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Mortality due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the resulting coronavirus disease 2019 (COVID-19) among transplant recipients is high 1 . In December 2020 the BNT162b2 (Pfizer-BioNTech) and the mRNA-1273 (Moderna) vaccines received emergency use authorization in the United States. These mRNA vaccines administered in a two-dose series were more than 94% effective in preventing COVID-19 in clinical trials, without safety concerns identified 2,3 . Transplant recipients were excluded from the clinical trials. Although decreased efficacy and immunogenicity were expected for transplant recipients, transplant recipients were included in the early vaccination prioritization groups and transplant societies, including the American Society of Transplantation, urged transplant recipients to get vaccinated as soon as vaccine was available.

BACKGROUND. The liver transplant risk score (LTRS) was developed to stratify 90-day mortality of patients referred for liver transplantation (LT). We aimed to validate the LTRS using a new cohort of patients. METHODS. The LTRS stratifies the risk of 90-day mortality of LT recipients based on their age, body mass index, diabetes, model for end-stage liver disease (MELD) score, and need for dialysis. We assessed the performance of the LTRS using a new cohort of patients transplanted in the United States between July 2013 and June 2017. Exclusion criteria were age

Post-transplant donor specific antibody (DSA) is associated with poor renal allograft outcomes. However, variable timing of DSA assessment and inclusion of patients who undergo desensitization treatments have hindered our understanding of its consequences and limited its predictive value. Here we prospectively studied non-desensitized patients to determine factors associated with poor four-year outcomes in patients who developed post-transplant DSA. Using serial monitoring, 67 of 294 patients were found to develop DSA by one year. Compared to patients who do not develop DSA, those with DSA exhibit an increased incidence of both clinical and subclinical T-cell-mediated rejection (TCMR). The combination of TCMR plus DSA led to an almost three-fold increase in graft loss compared to either DSA or TCMR alone. Moreover, DSA was associated with higher Banff grade TCMR and chronic changes at one year. Antibody-mediated rejection was uncommon and always associated with TCMR. Amongst factors independently associated with DSA plus TCMR; non-adherence is potentially modifiable. Non-adherence, measured as intra-patient variability of calcineurin trough levels during the first post-transplant year, further risk-stratified patients with DSA plus TCMR such that about 75% of these patients had impending graft loss by four years, whereas adherent patients with DSA plus TCMR had outcomes comparable to other patient groups. Thus, early post-transplant DSA, especially in non-adherent patients, is associated with increased incidence of TCMR and represents a high-risk group of patients who might benefit from targeted therapeutic interventions.

The use of kidneys donated after circulatory death (DCD) provides an invaluable expansion of the organ supply for transplantation. Here we investigated the effect of DCD on fibrotic changes on 1-year post-transplant surveillance kidney allograft biopsy. Recipients of a deceased donor kidney transplant between 2013 and 2017 at a single institution, who survived 1 year and underwent surveillance biopsy, were included in the analysis (n = 333: 87 DCD kidneys, 246 kidneys donated after brain death [DBD]). Banff scores for interstitial fibrosis and tubular atrophy were summed as IFTA and compared between the groups. DCD and DBD groups were comparable for baseline characteristics. Delayed graft function was 39% in DCD vs. 19% in DBD, p = 0.0002. Patient and graft survival were comparable for DCD and DBD cohorts. IFTA scores were higher in DCD compared to DBD (2.43±0.13 vs. 2.01±0.08, p = 0.0054). On multivariate analysis, the odds of IFTA>2 in the DCD group was 2.5x higher (95%CI: 1.35-4.63) than in the DBD group. Within the DCD group, kidneys with IFTA>2 had inferior 5-year graft survival (p = 0.037). In conclusion, compared DBD kidneys, DCD kidneys developed a greater degree of fibrotic changes on 1-year post-transplant surveillance biopsy, which affected graft longevity within the DCD cohort. This article is protected by copyright. All rights reserved.

Early immunological biomarkers that predict rejection and chronic allograft loss are needed to inform preemptive therapy and improve long-term outcomes. Here, we prospectively examined the ratio of interleukin-10 (IL-10) to tumor necrosis factor-α (TNFα) produced by transitional-1 B cells (T1B) 3 months after transplantation as a predictive biomarker for clinical and subclinical renal allograft rejection and subsequent clinical course. In both Training (n = 162) and Internal Validation (n = 82) Sets, the T1B IL-10/TNFα ratio 3 months after transplantation predicted both clinical and subclinical rejection anytime in the first year. The biomarker also predicted subsequent late rejection with a lead time averaging 8 months. Among biomarker high-risk patients, 60% had early rejection, of which 48% recurred later in the first posttransplant year. Among high-risk patients without early rejection, 74% developed rejection later in the first year. In contrast, only 5% of low-risk patients had early and 5% late rejection. The biomarker also predicted rejection in an External Validation Set (n = 95) and in key patient subgroups, confirming generalizability. Biomarker high-risk patients exhibited progressively worse renal function and decreased 5-year graft survival compared to low-risk patients. Treatment of B cells with anti-TNFα in vitro augmented the IL-10/TNFα ratio, restored regulatory activity, and inhibited plasmablast differentiation. To conclude, the T1B IL-10/TNFα ratio was validated as a strong predictive biomarker of renal allograft outcomes and provides a rationale for preemptive therapeutic intervention with TNF blockade.

We studied diverse rejection management strategies across centers by conducting a UNOS survey of kidney transplant program directors in 2017. There were 104 total responses from 235 kidney transplant programs representing 88 unique transplant programs (response rate 37%). Information was collected on center-specific management practices. Pertinent center-specific data were obtained from the OPTN database. Of the respondents, 33% were considered large centers (>100 transplants/year). Thymoglobulin was the most commonly used induction agent at 84%, 72% responders do rapid steroid withdrawal, and mycophenolic acid (MPA) is the major antimetabolite (100%). For diagnosing TCMR, 100% used indication biopsy, 28% used protocol biopsy, 2% used serum biomarkers, and none used urine cytokines. For ABMR, 99% used indication biopsy, 34% used protocol biopsy, 72% used DSA, 21% used C1q positive DSA, and none used gene profiling (ENDATS). The treatment of subclinical and clinical TCMR included iv/PO steroids. PP/IVIG were the commonest treatments for ABMR. The use of rituximab, bortezomib, and eculizumab increased from C4D-ABMR to recurrent ABMR. There are diverse management practices for diagnosing and treating rejection. An effort to harmonize these diverse practices for management of TCMR and ABMR will give an opportunity to pool data for evaluating clinical outcomes.

Transplantation of kidneys from deceased donors with acute kidney injury (AKI) can expand the donor pool. We investigated the effect of donor AKI on renal function and chronic changes on protocol biopsies at 1-year post-transplant. Donor AKI was defined according to Acute Kidney Injury Network (AKIN) criteria. Between 2013 and 2017, 333 kidneys were transplanted and subsequently biopsied after 1 year. Fifty-three kidneys from AKI donors (AKIN stage I n = 42, stage II n = 8, stage III n = 3) were compared to 280 kidneys from non-AKI donors. At 1-year follow-up, patient and graft survival were comparable. Donor AKI was not predictive of IFTA (Banff interstitial fibrosis plus tubular atrophy scores) at 1-year post-transplant biopsy (2.10 ± 1.28 in AKI, 2.09 ± 1.22 in non-AKI, P = .95). Donor AKI was also not associated with progression of IFTA from 3 to 12 months (P = .69), or inferior glomerular filtration rate (eGFR, P = .94). In a multivariate analysis, the odds of IFTA >2 were comparable between AKI and non-AKI groups. In conclusion, the transplantation of kidneys from donors with predominantly stage I AKI results in comparable function and degree of fibrosis on protocol biopsies 1-year post-transplant. Selected grafts from donors with AKI are a valuable tool for expanding the donor pool for kidney transplantation.

The impact of subclinical inflammation (SCI) noted on early kidney allograft biopsies remains unclear. This study evaluated the outcome of SCI noted on 3-month biopsy. A total of 273/363 (75%) kidney transplant recipients with a functioning kidney underwent allograft biopsies 3-months posttransplant. Among those with stable allograft function at 3 months, 200 biopsies that did not meet the Banff criteria for acute rejection were identified. These were Group I: No Inflammation (NI, n = 71) and Group II: Subclinical Inflammation (SCI, n = 129). We evaluated differences in kidney function at 24-months and allograft histology score at 12-month biopsy. SCI patients had a higher serum creatinine (1.6 ± 0.7 vs 1.38 ± 0.45; P = .02) at 24-months posttransplant, and at last follow-up at a mean of 42.5 months (1.69 ± 0.9 vs 1.46 ± 0.5 mg/dL; P = .027). The allograft chronicity score (ci + ct + cg + cv) at 12-months posttransplant was higher in the SCI group (2.4 ± 1.35 vs 1.9 ± 1.2; P = .02). The incidence of subsequent rejections within the first year in SCI and NI groups was 24% vs 10%, respectively (P = .015). De novo donor-specific antibody within 12 months was more prevalent in the SCI group (12/129 vs 1/71, P = .03). SCI is likely not a benign finding and may have long-term implications for kidney allograft function.

Due to shortage of donor, kidney transplants (KTs) from donors with acute kidney injury (AKI) are expanding. Although previous studies comparing clinical outcomes between AKI and non-AKI donors in KTs have shown comparable results, data on high-volume analysis of KTs outcomes with AKI donors are limited. This study aimed to analyze the selection trends of AKI donors and investigate the impact of AKI on graft failure using the United states cohort data. We analyzed a total 52,757 KTs collected in the Scientific Registry of Transplant Recipient (SRTR) from 2010 to 2015. The sample included 4,962 (9.4%) cases of KTs with AKI donors (creatinine ≥ 2 mg/dL). Clinical characteristics of AKI and non-AKI donors were analyzed and outcomes of both groups were compared. We also analyzed risk factors for graft failure in AKI donor KTs. Although the incidence of delayed graft function was higher in recipients of AKI donors compared to non-AKI donors, graft and patient survival were not significantly different between the two groups. We found donor hypertension, cold ischemic time, the proportion of African American donors, and high KDPI were risk factors for graft failure in AKI donor KTs. KTs from deceased donor with AKI showed comparable outcomes. Thus, donors with AKI need to be considered more actively to expand donor pool. Caution is still needed when donors have additional risk factors of graft failure.

This prospective observational cohort study compared the impact of subclinical tubulitis with or without interstitial inflammation to interstitial inflammation alone and to no inflammation in early post kidney transplant biopsies. A study cohort of 415 patients (living and deceased donor recipients) was divided into three groups on the basis of their three-month biopsy: 149 patients with No Inflammation (NI), 83 patients with Isolated Interstitial Inflammation (IIF), and 183 patients with Tubulitis [(with or without interstitial inflammation) (TIF) but not meeting criteria for Banff IA]. TIF was further divided into 56 patients with tubulitis without interstitial inflammation (TIF0) and 127 patients with tubulitis alongside interstitial inflammation (TIF1). TIF was significantly associated with higher incidence of subsequent T-cell mediated rejection (clinical or subclinical) at one year compared to IIF (31% vs 15%) and NI (31% vs 17%). Chronicity on one-year biopsy was significantly higher in TIF compared to IIF (22% vs 11%) and NI (22% vs 7%). De novo donor-specific antibody development was significantly higher in TIF compared to NI (6% vs 0.7%). Tubulitis subgroups (TIF0 and TIF1) revealed comparable effects on de novo donor-specific antibody and interstitial fibrosis/tubular atrophy development. However, tubulitis with interstitial inflammation had a significantly higher incidence of subsequent rejection and posed an increased hazard for the composite end point (subsequent acute rejection and death censored graft loss) compared to other groups [adjusted hazard 2.1 (95% confidence interval 1.2-3.5)]. Thus, subclinical tubulitis is a marker of adverse immunological events, but tubulitis with interstitial inflammation has a worse prognosis. Hence, the Banff 1997 (TIF1) and Banff 2005 classifications (TIF) for borderline change may have different implications.

We investigated the effect of clinical and subclinical T cell-mediated rejection (C-TCMR and SC-TCMR) on allograft histology, function, and progression.Adult kidney recipients with 2 protocol biopsies were divided into No-TCMR on biopsies (n = 104), SC-TCMR (n = 56), and C-TCMR (n = 32) in at least 1 biopsy. Chronicity (ci + ct + cg + cv) scores, renal function, and the burden of renal disease measured by area under the curve (serum creatinine, mg mo/dL) were compared.Baseline characteristics were similar except for mean donor age and Kidney Donor Profile index scores. Patients with C-TCMR had higher mean serum creatinine, lower mean estimated glomerular filtration rate, and higher area under the curve with 95% confidence interval (75.2 [67.7-82.7]) as opposed to patients with SC-TCMR and No-TCMR (58.3 [53.6-62.9], 65.1 [58.8-71.5]), P = 0.0004. Chronicity scores were higher at 3 months in C-TCMR (2.30 ± 1.58) compared with SC-TCMR (2.02 ± 1.42) and No-TCMR (1.31 ± 1.18), P = 0.0001 and also at 12 months. At last follow-up, 18.8% patients with C-TCMR had ≥50% decline in estimated glomerular filtration rate from 3 months compared with 7% and 1% among No-TCMR and SC-TCMR groups (P = 0.038). Multivariate analyses revealed higher odds of Δ-creatinine ≥ 0.5 mg/dL from 3 months to last follow-up for C-TCMR (3.39 [95% confidence interval, 1.25-9.20]) versus No-TCMR (P = 0.016).Kidney transplant recipients with C-/SC-TCMR have heightened early allograft chronicity and worse renal function compared with those with No-TCMR. Progressive renal dysfunction was noted among patients with C-TCMR as opposed to SC-TCMR and No-TCMR.

Supplemental digital content is available in the text., Background High calcineurin inhibitor (CNI) intrapatient variability (IPV) has been associated with poor kidney allograft outcomes. However, the relationship between early allograft histological changes, their progression, and CNI-IPV is less well studied. Hence, we evaluated effect of CNI-IPV defined by the degree of fluctuation of CNI levels in all kidney transplant patients over 2 to 12 months posttransplant on early allograft inflammation, subsequent chronicity, and later clinical outcomes. Methods Two hundred eighty-six patients transplanted from January 2013 to November 2014 were enrolled with protocol and indication biopsies. The mean CNI-IPV was 28.5% and a quarter of our cohort had IPV of 35% or greater (high CNI IPV). Baseline demographic differences were similar between high and low CNI IPV groups. Results High CNI-IPV was associated with a higher incidence of acute rejection (AR) within 1 year (52% vs 31% P < 0.001), more persistent/recurrent AR by 1 year (18.2% vs 6.2%, P = 0.002), higher-grade AR (≥Banff 1B, 27.5% vs 7.3%, P < 0.001), and worse interstitial fibrosis/tubular atrophy (P = 0.005). High CNI-IPV was associated with increased graft loss (GL) and impending graft loss (iGL, defined as eGFR30% decline in eGFR from baseline), regardless of donor-specific antibody, delayed graft function, rejection, or race. In a multivariate Cox Proportional Hazards Model, high CNI-IPV was independently associated with GL + iGL (hazard ratio, 3.1; 95% confidence interval, 1.6–5.9, P < 0.001). Conclusions High CNI-IPV within 1 year posttransplant is associated with higher incidence of AR, severe AR, allograft chronicity, GL, and iGL. This represents a subset of patients who are at risk for poor kidney transplant outcomes and potentially a modifiable risk factor for late allograft loss.

Background. Early acute kidney rejection remains an important clinical issue. Methods. The current study included 552 recipients who had 1–2 surveillance or indication biopsy within the 1 y posttransplant. We evaluated the impact of type of allograft inflammation on allograft outcome. They were divided into 5 groups: no inflammation (NI: 95), subclinical inflammation (SCI: 244), subclinical T cell–mediated rejection (TCMR) (SC-TCMR: 110), clinical TCMR (C-TCMR: 83), and antibody-mediated rejection (AMR: 20). Estimated glomerular filtration rate (eGFR) over time using linear mixed model, cumulative chronic allograft scores/interstitial fibrosis and tubular atrophy (IFTA) ≥2 at 12 mo, and survival estimates were compared between groups. Results. The common types of rejections were C-TCMR (15%), SC-TCMR (19.9%), and AMR (3.6%) of patients. Eighteen of 20 patients with AMR had mixed rejection with TCMR. Key findings were as follows: (i) posttransplant renal function: eGFR was lower for patients with C-TCMR and AMR (P

Background The burden of cytomegalovirus infection in CMV high-risk (donor positive to recipient negative) kidney transplant recipients getting thymoglobulin induction and six months of valganciclovir is not well characterized. Additionally, the role of post-prophylaxis surveillance remains unclear. Methods One-year observational study of forty-eight high-risk CMV kidney transplant recipients transplanted under thymoglobulin between January 2013 and July 2014. All received valganciclovir for six months, followed by monthly CMV PCR for three months. Results CMV infection defined as viremia with or without symptoms occurred in 40% (19/48). Of these, 47% (9/19) occurred during prophylaxis, 32% (6/19) during surveillance and 21% (4/19) during post-surveillance period (9–12 months). Among breakthrough infections, suboptimal valganciclovir dosing was present in 55% (5/9). With routine surveillance, there was a trend toward lower CMV-related hospitalization (17% vs 56% and 75% during prophylaxis and post-surveillance, respectively [P=.23]) and lower mean peak viral loads (19 432 copies/mL vs 97 925 copies/mL and 536 021 copies/mL during prophylaxis and post-surveillance, respectively [P=.07]). Conclusion CMV infection remains a significant problem with thymoglobulin induction despite six months of valganciclovir. Suboptimal valganciclovir dosing was common among breakthrough infections. Monthly surveillance post-prophylaxis appears to detect early CMV infection with lower degree of viremias requiring fewer hospitalizations.

Early histological progression that associates with delayed graft function (DGF) and its relationship to graft outcomes is less well-understood. We systematically evaluated early acute and chronic histological changes associated with DGF through serial biopsies (protocol: 3 and 12 months; for-cause) and related them to graft outcomes. 56/294 (19.04%) of our patients had DGF. DGF was associated with a progressive increase in both Banff 't' and 'i' scores from 2 weeks to 3 and 12 months with a resultant increase in T cell mediated rejection (TCMR) that was significantly greater than those with primary graft function (PGF). This increase in TCMR was predominantly sub-clinical TCMR diagnosed on protocol biopsy. Furthermore, TCMR in patients with DGF was recurrent/persistent at 12 months. Importantly, the combination of DGF and TCMR was associated with significantly worse interstitial fibrosis and tubular atrophy (IFTA) and interstitial fibrosis with inflammation (IF + 'i') as early as 3 months and worse renal function. Finally, DGF with TCMR was associated with significantly worse graft loss. In this regard, DGF without TCMR had comparable chronic histology and outcomes to PGF. Thus, DGF with TCMR (predominantly sub-clinical), represents a high-risk patient group who may benefit from early novel immunosuppression augmentation strategies to improve graft outcomes.

The kidney wait list has outgrown the supply of available organs every year. Efforts are being made to minimize discard rate of organs. One such area is the use of kidneys with glomerular microthrombi (MT). We retrospectively examined graft/patient outcomes in 28 cases with MT in pre-implantation biopsies. All patients had follow-up of at least 36 months, or until graft loss or death. In total, 17 of the 18 patients who underwent follow-up biopsy within 90 days of transplantation had cleared all MT. Most patients had excellent long-term graft function. On a closer review of the biopsies included in our study, we found that even in the organs with the most widespread thrombosis, the median percentage of glomeruli with more than 50 percentage of the capillary loops occluded was 8% (range 0-17%). The current practice of mentioning the % of glomeruli with thrombi cannot adequately capture the extent of donor organ pathology, as the actual % glomerular area involved can vary greatly from case to case. Future studies should attempt to quantify donor thrombi by a more robust method and revisit the issue of using clinico-pathologic parameters to predict allograft function in the setting of MT.

Short-term outcomes in renal transplantation have improved significantly in the past few years. However, the improvement in long-term outcomes has been modest. The reasons for graft failure beyond the first year of transplantation have been attributed to several different factors. We believe that subclinical rejection (SCR) may be 1 of the factors that contribute to graft loss in the long run. We also believe that there are data to suggest that SCR leads to progressive fibrosis and loss of graft function. This has been demonstrated even in patients who have mild degrees of subclinical inflammation. This review outlines the major studies that have been published on this important topic. It also outlines potential risk factors for the development of SCR. The current approach and diagnostic methods are discussed as well as their pros and cons. Newer noninvasive methods of diagnosis as well as molecular diagnostics and their merits and shortcomings are also discussed in some depth. Thus, the proposed state of the art review on SCR will create a renewed interest at all levels including transplant clinicians, transplant researchers, pharmaceutical industries as well as regulatory organizations.

Background The approach to the diagnosis and management of subclinical rejection (SCR) in kidney transplant recipients remains controversial. Methods We conducted a survey through UNOS across US transplant centers regarding their approach to surveillance biopsies and reasons for the nonperformance of surveillance biopsies. Results Responses were obtained from 106/238 centers (45%), and only 18 (17%) of the centers performed surveillance biopsies on all patients and 22 (21%) performed biopsy for select cases. The most common time points for surveillance biopsies were 3 and 12 months post-transplant. The common reasons for not performing biopsies were low yield (n = 44, 65%) and the belief that it will not change outcome (n = 24, 36%). The incidence of SC-TCMR was ≥ 10% among 39% of centers. The mean serum creatinine was slightly worse by 0.06 mg/dL at 1 year and 0.07 mg/dL at 3 years among centers performing biopsy, P

The number of overweight and obese patients undergoing renal transplantation has drastically increased in the last two decades. Studies on graft survival and complication rates of these obese patients have had conflicting results, with some reporting a significant risk and others reporting relatively good outcomes. We examined 1-year outcomes in obese and nonobese patients who underwent living donor transplants at our transplant program, a slightly different approach than prior studies of deceased donor transplants into patients with high body mass index (BMI). The mean serum creatinine clearance by the modified MDRD equation at the end of 1 year in the nonobese group was 58.9 mL/min whereas the mean creatinine clearance in the obese group was 48.9 mL/min (P = .09). The length of stay, incidence of delayed graft function, and 1-year graft survival did not differ between the obese and nonobese groups. The results of this single-center experience with living donor transplant into obese subjects suggest no differences in outcomes with regard to surgical or wound complications, delayed graft function, or serum creatinine at 1 year.

Kidney transplantation is the preferred therapy for patients with end-stage renal disease (ESRD). With improvements in allograft and patient outcomes, patients with prior kidney allograft failures are increasingly becoming candidates for repeat transplantation.1 According to the annual Scientific Registry for Transplant Recipients (SRTR) report for the year 2011, approximately 12% of kidney transplant recipients had prior renal allograft failure.2 In addition, renal failure is common in recipients of other nonrenal solid organ transplants with rates of CKD of up to 16% and in those with CKD, an ESRD incidence of up to 30% over 36 months post-nonrenal organ transplantation which varies from organ to organ.3-6 With improvements in medical care, patients with nonrenal solid organ transplants are living longer to become candidates for kidney after solid organ transplantation.7 This group which constituted less than 1% of the waitlist candidates before 1995 increased to 3.3% in 2008 and were more likely to be listed preemptively (38% vs 21% in those without prior nonrenal solid organ transplantation).8 According to the SRTR annual report, 2.6% of transplants performed in year 2011 were in recipients of prior nonrenal solid organ transplants.2 Only a few previous studies have compared renal allograft outcomes in recipients who have undergone other solid organ transplants compared with those undergoing primary or repeat kidney transplantation. These previous studies were based on national databases with large center to center variations in practices and issues with nonuniform coding.9,10 The current study is a retrospective single-center study that analyzes specifically the renal allograft outcome after primary kidney, repeat kidney and kidney-after-other solid organ transplant. We evaluated various demographic, donor/recipient, and posttransplant variables across the 3 groups.

Background: Allograft rejection is associated with T cell activation. T cell activation leads to secretion of soluble IL-2 receptor and elevated serum soluble IL-2 receptor (sIL-2R) levels. However, the clinical implication of individual elevated sIL-2 receptor levels is unclear. We followed levels of sIL-2R pre- and post-transplantation to determine if sIL-2R levels predict rejection episodes or degree of graft function. Materials and methods: Serum samples of 12 patients who underwent living or cadaveric renal transplant were followed weekly with serial sIL-2R levels. These levels were followed until the serum creatinine reached a baseline. Of the 12 patients, three patients developed delayed graft function. The remaining nine patients were followed for a period of 3 months. Sera of these nine patients in the initial 3 months post-transplant were monitored for sIL-2R levels. For comparison, sIL-2R levels were also measured in 150 healthy volunteers and five dialysis patients. Results: Recipients undergoing severe rejection episodes had higher overall serum levels of sIL-2R (1515 ′ 496 U/mL) as compared with recipients who had stable renal transplants and no episodes of rejection (698 ′ 333 U/mL) (P = 0.034). Comparison of sIL-2R ratios (post-transplant sIL-2R level/pre-transplant sIL-2R level) revealed that ratios of 0.6 or higher were more frequently seen in patients who subsequently underwent severe rejection episodes. Dialysis patients were found to have higher sIL-2R levels (2605 ′ 1312 U/mL) compared with renal transplant patients (1047 ′ 192 U/mL) (P < 0.001) and healthy volunteers (349 ′ 185 U/mL) (P < 0.001). Conclusion: Our results suggest that individual levels of sIL-2R are not predictive of rejection in the early post-transplant period, but s-IL2R ratios greater than 0.6 may be predictive of severe rejection episodes.

Clinical outcomes in obese kidney transplant recipients have been inconclusive. Most of these studies have been done in deceased donor transplants. We compared the outcomes of living donor kidney transplants in obese and nonobese transplant recipients. Data from 54 living donor transplants between January 1999 and November 2002 were analyzed. One patient was excluded due to a high panel reactive antibody (PRA). Of the remaining 53 patients, 37 (70%) had a BMI of less than 30 (nonobese) and 16 (30%) had a BMI equal to or greater than 30 (obese). Clinical outcomes with respect to various parameters (as shown in the table) were compared. No statistical difference in outcomes was noted between the outcomes in the two groups of patients. We found comparable outcomes in obese and nonobese recipients of living donor kidney transplants. The policy to withhold transplantation in obese recipients needs careful scrutiny, especially if the transplant can be performed with a living donor. TABLE—ABSTRACT P34 . BMI BMI ≥ 30 (n = 16) P value Age (yrs) 43 ± 16 50 ± 16 0.11 Sex (M/F) 22/15 12/4 Race (AA/non AA) 4/33 0/16 Creat at 1 yr (mg/dl) 1.44 ± 0.41 1.63 ± 0.45 0.14 Length of Stay (days) 6.4 ± 5 8.4 ± 7 0.68 Delayed graft function 2.7% 19% 0.077 1 yr graft survival 97% 94% 0.51 Acute rejection 8% 19% 0.35 Wound complications 13.5% 19% 0.68 Other complications 11% 25% 0.22 Patient survival 100% 100%