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NDT Advance Access published online on July 19, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm459
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The outcome of renal transplantation among systemic lupus erythematosus patients

Madhukar Chelamcharla1, Basit Javaid2, Bradley C. Baird1 and Alexander S. Goldfarb-Rumyantzev1,3

1Division of Nephrology and Hypertension, University of Utah, Salt Lake City, UT, 2Division of Nephrology, Kidney and Kidney-Pancreas Transplant Program, Stanford University, Stanford, CA and 3VA Salt Lake City Health Care System, Salt Lake City, UT, USA

Correspondence and offprint requests to: Alexander Goldfarb-Rumyantzev, MD, PhD, Division of Nephrology and Hypertension, University of Utah Health Sciences Center, 85 North Medical Dr., East Rm 201, Salt Lake City, UT 84112, USA. Email: alex.goldfarb{at}hsc.utah.edu



   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Background. Clinical outcome of renal transplantation among systemic lupus erythematosus (SLE) patients remains a topic of controversy. Most of the previous reports were based upon small single-centre studies that were not always well-designed.

Methods. We conducted the retrospective analysis using data from USRDS and UNOS databases. Patients were divided into five groups based on the cause of end-stage renal disease (ESRD): diabetes mellitus (DM), SLE, glomerulonephritis, hypertension and other causes. Between 1990 and 1999, 2886 renal transplantation recipients with ESRD due to SLE were identified from a total of 92 844 patients.

Results. The mean follow-up period of this study was 4.7 ± 2.4 years. While unadjusted analysis using Kaplan–Meier curves demonstrated an association between SLE and improved allograft survival compared with DM, in multivariate analysis the SLE group had worse allograft [hazard ratio (HR) 1.09, P < 0.05] and recipient (HR 1.19, P < 0.05) survival compared with the DM group. Subgroup analysis based on the type of donor showed that SLE patients who received deceased donor allograft had worse allograft and recipient survival (HR 1.14, P = 0.002 and HR 1.30, P = 0.001, respectively) compared with non-SLE deceased donor allograft recipients. Among living allograft recipients, there were no significant differences in either allograft or recipient survival compared with non-SLE recipients.

Conclusions. SLE as a cause of ESRD in renal transplant recipients is associated with worse allograft and recipient survival compared with DM; this association is true for the entire population and for the recipients of deceased donor (but not living donor) transplant. Deceased donor allograft recipients have worse outcomes compared with living allograft recipients.

Keywords: epidemiology; lupus; outcome; prediction; renal transplantation; survival



   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Acknowledgements
 References
 
Factors predicting long-term kidney transplant outcome have been examined in the past. Both genetic [1,2] and environmental factors [3–6] were implicated in short- and long-term kidney allograft and recipient survival.

Since the survival of patients with systemic lupus erythematosus (SLE) improved after the advent of high-dose corticosteroid therapy, it became an important cause of end-stage renal disease (ESRD). In the US, in the year 2004, SLE nephritis accounted for 1.1% of all ESRD cases [7]. Until 1975, chronic haemodialysis was the preferred treatment for ESRD secondary to lupus nephritis and kidney transplantation was discouraged due to concerns of disease recurrence and allograft rejection. These concerns were allayed after the American Colleges of Surgeons/National Institute of Health (ASC/NIH) Transplant Registry reported that the allograft and recipient survival rates of SLE nephritis patients were comparable with non-SLE kidney transplant recipients [8]. Subsequently, several additional reports have demonstrated similar results and renal transplantation is the established mode of treatment for ESRD due to SLE nephritis [9–29]. Some of the previous studies were based on relatively small samples, while others reported the results of unadjusted analysis, where potential confounding factors were not accounted for. At the same time there are reports that have demonstrated contradictory results and were suggestive of increased risk of allograft loss [30–33] especially among deceased donor allograft recipients.

We conducted this retrospective analysis of United States Renal Data system (USRDS) and United Network for Organ Sharing (UNOS) data to compare allograft and recipient survival in kidney transplant recipients with ESRD secondary to SLE nephritis in comparison with those who had ESRD due to other causes.



   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Acknowledgements
 References
 
Data set
We analysed the records of all kidney allograft recipients (both paediatric and adults) who underwent transplantation between 1 January 1990 through 31 December 1999 with a follow-up period through 31 December 2000, using pre-transplant information collected by the USRDS and transplant-related data collected by the UNOS. For recipients of multiple transplants, the most recent procedure was considered the transplant of interest. A total of 92 844 patients who underwent kidney transplantation during that period were identified. Recipients were classified into five groups based on the primary cause of ESRD: diabetes mellitus (DM), glomerulonephritis (GN), hypertensive nephrosclerosis (HTN), SLE and other causes (Other). Recipients with ESRD secondary to DM were used as a reference group and allograft and recipient outcomes of all other groups were compared with it. The primary analysis included all renal transplant recipients, including both adults and paediatric recipients with both single and multiple transplants. A subgroup analysis comprised of adult patients who received their first kidney transplantation, was also performed with separate analysis of living and deceased donor allograft recipients. This additional analysis was necessary, since paediatric patients and patients who received multiple transplants are likely to be unique in many aspects that cannot be easily modelled by using simple predictors such as age and the number of transplants. This retrospective study was approved by the University of Utah's Institutional Review Board.

Outcome measures and definitions
There were two outcomes in this study: the duration of allograft survival and the duration of the recipient survival. The duration of allograft survival was defined as the time between the date of study transplantation and the failure of the allograft. The allograft failure date is defined as the date of return to dialysis, re-transplant or death due to kidney-related cause. On the other hand, death for non-kidney-related cause with functioning graft was used as a censor for the graft survival study (i.e. death-censored graft survival). In other words, our definition of allograft failure excludes recipients who died with functioning allografts (i.e. death-censored analysis), the latter determined in the USRDS as a single binary variable. In cases where this variable was missing, and the patient's death date was found to be equal to the allograft failure date, we assumed that the patient died with a functioning allograft, unless the cause of death was coded as one of the following: 3200 (graft failure: primary failure), 3201 (graft failure: rejection), 3202 (graft failure: technical), 3299 (graft failure: other) or 3903 (miscellaneous: renal failure). Allograft outcome was censored at the earliest of the following events: lost to follow-up, patient death or the study completion date (31 December 2000) and was analysed as time-to-graft-failure or censor.

The duration of recipient survival was defined as the time between study transplantation and recipient death. Patient follow-up was censored at the earliest of lost to follow-up or study completion date (31 December 2000), and was analysed as time-to-recipient death or censor.

Independent variables
Primary variable of interest
The cause of ESRD was our primary variable of interest in order to examine the allograft and recipient outcome in patients who developed ESRD due to SLE nephritis. We compared SLE recipients to the group of recipients with diabetic nephropathy in both unadjusted and adjusted analysis. In addition to that we performed a separate analysis where the SLE recipients were compared with all other recipients with ESRD caused by any other disease except SLE.

Covariates
The Cox models were adjusted for the following covariates believed to be potential confounders:

  1. Recipient variables: age, gender, race, height, weight, comorbidity score, history of prior transplant, total duration of ESRD, total number of transplants, number of pre-transplant blood transfusions and most recent and peak panel reactive antibody (PRA) levels.
  2. Donor variables: type of donor (deceased or living), heart beating donor or not, age, gender, race, height and weight.
  3. Transplant procedure variables: year of transplantation, number of matched HLA antigens and cold ischaemia time.

To adjust for recipient comorbidities, we calculated a comorbidity score similar to the one proposed by Davis, which has been shown to be strongly associated with the survival in a prospective study of 97 peritoneal dialysis (PD) patients [34]. The comorbidity score used in this study was calculated based on the following coexisting conditions, each of them contributing one point to the score: cardiovascular disease (defined in the USRDS as symptomatic cardiovascular disease or angina/coronary artery disease), symptomatic peripheral vascular disease, diabetes mellitus and hypertension. This indicator of comorbidity was successfully used in our prior studies [4,35]. Information about co-existing conditions was obtained from the TXUNOS file, based on the information collected from the Transplant Candidate Registration Form; therefore, the comorbidities used for this study are those that patients had at the time of listing for the study transplant. We did not use data from the CMS-2728 form in order not to exclude patients who were not Medicare-eligible prior to 1995 (prior to 1995, dialysis units and transplant centres were required to fill out the Medicare Evidence form only for Medicare-eligible patients). To reduce lead time bias the models were also adjusted for total duration of ESRD prior to transplantation. Unrealistic values of the independent variables found in the database were eliminated. In particular, for donors and recipients younger than 13 years of age, the United States CDC Growth Charts were used as a guide for determining valid ranges. The heights and weights of recipients and donors aged 13 and older were based on the acceptable ranges: height (120–275 cm), weight (20–180 kg).

Statistical methods
Patient records with missing information regarding allograft or patient survival were excluded from the study. For other missing values, we categorized the variable and included ‘missing’ as a separate category. Patient characteristics of individual groups were compared using two tailed t-tests, Wilcoxon rank-sum tests or {chi}2-tests depending on the type of the variable. For survival analysis, Kaplan–Meier graphs were used to display actuarial survival curves and Cox regression models were used to analyse time to event. Data were analysed using SAS v.9 (SAS Institute, Cary, NC, USA).



   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Acknowledgements
 References
 
Baseline characteristics
The total number of recipients of the kidney transplants between 1990 and 1999 were 92 844. There were 89 270 adult (≥18 years old) patients. Clinical characteristics of all recipients are presented in Table 1. In the entire study population, 60% of the recipients were males, 70% were White, the mean age at the time of the transplantation was 43 years. In about one in four, DM was the cause of ESRD and roughly one-in-eight (13%) had at least one prior transplant (n = 11 714). The mean follow-up period of this study was 4.7 ± 2.4 years. When the clinical characteristics of the recipients with SLE were compared with those with ESRD due to other causes, SLE patients were found to be younger, have higher proportion of females and African-Americans and a greater proportion of living donors. SLE patients also had a lower mean comorbidity score, higher most recent PRA level, longer pre-transplant ESRD duration and they received more blood transfusions. There is no significanct difference in the immunosuppressive regimen used in recipients with and without lupus nephropathy. The prevalence of cardiovascular disease was 6.9% in SLE recipients and 9.7% in non-SLE recipients.


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  		Table 1. Baseline characteristics of the study populationa

 
We compared the frequency of acute rejection between SLE and non-SLE-related transplant recipients using a 2 x 2 contingency table. We did not find any significant difference in the frequency of acute rejection between these groups ({chi}2 = 0.0246, P = 0.8753). We evaluated the causes of graft failure and recipient death that were listed for SLE and non-SLE groups and did not observe any unusual patterns. However, meaningful analysis of the data might be difficult in this particular data set due to a large amount of missing information.

For recipients with SLE-related ESRD, the causes of death were as follows: myocardial infarction 6%, cardiac arrest 13.9%, stroke 5.1%, cardiac arrhythmia 2.5%, cardiomyopathy 2.9%, septicaemia 20.6%, pneumonia 4.5%, malignancies 2.9%. For recipients with other than SLE aetiology of ESRD the causes of death were as follows: myocardial infarction 11.0%, cardiac arrest 16.1%, stroke 5.3%, cardiac arrhythmia 4.4%, cardiomyopathy 2.2%, septicaemia 13.0%, pneumonia 4.0%, malignancies 6.1%. In the SLE group, 59.3% of all deaths were deaths with functioning grafts, while in the non-SLE population 79.7% of all deaths were deaths with functioning grafts.

The causes of graft failure were distributed as follows: for SLE recipients: acute rejection 34.9%, graft thrombosis 19.8%, hyperacute rejection 3.8%, infection 2.8%; for non-SLE recipients: acute rejection 28.2%, graft thrombosis 23%, hyperacute rejection 2.7%, infection 3.3%.

Survival analysis
We analysed the entire study population using DM as a reference group. One, three, and five year allograft survival rates in the DM group were 85, 55 and 31%, respectively. SLE recipients had comparable allograft survival rates of 86, 56 and 33% at the same time points. Similarly, recipient survival rates at 1, 3 and 5 years were 92, 61, and 36% for the DM group and 96, 68, and 44% for the SLE group. Kaplan–Meier survival analysis demonstrated a lower unadjusted risk of allograft failure and patient death for SLE recipients compared with the DM group (Figures 1 and 2). When multivariable analysis was performed after dividing the recipients into five groups based on the cause of ESRD, SLE recipients had worse allograft survival [hazard ratio (HR) 1.09, P < 0.05] and recipient survival (HR 1.18, P < 0.05) compared with the reference group (DM) (Table 2).


Figure 1
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  		Fig. 1. Actuarial graft survival curves of recipients grouped by primary cause of ESRD. Kaplan–Meier plots demonstrate lower unadjusted risk of allograft failure for SLE recipients compared with the DM group. ({chi}2 = 613.89, P < 0.001).

 

Figure 2
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  		Fig. 2. Actuarial recipient survival curves grouped by primary cause of ESRD. Kaplan–Meier plots demonstrate lower unadjusted risk of patient death for SLE recipients compared with the DM group ({chi}2 = 2217.25, P < 0.001).

 

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  		Table 2. Proportional hazards regression estimates of graft survival and recipient survival according to the cause of ESRDa

 
Subgroup analyses
We performed further analysis after excluding the paediatric population (age <18 years) and recipients of more than one kidney transplant. The remaining adult, single-transplant recipients were divided into two subgroups based on type of donor (living or deceased) and separate analyses were performed for each subgroup. In this analysis, instead of using DM as the reference group, we compared SLE recipients with all non-SLE recipients. Among the deceased donor allograft recipients, allograft survival was worse for the SLE group compared with non-SLE deceased donor recipients (HR 1.14, P < 0.005). Recipient survival was also inferior in the SLE group compared with non-SLE deceased donor recipients (HR 1.30, P < 0.001). The increased risk of allograft failure and recipient death among living donors with SLE did not reach statistical significance.

We analysed the association of SLE with graft and recipient survival in the subgroups of patients divided by race. When compared with all other causes of ESRD, the difference in graft survival for SLE patients did not reach statistical significance in any racial groups, except for White recipients where the HR for graft failure was 1.19 (P < 0.005). When analysing the risk of recipient death associated with SLE as a cause of ESRD, significant results were demonstrated in Asian recipients (HR 1.81, P < 0.05) and White recipients (HR 1.23, P < 0.005).



   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Acknowledgements
 References
 
SLE patients that undergo renal transplantation might be different from non-SLE recipients in many respects. They are generally younger, with fewer comorbidities, a majority of them are women with a greater percentage of African-American patients. SLE patients might have a unique immunological profile, they are more likely to have received blood transfusions and their PRA levels are higher than non-SLE recipients. They also have higher than average theoretical risk of allograft failure due to recurrence of SLE activity and thrombosis [36–40]. Infections are a common cause of morbidity and mortality in SLE patients and may contribute to poor allograft and recipient outcomes [41,42]. In addition, cardiovascular disease occurs more frequently in lupus nephritis patients and contributes to increased mortality and morbidity [43]. Because of these unique characteristics, allograft and recipient survival of SLE nephritis patients who underwent renal transplantation have been a subject of great interest reflected in several publications since 1975, when transplantation started to be considered a reasonable treatment option for ESRD due to SLE nephritis [8]. The results of the studies reported in the literature are controversial, with some studies showing poor allograft survival associated with SLE, whereas others reported allograft and recipient survival rates comparable with non-SLE recipients. Table 3 illustrates the results of the selected studies.


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  		Table 3. Selected studies of renal transplantation outcome in recipients with ESRD due to SLE

 
Most of these studies were conducted in single centres, included a limited number of patients and did not have a control group. In the few studies that included a control group, the control population was heterogeneous and consisted of historic controls, non-diabetics, only those with non-SLE glomerulonephritis, or all those with non-SLE ESRD, making comparisons between these studies difficult. Follow-up periods of prior reports were also different and ranged from 1 month to 10 years. A data analysis comparable with that presented here has been done by Ward [29] using the USRDS and UNOS data of transplantations performed between 1987 and 1994. The results of that analysis were somewhat contradictory to our results and showed that in an unadjusted model, the risk of allograft failure among SLE patients who received deceased donor allografts was worse compared with non-SLE-deceased donor recipients (HR 1.13, P < 0.05). However, after adjusting for potential confounding factors, the risk of allograft failure and recipient survival was no longer significantly different from non-SLE recipients. Similarly, there were no significant differences in allograft and recipient survival rates between SLE and non-SLE groups who received living allograft.

Although our study was also based on USRDS data, the results are quite different. In unadjusted analysis, the outcome of SLE recipients was essentially the same as the outcome in non-SLE recipients. We need to mention here, that the percent survival values presented in the results for the patient subgroups are lower than presented in literature, which most likely has to do with the statistical phenomenon rather than actual survival rate. In our analysis, recipients who were transplanted towards the end of the study had a follow-up time of <1 year, and therefore were censored at the end of the study without reaching the outcome. These censored records were not used in the calculation, even though most of the recipients would probably survive 1 year if observed longer. However, those recipients who reached the outcome (death or graft failure) were included in the calculation and therefore drove the survival rate down. Since the same analysis was used for each subgroup we decided that while the absolute percent survival rate is probably artificially low, it is a valid tool to compare the subgroups. This analysis along with Kaplan–Meier curves demonstrated that if analysis is not adjusted for covariates, the survival rate of SLE recipients is not worse than in diabetics. However, after adjustment for potential confounders, SLE recipients demonstrated significantly worse outcome.

There are significant differences between these two analyses. Our study population was transplanted roughly 5 years later than the study population examined by Ward. Our primary analysis included all kidney transplantation records between 1990 and 1999 (n = 92 844), whereas Ward's data set included only 45 451 records that underwent kidney transplantation between 1987 and 1994. The total number of SLE recipients in our data set is 2886, whereas Ward's study included a total of 1162 SLE recipient records. Even though 1162 is not a small number, when divided into living and deceased donor allograft groups, there were 772 patients in the deceased donor group and only 390 patients in the living donor group. With these relatively small numbers, the analysis might have lacked enough power to show differences in outcomes between SLE and non-SLE groups. Our data set with about 2.5 times more SLE recipients might have enough statistical power to demonstrate the existing differences in outcomes compared with the non-SLE group, at least in the primary analysis. When separate analyses were performed for the recipients of living and deceased allograft groups, in the latter group with a greater number of patients, the outcome was statistically significant, while as in the smaller living donor group, the differences have not reached statistical significance. There are some additional methodological differences between the two studies. We used all renal allograft recipients in our study, adult and pediatric, single and multiple allograft recipients, as well as living and deceased donor allograft recipients. Ward's analysis included only adult transplant recipients who received single kidney transplantation. We used DM as the reference group and compared the outcomes of all other groups against the reference group, where as Ward's analysis compared SLE recipients with all non-SLE recipients pooled together. The reason we decided to use DM patients as a reference group (rather than all other recipients with a disease other than SLE, or recipients with GN since they might have received immunosuppressive therapies similar to SLE patients in the past) are as follows. The group is well defined, homogenous, yet has a large number of patients; also DM recipients have worse outcome than other transplant recipients, which makes the comparison clinically relevant.

In addition to primary analysis, we conducted further subgroup analysis simulating Ward's study, where we restricted our patient population to only adult patients who underwent single kidney transplantation. Subgroup analyses were performed after dividing patients into living and deceased donor allograft groups. These results showed that adult SLE patients who received only single deceased donor (but not living donor) allograft, have worse allograft and recipient survival outcomes compared with their non-SLE counterparts.

Finally, Ward did not include PRA level and comorbidity score as covariates in the multivariable analysis. These variables might be very important as a potential confounding factors. Higher PRA level observed in SLE patients (Table 1) may adversely affect the transplant outcome. Similarly, the comorbidity score is an important factor affecting allograft and recipient survival. In fact, in our primary analysis, addition of only comorbidity score to bivariate analysis, eliminated the lower HR associated with SLE for allograft survival (HR 0.93, P = 0.03 vs HR 0.95, P = 0.12, for unadjusted model and comorbidity-adjusted model, respectively). Similarly, recipient survival also decreased after adjusting for comorbidity score (HR 0.70, P < 0.001 vs 0.79, P < 0.001, for unadjusted and comorbidity-adjusted models, respectively).

We specifically addressed the issue of comparing outcome of living and deceased donors. While the superiority of the living organ intuitively seems obvious, there are data that might potentially suggest the opposite. There is preliminary evidence that systemic SLE has familial inheritance through human leucocyte antibodies (HLA)-linked susceptibility genes [44]. Some investigators have raised concerns that allografts received from living related donors that carry the same disease susceptibility genes may increase the likelihood of disease recurrence in the recipients. Cats et al. [33] have found that 1 year allograft survival rates were significantly worse in SLE patients when the allografts were obtained from parental donors. However, in our analysis, allograft and recipient survival rates of living allograft recipients were not significantly different between SLE and non-SLE groups. SLE patients that received living allograft had better outcomes compared with deceased donor allograft recipients.

Regarding the mechanisms of observed inferior outcome of transplant recipients with ESRD caused by SLE, several of these points might be proposed. As indicated above, SLE patients differ from the general transplant population in their demographics, immunological status (e.g. PRA level), comorbidities, etc. These differences were also observed in our study. Even though we adjusted the models for these variables, some residual effect could still be present. In addition, some of the potential mechanisms were not accounted for in the multivariate models. In particular, we did not include antiphospholipid antibody and coagulability status, rate of infection complications and the recurrence of SLE activity in the post-transplant period. Other possible mechanism might have to do with prior immunosuppressive therapy for SLE and immunological effects of SLE.

Considering inferior outcome of patients with SLE and renal transplant, there is a need for closer follow-up of patients with kidney transplant and SLE nephropathy. Unfortunately, based on this retrospective data analysis, authors cannot give more specific recommendations regarding post-transplant care of these patients. In general, the results of a retrospective analysis are usually insufficient evidence to radically change clinical practice.

Certain limitations should be realized when interpreting the results of this retrospective analysis of the national data. As analysis is based on the existing data set, investigators were limited by the data available, therefore certain relevant questions could not be addressed. In particular, while it would be interesting to evaluate the role of disease activity at the time of transplantation, the data of the serological evidence of activity were not available to investigators and this question might therefore be better addressed by the single-centre data analysis. Certain other interesting questions could be addressed as a follow-up to this analysis. Since SLE patients with kidney transplant have inferior outcome compared with other recipient groups, it would be interesting to compare their outcome to those SLE patients remaining on dialysis on the waiting list. Without this additional analysis, the authors believe that transplantation should still remain the preferred treatment modality of the SLE patients with ESRD. While demonstrating that SLE as a cause of ESRD is associated with inferior transplant outcome, this retrospective data analysis does not provide explanation for the mechanism of this association. One might hypothesize that disease recurrence, long-term use of immunosuppression in pre-transplant period, systemic nature of the disease, as well as other pathophysiological mechanisms associated with SLE might play a role.

In conclusion, SLE as a cause of ESRD in renal transplant recipients is associated with worse allograft and recipient survival compared with DM; this association is true for the entire population and for the recipients of deceased donor (but not living donor) transplantation when analysed separately. Deceased donor allograft recipients have worse outcomes compared with living allograft recipients.



   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
References
 
This study was supported in part by the Dialysis Research Foundation (Ogden, UT, USA). The data reported here have been supplied by the USRDS. The interpretation and reporting of these data are the responsibility of the authors and in no way should be seen as official policy or interpretation of the US Government.

Conflict of interest statement: None declared.



   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 

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Received for publication: 2. 3.07
Accepted in revised form: 13. 6.07


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