Central obesity is common in renal transplant recipients and is associated with increased prevalence of cardiovascular risk factors.

Abstract

Aim: Obesity following renal transplantation is common and may be associated with cardiovascular disease. We sought to investigate the prevalence of central obesity in renal transplant recipients (RTR) and its association with cardiovascular risk factors.

Methods: Weight, height, body mass index (BMI), waist and hip circumference, and biochemical cardiovascular risk factors were prospectively measured in 199 RTR, and were compared against published data from the Australian general population.

Results: When obesity was defined by BMI, there was no difference between RTR and the Australian population irrespective of age. Significantly more female RTR had central obesity (defined as waist circumference [greater than or equal to]90 cm for men and [greater than or equal to]80 cm for women) when compared with the general population, and this was apparent at a younger age. In younger women (<45 years), 76% of RTR had central obesity compared with 17% of women from the general population (P < 0.0001). This trend was also seen in older female RTR. Younger male RTR (<45 years) had a greater prevalence of central obesity than aged-matched men in the general population (66% vs 44%, respectively, P < 0.001). This trend was not seen in older male RTR. Centrally obese RTR gained significantly more weight post transplant than those who were lean (9.5 kg vs 2.4 kg, respectively, P < 0.0001), and were more likely to have a history of childhood obesity (P = 0.04). On multivariate analysis, central obesity was independently associated with weight gain post transplant (P < 0.001), a history of hyperlipidaemia (P = 0.01) and a history of hypertension (P = 0.02).

Conclusion: Central obesity is a common problem for all RTR, particularly women and men aged below 45 years. Measures of central obesity should be used for RTR in clinical practice. BMI is not a suitable measure to determine central obesity. Central obesity is associated with cardiovascular risk factors, and further studies targeting multi-disciplinary lifestyle interventions are recommended.

Key words: central obesity, glucose tolerance, insulin resistance, renal transplant recipient.

INTRODUCTION

Obesity following renal transplantation is common, and is associated with a sedentary lifestyle, metabolic effects of steroids and obesity prior to transplant. (1) Other factors associated with weight gain post transplant are female gender, African American race, young age and low income. (2,3) Obesity in renal transplant recipients (RTR) has been linked to cardiovascular disease (CVD) and other adverse health outcomes, including hypertension, dyslipidaemia, insulin resistance, post-transplant diabetes mellitus (PTDM), chronic allograft nephropathy, and graft loss and death. (1) CVD is the leading cause of mortality in RTR, accounting for more than 50% of deaths. (4) Central obesity is common in RTR and is associated with cardiovascular morbidity and mortality. (3,5) Central (or visceral) fat is considered more detrimental than subcutaneous fat as it is associated with a number of metabolic and cardiovascular disturbances, namely the increased production of free fatty acids, which may impair the action of insulin, leading to insulin resistance. (6) Waist circumference (WC) has been demonstrated as a good predictor of visceral fat and is easily measured in clinical practice. (6,7)

Although weight gain is a well-known consequence of renal transplantation, monitoring weight changes and cardiovascular risk factors such as WC, insulin resistance and dyslipidaemia are not necessarily routine practice in renal transplant centres. We sought to: (i) investigate the prevalence of central obesity in RTR at our centre and compare with the general Australian population; and (ii) determine the association between central obesity and cardiovascular risk factors (blood pressure, fasting lipids and oral glucose tolerance test (OGTT)).

PATIENTS AND METHODS

Subjects

The study protocol was approved by the Princess Alexandra Hospital Human Research Ethics Committee, which conforms to the provisions of the Declaration of Helsinki. All patients at the Princess Alexandra Hospital Renal Unit (PAHRU) were screened according to the following criteria: [greater than or equal to]6 months post transplant and with a functioning renal transplant; not known to be diabetic (self-reported or on oral hypoglycaemic agents); and regularly followed up at the PAHRU on a two- to three-monthly basis. Two hundred and eighty eligible patients were approached to undertake an OGTT for inclusion in the study, and observational data were collected on this cohort between January 2004 and January 2005. One hundred and ninety-nine patients (71%) underwent screening and were included in the present study. Written informed consent was obtained from all study participants. Some of the eligible patients did not attend for an OGTT for the following reasons: not interested in the study (n = 11, 13.6%); failed to attend OGTT appointment (n = 18, 22.2%); refused to have OGTT (n = 5, 6.1%); lived too far away (n = 20, 24.7%); physically or mentally disabled (n = 2, 2.5%); kidney pancreas transplant (n = 10, 12.3%); glomerular filtration rate <25 mL/minute (n = 7, 8.6%); too unwell for study (n = 2, 2.5%); kidney heart transplant (n = 2, 2.5%); or attended clinic infrequently (n = 4, 5%). The present study sample was found to be representative of the study population (see Results section). Screening of all patients six months post transplant continues as part of standard clinical care in the PAHRU.

Assessment of cardiovascular risk factors included a history of any of the following: (i) a previous cardiac event (defined as a nonfatal myocardial infarction, acute coronary syndrome requiring hospitalisation, coronary artery bypass graft or percutaneous coronary intervention); (ii) peripheral vascular disease (defined as angioplasty, bypass or amputation); (iii) cerebrovascular disease (defined as transient ischaemic attack or stroke with neurological deficit); (iv) hypertension (defined as previous or current use of antihypertensive agents or self-reported); (v) dyslipidaemia (defined as previous or current use of lipid-lowering therapy or self-reported); and (vi) smoking status (current, former or never). A history of childhood obesity (<18 years) was obtained by self-report, with a yes or no response.

An OGTT was performed after an overnight fast and included measurements of fasting, one- and two-hour insulin and glucose concentrations. (8) Medications were noted and blood pressure was measured by a trained nurse using a standard sphygmomanometer for all patients. The most recent accessible Australian population data were obtained from the National Nutrition Survey (NNS). (9) Missing data (approximately 5%) from the NNS are not included. Anthropometric measurements from the present study population of RTR were compared against those from the NNS and categorised according to gender and age.

Anthropometric measures

Weight (kg, measured on a calibrated digital scale Tanita BWB-600, Tanita, Japan) and height (cm) were measured with patients wearing light clothing and without shoes. Body mass index (BMI) categories were classified according to World Health Organisation criteria: 18.5-24.9 (healthy weight), 25.0-29.9 (overweight) and [greater than or equal to]30 kg/[m.sup.2] (obese). (10)

Waist circumference (cm) was measured at the midpoint between the lower border of the ribs and the top of the iliac crest on a horizontal plane. Hip circumference (cm) was measured at the point where the buttocks extended the maximum, when viewed from the side. (11) Waist to hip ratio (WHR) was calculated by dividing WC by hip circumference. For the present study, WC [greater than or equal to]90 cm (male) or [greater than or equal to]80 cm (female) were considered centrally obese, as is consistent with the NNS. WHR >0.9 (male) and >0.8 (female) were considered centrally obese. (10)

Biochemical information

Fasting venous blood samples were obtained from RTR for determination of glucose, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, VLDL cholesterol, urea and creatinine levels.

Statistics

All variables shown are mean values [+ or -] standard deviation (SD) for continuous parametric data, median (interquartile range) for continuous nonparametric data, or frequency (%) for categorical data. Student's t-tests or one-way analysis of variance (ANOVA) were used except when variables were non-Gaussian in distribution, in which case the Mann-Whitney U-test was applied. Chi-squared tests were used for categorical data. Pearson's and Spearmann's correlation coefficients were calculated to determine correlative relationships between anthropometric measures.

Univariate and multivariate binary logistic regression analyses were performed. Variables meeting the statistical criteria of P < 0.1 on univariate regression analysis were applied to a logistic regression model and using likelihood ratios in a backwards step-wise elimination procedure to determine the most appropriate models. A maximum of seven variables were allowed in the original models. The explanatory (predictor, independent) variables were weight gain post transplant, fasting blood glucose levels, HDL cholesterol, history of hyperlipidaemia, history of hypertension and history of childhood obesity. One model was developed to examine each of the two outcome (dependent) variables, BMI and central obesity (binary variables). The outcome variable BMI was categorised into either >25 kg/[m.sup.2] or [less than or equal to]25 kg/[m.sup.2]. Central obesity was categorised by WC [greater than or equal to]90 cm (men) and [greater than or equal to]80 cm (women), or WC <90 cm (men) and <80 cm (women). The model included gender, weight gain post transplant, fasting blood glucose, HDL cholesterol, triglycerides, history of hyperlipidaemia, history of hypertension and history of childhood obesity. Standard regression diagnostic techniques, including check of appropriateness of the model and Hosmer-Lemeshow tests, were carried out. Statistical significance was considered at P < 0.05 a priori. Data analysis was performed with SPSS statistical software version 11.5 (SPSS, Chicago, IL, USA).

RESULTS

Characteristics of lean and centrally obese patients are shown in Table 1. Of the 199 RTR who participated, 109 (55%) had normal glucose tolerance, while 57 were diagnosed as impaired glucose tolerance and 33 patients had type 2 diabetes mellitus. There were similar proportions of patients with abnormal glucose tolerance in the lean and centrally obese patient groups (24% vs 30%, respectively, Table 1). Eligible patients who did not attend for an OGTT (non-attendees, n = 81) were younger than the study population (44 [+ or -] 13 years vs 52 [+ or -] 12 years, P < 0.001), but were otherwise well matched with respect to gender, race, transplant duration, BMI, type of donor, cause of renal failure and immunosuppression.

Anthropometric data are presented separately for women and men in Tables 2 and 3, respectively. In women, younger RTR (<45 years) were significantly more centrally obese than age-matched women in the general population (Table 2). A total of 76% of female RTR had a WC above target, compared with 17% of younger women in the general population (Table 2). Similarly, 81% of female RTR had a WHR above target compared with 25% of women in the general population (Table 2). This relationship was also noted in older female RTR ([greater than or equal to]45 years), who showed a higher prevalence of central obesity and increased WHR compared with aged-matched women in the general population. Interestingly, obesity as measured by BMI was not different between either younger or older female RTR and the general population (Table 2).

Younger male RTR (<45 years) showed a similar picture of central obesity as their female counterparts. In total, 66% of male RTR had a WC above target compared with 44% of age-matched men in the general population (Table 3). Similarly, 69% of male RTR had a WHR above target compared with 38% of the general population (Table 3). There were no significant differences in BMI between young male RTR and aged-matched men in the general population (Table 3). Older male (aged [greater than or equal to]45 years) RTR did not show any significant difference in WC, WHR or BMI compared with aged-matched men in the general population (Table 3).

Table 1 shows that centrally obese RTR gained significantly more weight post transplant than those who were not centrally obese, and were more likely to have had a history of childhood obesity. Those who gain more weight post transplant are more likely to be centrally obese: all 49 (100%) patients in the highest quartile of weight gain compared with 29 of 49 (59%) patients in the lowest quartile (P < 0.001). Centrally obese RTR had an increased prevalence of hyperlipidaemia and hypertension compared with lean RTR. Independent predictors of overweight and central obesity in RTR with a BMI > 25 kg/[m.sup.2] and central obesity are shown in Table 4. After univariate regression analysis, the variables chosen for inclusion in the multivariate logistic regression were gender, weight gain post transplant, fasting blood glucose, HDL cholesterol, triglycerides, a history of hyperlipidaemia, a history of hypertension and a history of childhood obesity. After step-wise backward regression analysis, the variables independently associated with BMI > 25 kg/[m.sup.2] (n = 123) were weight gain post transplant and high fasting blood glucose levels and a relationship with low HDL levels (Table 4a). When this method was repeated for central obesity, the variables independently associated were weight gain post transplant, a history of hyperlipidaemia and a history of hypertension (Table 4b).

DISCUSSION

In the present study, measures of adiposity (WC and BMI) have been shown to be associated with cardiovascular risk factors, such as weight gain, high fasting blood glucose levels, low HDL cholesterol, a history of hyperlipidaemia and a history of hypertension, in RTR. In the general population, measures of central obesity such as WC and WHR have been found to better predict CVD risk than BMI. (12) Presently it is unknown whether markers of central obesity are better predictors of long-term clinical outcomes such as CVD in RTR. Ongoing follow up of this group is occurring to determine this. In the interim, these measures should be routinely included in clinical practice in order to help quantify cardiovascular risk in this high-risk population.

Obesity is a common problem in RTR and is associated with adverse outcomes, such as hyperlipidaemia, hypertension, PTDM, graft loss and death. (1,13) An age-related difference in obesity prevalence was identified in male RTR, with younger patients experiencing proportionately greater rates of central obesity compared with older RTR. Both younger and older women experienced greater rates of central obesity when compared with age-matched women in the general population. BMI was not a sensitive indicator of increased central obesity in either male or female RTR. The anthropometric data from our centre have been compared with the NNS data, which are now 10 years old. This factor may have influenced the comparison of our results with NNS data. However, NNS obesity rates of 13-21% (women) and 15-23% (men) are comparable to more recent prevalence data from Ausdiab, which demonstrated 21% obesity as measured by BMI. (14) It is unknown whether increases in obesity over the past 10 years in the general population were experienced at a similar rate in the renal transplant population.

An increased prevalence of overweight and obesity in RTR has been identified at other centres. (15) In a study of 130 RTR, Heaf et al. used BMI to identify significant rates of overweight (39%) and obesity (14%). (16) Studies have shown that younger age and female gender are factors associated with weight gain in the first year after renal transplant. (2,3) Steroid immunosuppressive therapy has been implicated in the pathogenesis of weight gain after transplant. (2,3,5,6,17,18) Corticosteroids are known to promote weight gain through stimulating appetite, effecting adipocytes and resting energy expenditure and altering lipid oxidation, which encourages central fat deposition. (5,18,19) In our centre, 161 (82%) of RTR were on a corticosteroid at the time of data collection. The use of corticosteroid therapy in RTR remains controversial. The disadvantages, including weight gain and risk of developing diabetes mellitus, need to be weighed against the benefits of therapy, including improved outcomes and ability to minimise calcineurin inhibitor exposure. (20) Body fat composition of RTR has been investigated in a number of studies. (16,17,19,21,22) Van den Ham et al. observed that post-transplant weight gain is mainly due to an increase in fat mass, with truncal fat mass being the most pronounced and rates of increased WHR up to 34% in female RTR. (22) This is similar to our results as truncal (or central) fat mass (as measured by WC) was a significant problem for female and younger male RTR. It has been speculated that weight gain post transplant may be caused by an increase in calorie intake after ceasing to adhere to the strict dietary requirements of dialysis and reversal of the uraemic state improving appetite. (23)

The identification of central obesity and cardiovascular risk factors at a younger age in RTR is of significant clinical concern as there may be an increased risk for associated morbidity, reduced quality of life and premature death from CVD. The results of the present study highlight the need to change clinical practice, so that screening for cardiovascular risk factors occurs in all patients after renal transplant, and not be limited to those in a classical 'high risk' age group (e.g. >40 years). The present study clearly shows that traditional methods of measuring obesity (e.g. BMI) and measures of central obesity (e.g. WC, WHR) are both important determinants of cardiovascular risk in RTR. Central obesity, as measured by WC and WHR, was more likely to predict patients who had greater weight gain post transplant, a history of hyperlipidaemia and hypertension, which are key risk factors for the development of CVD. It is interesting to note that RTR who were centrally obese were more likely to be obese as children. This finding further supports evidence indicating that childhood obesity is a predictor for adulthood obesity (24,25) (which may include central obesity). Public health initiatives that tackle childhood obesity early to prevent the cycle of weight gain into adulthood could possibly benefit renal transplant populations in the future.

The study population was considerably older (mean age 51-53 years) compared with those investigated by du Plessis et al., in which the mean age of participants was between 35 and 41 years. (15) While age may be a confounding factor in the development of central obesity, the age range in the current study was representative of the PAHRU and similar to the median age of functioning transplant recipients in Australia and other published studies, (16,19) Cross-sectional data analysis prevents the determination of cause and effect of central obesity in the present study population; therefore, the mechanisms associated with the increased risk of cardiovascular risk factors were not addressed. Increased dietary intake or lack of physical activity are factors which may impact on cardiovascular risk, and future studies should include measurement of these factors using validated tools.

Successful weight management involves dietary manipulation and increased physical activity. (23) Dietary intervention in RTR has been shown to reduce weight and improve lipid profiles. (23,26-28) In the majority of studies, the American Heart Association Step diets have been used, which focus on calorie restriction and reducing total and saturated fat intake. Physical activity (PA) can significantly reduce the risk of obesity, CVD and type 2 diabetes mellitus in the general population. (29) Nielens et al. observed an increase in PA after renal transplant compared with PA during dialysis. (30) However, it is unlikely that the increase in PA is sufficient to balance the increase in caloric intake. PA has been shown to have a favourable effect on body composition in RTR, as higher levels have been associated with a higher percentage of lean body mass and lower percentage of fat mass. (19) Given the results of the present study and the success of previous structured dietary interventions, the role of dietetic professionals in renal transplant units should be further explored. Clinical pathways for management of RTR should include regular dietary intervention to identify and manage central obesity and educate patients on the most appropriate methods for maintaining a healthy weight and preventing post-transplant complications. Physical activity should also be encouraged as a strategy to enhance weight loss and improve body composition.

ACKNOWLEDGEMENTS

The authors are appreciative to all study participants and gratefully acknowledge the help with data collection and recording by Anne Maree Elliot and Jodie Tarnawskyj.

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20 Kasiske BL, Chakkera HA, Louis TA, Ma JZ. A meta-analysis of immunosuppression withdrawal trials in renal transplantation. J Am Soc Nephrol 2000; 11: 1910-17.

21 Isiklar I, Akin O, Demirag A, Niron EA. Effects of renal transplantation on body composition. Transplant Proc 1998; 30: 831-2.

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23 de Vries APJ, Bakker SJL, van Son WJ. Dietary intervention after renal transplantation. Transplantation 2003; 75: 1604.

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Linda ORAZIO, (1,2) Kirsty ARMSTRONG, (1,3) Merrilyn BANKS, (2) David JOHNSON, (1,3) Nikky ISBEL (1,3) and Ingrid HICKMAN (4)

Departments of (1) Renal Medicine and (2) Nutrition and Dietetics, (3) School of Medicine, and (4) Diamantina Institute for Cancer Immunology and Metabolic Medicine, Princess Alexandra Hospital, Brisbane, Queensland, Australia

L. Orazio, BHSc (Hon), APD, Dietitian 

I. Hickman, PhD, APD, NHMRC Australian Clinical Research Fellow

N. Isbel, PhD, Consultant Nephrologist 

M. Banks, M Hlth Sc, APD, Manager

K. Armstrong, PhD, Renal Research Fellow

D. Johnson, PhD, Director

Correspondence: L. Orazio, Ipswich Road, Woollongabba, Brisbane, Qld 4102, Australia. Email: [e-mail]

Table 1 Patient characteristics

                            Lean               Centrally obese    P-
                            (n = 46)           (n = 153)          value

Age (years)                 50.98 [+ or -]      52.54 [+ or -]     0.47
                              15.14               11.81
Gender: male/female         30/16               86/67              0.28
Transplant duration          8.04 (3.8-15.2)     6.13 (2.7-11.9)   0.13
  (years) (a)
Weight at transplant (kg)   58.97 [+ or -]      74.34 [+ or -]    <0.001
                              9.63                15.49
Weight gain since            2.40 [+ or -]       9.46 [+ or -]    <0.001
  transplant (kg)              5.42                9.87
Waist circumference (cm)    80.41 [+ or -]     102.23 [+ or -]    <0.001
                              6.56               13.64
Waist to hip ratio           0.87 [+ or -]       0.96 [+ or -]    <0.001
                               0.072               0.097
BMI (kg/[m.sup.2])          21.92 [+ or -]      28.71 [+ or -]    <0.001
                              2.91                4.86
Fasting glucose (mmol/L)     5.5 [+ or -]        5.6 [+ or -]      0.43
                               1.41                0.99
Total cholesterol (mmol/L)   5.12 [+ or -]       5.10 [+ or -]     0.86
                               1.08                0.99
Triglyceride (mmol/L)        1.74 [+ or -]       1.94 [+ or -]     0.23
                               0.96                0.97
Creatinine ([micro]mol/L)    0.143 [+ or -]      0.14 [+ or -]     0.49
                               0.05                0.05
Hx CVD                      10 (22)             31 (20)            0.84
Hx hyperlipidaemia          19 (41)             99 (65)            0.006
Hx HT                       28 (61)            123 (80)            0.01
Hx childhood obesity         0                  14 (9)             0.04
Family hx DM                15 (33)             48 (31)            0.86
Presence of DM               8 (17)             25 (16)            0.82
Abnormal OGTT               11 (24)             46 (30)            0.46

(a) Data presented as median (interquartile range).
Data presented as mean [+ or -] standard deviation or frequency (%),
unless otherwise stated.
Central obesity defined as waist circumference
[greater than or equal to]90 cm (male) [greater than or equal to]80 cm
(female).
CVD = cardiovascular disease; DM = diabetes mellitus; HT = hypertension;
Hx = history; OGTT = oral glucose tolerance test.

Table 2 Comparison of female anthropometric measurements of RTR and the
Australian population stratified according to age

                                         Age < 45 years
                                      Gen pop (a)  RTR
                                      (n = 3630)   (n = 21)
                                      n (%)        n (%)     P-value

WC >target (b)                         633 (17)    16 (76)   <0.001
WC <target                            2997 (83)     5 (24)
WHR >target (c)                        720 (25)    17 (81)   <0.001
WHR <target                           2711 (75)     4 (19)
BMI <25 kg/[m.sup.2]                  2119 (58)    10 (48)    0.140
BMI 25-29.9 kg/[m.sup.2]               836 (23)     5 (24)
BMI [greater than or equal to]30 kg/   478 (13)     6 (28)
  [m.sup.2]

                                      Age [greater than or equal to]45
                                      years
                                      Gen pop (a)  RTR
                                      (n = 3074)   (n = 62)
                                      n (%)        n (%)     P-value

WC >target (b)                        1089 (36)    51 (82)   <0.001
WC <target                            1985 (64)    11 (18)
WHR >target (c)                       1713 (58)    50 (80)   <0.001
WHR <target                           1281 (42)    12 (20)
BMI <25 kg/[m.sup.2]                  1130 (37)    22 (35)    0.360
BMI 25-29.9 kg/[m.sup.2]              1093 (36)    28 (45)
BMI [greater than or equal to]30 kg/   745 (21)    12 (19)
  [m.sup.2]

(a) Missing data from the NNS not included.
(b) Target [greater than or equal to]80 cm.
(c) Target >0.8.
P-value represents chi-squared test.
BMI = body mass index; Gen pop = general Australian population; NNS =
National Nutrition Survey; RTR = renal transplant recipients; WC = Waist
circumference; WHR = waist to hip ratio.

Table 3 Comparison of male anthropometric measurements of RTR and
Australian population stratified according to age

                                         Age < 45 years
                                      Gen pop (a)  RTR
                                      (n = 3663)   (n = 35)
                                      n (%)        n (%)     P-value

WC >target (b)                        1600 (44)    23 (66)    0.010
WC <target                            2063 (56)    12 (34)
WHR >target (c)                       1401 (38)    24 (69)   <0.001
WHR <target                           2262 (62)    11 (31)
BMI < 25 kg/[m.sup.2]                 1582 (43)    12 (34)    0.490
BMI 25-29.9 kg/[m.sup.2]              1529 (42)    18 (52)
BMI [greater than or equal to]30 kg/   539 (15)     5 (14)
  [m.sup.2]

                                      Age [greater than or equal to]45
                                      years
                                      Gen pop (a)  RTR
                                      (n = 2840)   (n = 82)
                                      n (%)        n (%)     P-value

WC >target (b)                        2217 (78)    64 (78)   0.90
WC <target                              63 (22)    18 (22)
WHR >target (c)                       2256 (79)    71 (87)   0.15
WHR <target                            584 (21)    11 (13)
BMI < 25 kg/[m.sup.2]                  701 (25)    29 (35)   0.12
BMI 25-29.9 kg/[m.sup.2]              1408 (50)    37 (45)
BMI [greater than or equal to]30 kg/   662 (25)    16 (20)
  [m.sup.2]

(a) Missing data from the NNS not included.
(b) Waist target [greater than or equal to]90 cm.
(c) WHR target >0.9.
P-value represents chi-squared test.
BMI = body mass index; Gen pop = general Australian population; NNS =
National Nutrition Survey; RTR = renal transplant recipients; WC = Waist
circumference; WHR = waist to hip ratio.

Table 4 Cardiovascular risk factors independently associated with (a)
BMI > 25 kg/[m.sup.2] and (b) central obesity after step-wise backward
regression analysis in RTR

                                        n = 199
                               Multivariate
Risk factor                    adjusted OR   95% CI     P-value

(a) BMI > 25 kg/[m.sup.2] (a)
  Weight gain                  1.1           1.06-1.15  <0.01
  FBG                          1.81          1.22-2.70  <0.01
  HDL cholesterol              0.45          0.20-1.00   0.05
(b) Central obesity (b)(c)
  Weight gain                  1.12          1.06-1.18  <0.01
  Hx Hlipid                    2.70          1.28-5.56   0.01
  Hx HT                        2.70          1.25-5.88   0.02

(a) [R.sup.2] = 0.295.
(b) [R.sup.2] = 0.321.
(c) Central obesity = WC [greater than or equal to]90 cm (men),
[greater than or equal to]80 cm (women).
The model included gender, weight gain post transplant, fasting blood
glucose, HDL cholesterol, triglycerides, history of hyperlipidaemia,
history of hypertension and history of childhood obesity. BMI = body
mass index; FBG = fasting blood glucose; Hx Hlipid = history of
hyperlipidaemia; Hx HT = history of hypertension.