PEDIATRICS Vol. 115 No. 2 February 2005, pp. 352-356 (doi:10.1542/10.1542/peds.2004-0289)
Obesity and Renal Transplant Outcome: A Report of the North American Pediatric Renal Transplant Cooperative Study
* Medical College of Georgia, Augusta, Georgia
EMMES Corporation, Rockville, Maryland
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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Objective. Obesity is increasing in the end-stage renal disease population. Studies that have evaluated the effect of obesity on transplant outcomes in adults have yielded varying results. This issue has received little attention in the pediatric population.
Methods. We performed a retrospective study of the effect of obesity on pediatric renal transplant outcomes using the North American Pediatric Renal Transplant Cooperative Study database. Registry data from 1987 through 2002 on 6658 children aged 2 to 17 years were analyzed. Obesity was defined by a BMI >95th percentile for age.
Results. Overall, 9.7% were obese with an increase noted in recent years (12.4% after 1995 vs 8% before 1995). Obese children were significantly younger and shorter and had been on dialysis for a longer time than nonobese children. There was no significant difference in the overall patient and allograft survival between the 2 groups. However, obese children aged 6 to 12 years had higher risk for death than nonobese patients (adjusted relative risk: 3.65 for living donor; adjusted relative risk: 2.94 for cadaver), and death was more likely as a result of cardiopulmonary disease (27% in obese vs 17% in nonobese). Overall, graft loss as a result of thrombosis was more common in obese as compared with nonobese (19% vs 10%).
Conclusions. Obesity is an increasing problem in children who present for transplantation and may have an adverse effect on allograft and patient survival.
Key Words: obesity • children • renal transplant • graft survival
Abbreviations: NAPRTCS, North American Pediatric Renal Transplant Cooperative Study • SDS, SD score • aRR, adjusted relative risk • USRDS, US Renal Data System • ESRD, end-stage renal disease
In the past several years, obesity in children and adolescents has become a major concern for pediatricians. Although most children with kidney failure are not overweight, increasing numbers are obese when dialysis or transplantation is initiated.1 Depending on transplant center preference, obesity may be considered an exclusion factor for transplantation out of concern that it could reduce graft and patient survival.2 In children, few data address this question.
Recently, we and others assessed the relationships between BMI and short-term (1-year) renal allograft function in children and adolescents and showed that pretransplant obesity was associated with worse 1-year allograft function.3,4 However, the impact of obesity on long-term outcome in pediatric patients with renal transplant has not been evaluated. Therefore, we designed a study to evaluate the impact of childhood obesity on long-term graft and patient survival using data from the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS).
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Since January 1, 1987, the NAPRTCS has maintained a scientific registry of pediatric transplants. Currently, data regarding >6500 transplants from 126 centers in the United States, Mexico, and Canada have been entered into the NAPRTCS database. For this retrospective study, the NAPRTCS data were analyzed for children who were aged 2 to 17 years and received kidney transplants between 1987 and 2002. Children who were younger than 2 years were excluded as normative data for BMI are not available for this age group.5 Data compiled included gender, race, age at the time of transplantation, dialysis modality, time on dialysis, donor source (living donor vs cadaver donor), primary diagnosis, transplant history, weight, height, history of delayed graft function, transfusion history, HLA typing of donor and recipient, cold ischemia time, use of induction therapy, episodes of acute rejection, and causes of graft and patient loss.
Delayed graft function was inferred by the requirement of dialysis during the first week after transplantation. Allograft failure was defined by return to dialysis or repeat transplant. Primary kidney disease was characterized as structural kidney disease, glomerulonephritis, focal segmental glomerulosclerosis, congenital nephrotic syndrome, hemolytic uremic syndrome, renal infarct, cystinosis, familial nephritis, or "other." Structural kidney disease refers to children with renal failure as a result of obstructive uropathy, aplasia/hypoplasia/dysplasia, prune belly syndrome, reflux nephropathy, polycystic kidney disease, medullary cystic disease/juvenile nephronophthisis, and pyelonephritis/interstitial nephritis. BMI was calculated as weight in kilograms divided by height in meters squared. Patients were considered to be obese when their BMI was greater than the 95th percentile for age5 at the time of transplantation. Weight SD scores (SDS) and height SDS were calculated using an age- and gender-specific formula based on the Third National Health and Nutrition Examination Survey 2000 growth chart set.5
For the statistical analysis, patients were divided into obese and nonobese groups on the basis of their baseline (pretransplant) BMI. Results are expressed as mean ± SD unless otherwise specified. Data were compared using 
2 and t tests. Kaplan-Meier graft survival estimates were determined by presence of obesity and donor source and were compared using log-rank test. Univariate (log-rank test) and multivariate (Cox regression) analyses were performed to determine the impact of obesity on graft and patient survival. Separate analyses were performed after subdividing the patients by age category and donor source. In the multivariate analysis, the relative risk values listed were adjusted for race, gender, transplant year, antihypertensive drug use during the first 30 days, time between dialysis initiation and transplantation, HLA match, delayed graft function, and previous transplant status. P 
0.05 was considered statistically significant.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Data were available on 6658 children who received 3511 living donor and 3147 cadaver donor transplants. At the time of transplantation, 649 (9.7%) were obese. As shown in Table 1, the distribution of gender and race was similar in obese and nonobese children. Children in the obese group were younger (mean age at transplant: 8.9 years vs 11.0 years; P < .001) and shorter (mean height SDS: –2.1 vs –1.9; P = .020) than the children in the nonobese group at transplant. The cause of renal failure differed between the obese and nonobese groups. A diagnosis of structural kidney disease as the primary renal disease was more prevalent in the obese group versus the nonobese group (52% vs 47%; P < .001). There was no difference in the frequency of other renal diseases between the 2 groups (data not shown). A history of peritoneal dialysis was more frequent in the obese group (42.5%) as compared with the nonobese group (39.1%; P = .001). Obese children also spent more time on maintenance dialysis (mean: 21.5 months) before transplant than nonobese children (mean: 18.5 months; P < .001). Donor age and source were similar in obese and nonobese groups. There was also no significant difference between the 2 groups with regard to the incidence of delayed graft function, degree of HLA mismatch, use of induction therapy, transfusion history, and cold ischemia time (data not shown). When children who received transplants between 1987 and 1995 were compared with children who received transplants between 1996 and 2002, it is noted that the percentage of children with obesity increased from 8.2% to 12.4% (P < .001).
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The mean follow-up after transplantation was 1585 days. The overall graft failure rate did not differ between the obese (22.3%) and the nonobese (24.1%) groups. Obese children did not have an increased risk for acute rejection as compared with nonobese recipients (data not shown). As shown in Table 2, chronic rejection was the most common cause of graft failure in both groups (nonobese patients: 37%; obese patients: 26%; P = NS). However, thrombosis accounted for 19% of graft loss in the obese group as compared with 10% of the nonobese group (P = .047).
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There were a total of 385 deaths. The overall patient mortality was not different between the obese children (36, or 5.5%) and nonobese children (349, or 5.8%). As shown in Table 3, infection was the leading cause of death in both groups (nonobese: 28%; obese: 25%; P = NS). It is also noted that death from cardiopulmonary disease occurred more frequently in the obese group (25%) than in the nonobese group (15%), but the difference did not reach statistical significance.
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Although there were no differences in the overall graft and patient survivals between the obese and nonobese patients, there was a significant interaction between transplant age and BMI status in both patient survival (P = .0014) and graft survival (P = .0163). Evaluation of patient survival showed that for children aged 6 to 12 years, the mortality rate was 5.4% for the nonobese group as compared with 12.1% for the obese group. Multivariate analysis showed that obese children aged 6 to 12 years had a significantly higher risk for death than nonobese patients (adjusted relative risk [aRR]: 3.65 living donor; aRR: 2.94 cadaver donor), Table 4. As noted in Fig. 1, the 5-year survival rate was significantly lower in obese children aged 6 to 12 years when compared with nonobese children of the same age (P < .001). Although the results did not reach statistical significance, cardiopulmonary causes of death were more common in obese children aged 6 to 12 years as compared with nonobese children of the same age (27% in obese vs 17% in nonobese; P = NS).
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Evaluation of graft survival showed that for adolescents who were aged 13 to 17 years and received a living donor transplant, allograft failure was more frequent in the obese group (27 of 133, or 20%) as compared with the nonobese group (228 of 1571, or 15%; P = .0188). As shown in Table 4, multivariate analysis confirmed these findings: adolescents who were aged 13 to 17 years and were obese at the time of receiving a living donor transplant had a greater risk for graft failure than nonobese patients in the same age category (aRR: 1.77). The most common cause of graft loss in obese adolescents who received a living donor transplant was vascular thrombosis: 7 (26%) of 27 in the obese group as compared with only 15 (7%) of 228 in the nonobese group (P = .004). In these adolescent groups, there were no significant difference in the frequency of graft loss as a result of chronic rejection: 22% in the obese group as compared with 31% in the nonobese group. Differences in outcome were not noted when obese and nonobese adolescents who received a cadaver donor transplant were considered.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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The prevalence of obesity in children has increased dramatically in the past several years. It is now estimated that 10% to 15% of children in the United States have a BMI
95th percentile.6 Similarly, our findings demonstrate that the percentage of children who receive kidney transplants and are obese is increasing. During the time period 1987–1995, only 8.2% of the pediatric transplant recipients who were registered in the NAPRTCS database were obese compared with 12.4% during the period 1996–2002. In addition, in children and adults, it has been shown that obesity may develop after transplantation, and weight gain may be more significant in those who were obese before transplantation.4,7 Mitsnefes et al4 found in children that the frequency of obesity doubled during the first year after transplantation. Similarly, Baum et al7 in a study of adult recipients found that initial BMI predicted weight gain after transplantation. The increased incidence of obesity in transplant recipients is alarming, because posttransplantation obesity is 1 of several factors that increase morbidity and mortality in adults. Factors that potentially affect graft survival in obese adult recipients include inadequate dosing of medications, increased risk for delayed graft function, and a discrepancy between recipient size and donor kidney size.3,8–11 Factors that potentially reduce patient survival are an increase in morbid cardiovascular events, wound infections, hyperlipidemia, and posttransplantation diabetes.3,8–11 Studies of adult recipients to determine the importance of obesity in patient and graft survival have yielded conflicting results.3,8,9,12–14 Obesity has been linked to reduced patient and graft survival by several investigators.3,8,9,12,15 Meier-Kriesche et al3 evaluated adult renal transplant recipients who were registered in the US Renal Data System (USRDS) for the effect of obesity on patient and graft survival. An elevated BMI was associated with increased mortality and risk for graft loss, with the most significant association noted in those with a BMI >36. Patients with higher BMIs were at greater risk for chronic graft failure, delayed graft function, and death from cardiovascular and infectious causes. In earlier work, these investigators found that even mild obesity had a negative impact on graft and patient survival.8
In contrast, other investigators have not found in adults any effect of obesity on patient or graft survival.10,13,14 The variability in these results may be related to recipient selection as noted below. Cardiac disease is known to be an important cause of morbidity and mortality in adult transplant patients.16,17 Modlin et al9 reported a 67% 5-year patient survival in obese recipients as compared with 89% in the nonobese group. Cardiac disease accounted for 39% of the deaths in the obese group versus 20% in nonobese patients.9 In contrast, Johnson et al15 reported a 5-year actuarial survival rate of 91% in both obese and nonobese patients. Of note, these investigators screened all patients for cardiovascular disease and eliminated anyone with an abnormal stress test or abnormal coronary angiogram.14 In this select population, these investigators also found no difference in graft survival in obese as compared with nonobese patients.14
In this NAPRTCS study, no difference in overall survival between obese and nonobese recipients was found. However, patient survival was significantly lower in obese 6- to 12-year-old children compared with nonobese children of that age. The reason for the high mortality rate in this age group is not evident. The most common cause of death in this age group was cardiopulmonary disease. Overall, considering all age groups, death from cardiopulmonary disease was more common in obese recipients (25%) as compared with nonobese children (15%). Although this difference was not significant (most likely because of small numbers of patients), the above observations raise concern about the impact of obesity on cardiovascular health in these young children. Recent reports have focused on the risk for cardiovascular disease in children with end-stage renal disease (ESRD). Cardiac disease has been found to be an important cause of morbidity and mortality in children who are on dialysis.18–21 It is the second most common cause of death in children who are on dialysis and after renal transplantation.1,21 Particularly concerning is the persistence of cardiac hypertrophy in children after transplantation.22–24 Left ventricular hypertrophy is 1 of the strongest independent risk factors for cardiac death in adults who are on chronic dialysis and after transplantation.25 Some studies in adults and children have also implicated obesity as an independent risk factor for increased left ventricular mass and left ventricular hypertrophy.26–28 Prospective studies in the pediatric population are needed to delineate further the impact of obesity on the cardiovascular system.
We also found that the graft loss as a result of vascular thrombosis was significantly increased in obese as compared with nonobese children. Previous NAPRTCS studies have linked young donor and recipient age (<6 years), prolonged cold ischemia time, previous transplant, and pretransplant peritoneal dialysis with graft thrombosis.29,30 Generally, an increase in vascular thrombosis has not been reported in obese adult recipients. Certainly, the increase in thrombosis that we observed may reflect technical complications in these obese patients. However, Halme et al15 reported that renal circulatory problems were a significant cause of graft loss during the first 30 days after transplantation in obese adult recipients as compared with nonobese control subjects. Studies of the coagulation system suggest that the risk for vascular thrombosis may be increased in obese patients. Obesity is known to be associated with a prothrombotic state. Increased plasma concentrations of fibrinogen, von Willebrand factor, and factor VII have been documented in obese individuals.31 Peritoneal dialysis has also been implicated in promoting coagulation.32,33 Although not statistically significant, analysis of our data demonstrated that obese recipients with graft loss as a result of vascular thrombosis were more likely to have received peritoneal dialysis before transplantation than hemodialysis. This association was most notable in the adolescent population. In obese adolescents who received living donor transplants, a statistically significant increase in graft loss as a result of vascular thrombosis was observed. The lack of an association in those who received cadaver transplants is puzzling and may be related to the small numbers in these subsets, a low frequency of peritoneal dialysis, or other differences that were not demonstrated.
Obese transplant recipients in the NAPRTCS database were generally younger and shorter and had been on dialysis longer than nonobese children. These findings contrast with data reported to the USRDS, where obese patients who initiated therapy in 2001 for ESRD were more likely to be older adolescents.1 In 2001, 16.3% of 15- to 19-year-olds with newly diagnosed ESRD were classified as obese as compared with 13.8% in 1996. However, the USRDS does not account for changes in weight while on dialysis. According to NAPRTCS dialysis registry, children who are younger than 6 years at the time of dialysis initiation improve their weight SDS while on dialysis. The reasons for weight gain during dialysis include additional caloric intake from the dextrose-based peritoneal dialysis fluid and the use of enteral supplemental feedings. NAPRTCS data confirm that young children are more likely than adolescents to receive peritoneal dialysis. Adolescents accounted for 62.1% of the hemodialysis population but only 37.5% of the peritoneal dialysis cohort. Our data show that obese children were also more likely to have been on peritoneal dialysis before receiving a transplant than their nonobese peers. Younger children are also more likely than older children to accept supplemental feedings to improve growth. NAPRTCS data shows that supplemental enteral feedings are more commonly provided to children who are on peritoneal dialysis (23%) as compared with children who are on hemodialysis (10%). In our population, nonobese children were older, more likely to have a history of glomerulonephritis or vasculitis, and more likely to be on hemodialysis before transplantation as compared with obese children.
This study has limitations, most notably the retrospective design and the inherent problems associated with use of a data registry. Details regarding previous glucocorticoid therapy and length of time on dialysis before transplantation, factors that might have an impact on the frequency of obesity at the time of transplantation, were not available in the database. Also, data were not available on the prevalence of hypertension in these young transplant recipients. In the NAPRTCS database, hypertension is defined by the treatment with antihypertensive medications during the first 30 days after treatment. This limited definition did not allow us to evaluate the effect of obesity on the prevalence of hypertension.
In summary, this investigation demonstrated that the frequency of obesity is increasing in the pediatric population that is eligible for renal transplantation. Our data suggest that obesity may limit patient and graft survival in some pediatric age groups and that vascular thrombosis might contribute to increased graft loss in these patients. Weight reduction before transplantation might be important in improving patient and graft survival. Pediatricians should educate families on the potential risks of excessive weight gain during dialysis and after kidney transplantation.
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FOOTNOTES |
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Accepted Jun 28, 2004.
Reprint requests to (M.M.M.) Division of Nephrology and Hypertension, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 7022, Cincinnati, OH 45229. E-mail: mark.mitsnefes{at}cchmc.org
Drs Hanevold and Mitsnefes participated equally in the design and analysis of the results of the study and in the preparation of the manuscript.
No conflict of interest declared.
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PEDIATRICS (ISSN 1098-4275). ©2005 by the American Academy of Pediatrics
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