Therefore, we can conclude that being
was 25.6 ⫾ 7.1 kg/m2 (P ⫽ .004). underweight is also a risk factor for renal Tx.
Frequency of allograft dysfunction in group A was a little A number of potential factors may account for the
more than groups B and C, and in group D, it was increasing prevalence of overweight and obesity in ESRD
significantly higher than others (P ⫽ .02). patients undergoing transplantation. First, demographic
There was statistical significance between BMI at the groups at greatest risk for chronic kidney disease (ie,
time of Tx and serum BUN (P ⫽ .011), serum Cr (P ⫽ diabetics and minorities) are also those with an increased
3000 RAISS-JALALI, MEHDIZADEH, RAZMKON ET AL

Table 2. Relationship Between Mean BUN, Creatinine, Patient Allograft Dysfunction, and Mortality, with BMI and WG
BMI WG

Group 1 Group 2 Group 3 Group 4 Group A Group B Group C Group D

No. (%) 56 (31%) 86 (47%) 28 (15%) 12 (7%) 38 (21%) 97 (53%) 39 (22%) 8 (4%)
Mean BUN (mg/dL) 20.4 21.1 24.3 27 22.5 21.4 21 21.7
Mean creatinine (mg/dL) 1.4 1.4 1.5 1.9 1.5 1.4 1.4 1.4
Frequency of allograft 12.5 10.5 17.9 50 17.9 12.5 12.8 33.3
dysfunction (%)
Mortality rate (%) 3.9 0 14.3 25 5.1 5.2 5.1 0

prevalence of overweight and obesity.15 Second, more 5. Modlin CS, Flechner SM, Goormastic M, et al: Should obese
patient subgroups at increased risk of obesity (eg, older patients lose weight before receiving a kidney transplant? Trans-
plantation 64:599, 1997
patients and blacks) are undergoing transplantation.16
6. Calle EE, Thun MJ, Petrelli JM, et al: Body-mass index and
Third, better management of uremia during ESRD over mortality in a prospective cohort of U.S. adults. N Engl J Med
recent years, as reflected by increasing Kt/V,16 could theo- 341:1097, 1999
retically improve dietary intake. Fourth, general behavioral 7. Meier-Kriesche HU, Arndorfer JA, Kaplan B, et al: The
and cultural influences that have encouraged excess caloric impact of body mass index on renal transplant outcomes: a
significant independent risk factor for graft failure and patient
consumption or inadequate physical activity also may be death. Transplantation. 73:70, 2002
manifest in patients with ESRD.17 8. Halme L, Eklund B, Kyllonen L, et al: Is obesity still a risk in
The reason for worse outcome in obese patients has not renal transplantation? Transpl Int 10:284, 1997
been clearly defined. In adults, obesity is considered a 9. Friedman AN, Miskulin DC, Rosenberg IH, et al: Demo-
graphics and trends in overweight and obesity in patients at time of
significant comorbidity after renal Tx leading to increased
kidney transplantation. Am J Kidney Dis 41:480, 2003
cardiac, pulmonary, surgical, and urological complica- 10. Clunk J, Lin CY, Curtis J: Variables affecting weight gain in
tions.18 Pirsch et al19 proposed that increased BMI could renal transplant recipients. Am J Kidney Dis 38:349, 2001
have an independent effect on the allograft due to immu- 11. Howard RJ, Thai VB, Patton PR, et al: Obesity does not
nological causes. portend a bad outcome for kidney transplant recipients. Transplan-
tation 73:53, 2002
We recommend decreasing weight before and after Tx 12. Hall JE, Brands MW, Henegar JR: Mechanisms of hyper-
for every potential recipient. Change in behavioral habits of tension and kidney disease in obesity. Ann N Y Acad Sci 892:91,
eating, consultation with a nutritionist, and exercise are 1999
perhaps the best ways in this regard. Finally, it is important 13. Drafts HH, Anjum MR, Wynn JJ, et al: The impact of
pre-transplant obesity on renal transplant outcomes. Clin Trans-
to note that obesity should not be a barrier for transplan-
plant 11:493, 1997
tation.12 14. Merion RM, Twork AM, Rosenberg L, et al: Obesity and
renal transplantation. Surg Gynecol Obstet 172:367, 1991
15. Mokdad AH, Serdula MK, Dietz WH, et al: The spread of
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