Cardiogenic shock and coronary endothelial dysfunction predict cardiac allograft vasculopathy after heart transplantation

Cardiac allograft vasculopathy remains one of the major causes of death post‐heart transplantation. Its etiology is multifactorial and prevention is challenging. The aim of this study was to prospectively determine factors related to cardiac allograft vasculopathy after heart transplantation. This research was planned on 179 patients submitted to heart transplant. Performance of an early coronary angiography with endothelial function evaluation was scheduled at three‐month post‐transplant. Patients underwent a second coronary angiography after five‐yr follow‐up. At the 5‐ ± 2‐yr follow‐up, 43% of the patients had developed cardiac allograft vasculopathy (severe in 26% of them). Three independent predictors of cardiac allograft vasculopathy were identified: cardiogenic shock at the time of the transplant operation (OR: 6.49; 95% CI: 1.86–22.7, p = 0.003); early coronary endothelial dysfunction (OR: 3.9; 95% CI: 1.49–10.2, p = 0.006), and older donor age (OR: 1.05; 95% CI: 1.00–1.10, p = 0.044). Besides early endothelial coronary dysfunction and older donor age, a new predictor for development of cardiac allograft vasculopathy was identified: cardiogenic shock at the time of transplantation. In these high‐risk patient subgroups, preventive measures (treatment of cardiovascular risk factors, use of novel immunosuppressive agents such as mTOR inhibitors) should be earlier and much more aggressive.     

Early findings of prospective anti‐HLA donor specific antibodies monitoring study in pancreas transplantation: Indiana University Health Experience

The significance of donor‐specific antibodies (DSA) is not well known in the setting of pancreas transplantation. Since December 2009, we prospectively followed pancreas transplant patients with single‐antigen‐luminex‐bead testing at one, two, three, six, and then every six months for the first two yr. Thirty‐five of the 92 patients that underwent pancreas transplantation (13 pancreas‐alone [PTA], 20 with a kidney [SPK], and two after a kidney [PAK]) agreed to participate in study. Median age at transplant was 45 yr and follow‐up was 23 months. Majority were Caucasian (n = 33) and male (n = 18). Rabbit anti‐thymocyte globulin induction was used. Median HLA‐mismatch was 4.2 ± 1.1. Eight patients (7SPK, 1PAK) developed post‐transplant DSA at median follow‐up of 76 d (26–119), 1 SPK had pre‐formed DSA. Seven patients had both class I and class II DSA, one with class I and one with class II only. Mean peak class I DSA‐MFI was 3529 (±1456); class II DSA‐MFI was 5734 (±3204) whereas cumulative DSA MFI (CI + CII) was 9264 (±4233). No difference was observed in the patient and donor demographics among patients with and without DSA. One patient in non‐DSA group developed acute cellular rejection of pancreas. From our data it appears that post‐transplant DSA in pancreas allograft recipients may not impact the early‐pancreatic allograft outcomes. The utility of prospective DSA monitoring in pancreatic transplant patients needs further evaluation and long‐term follow‐up.     

Do kidney histology lesions predict long‐term kidney function after liver transplantation?

Histological renal lesions observed after liver transplantation are complex, multifactorial, and interrelated. The aims of this study were to determine whether kidney lesions observed at five yr after liver transplantation can predict long‐term kidney function. Ninety‐nine liver transplant patients receiving calcineurin inhibitor (CNI)‐based immunosuppression, who had undergone a kidney biopsy at 60 ± 48 months post‐transplant, were included in this follow‐up study. Kidney biopsies were scored according to the Banff classification. Estimated glomerular filtration rate (eGFR) was assessed at last follow‐up, that is, 109 ± 48 months after liver transplantation. eGFR decreased from 92 ± 33 mL/min at transplantation to 63 ± 19 mL/min after six months, to 57 ± 17 mL/min at the kidney biopsy, to 54 ± 24 mL/min at last follow‐up (p < 0.0001). At last follow‐up, only three patients required renal replacement therapy. After the kidney biopsy, 13 patients were converted from CNIs to mammalian target of rapamycin inhibitors, but no significant improvement in eGFR was observed after conversion. Elevated eGFR at six months post‐transplant and a lower fibrous intimal thickening score (cv) observed at five yr post‐transplant were the two independent predictive factors for eGFR ≥60 mL/min at nine yr post‐transplant. Long‐term kidney function seems to be predicted by the kidney vascular lesions.     

Allograft and patient survival after sequential HSCT and kidney transplantation from the same donor—A multicenter analysis

Tolerance induction through simultaneous hematopoietic stem cell and renal transplantation has shown promising results, but it is hampered by the toxicity of preconditioning therapies and graft‐versus‐host disease (GVHD). Moreover, renal function has never been compared to conventionally transplanted patients, thus, whether donor‐specific tolerance results in improved outcomes remains unanswered. We collected follow‐up data of published cases of renal transplantations after hematopoietic stem cell transplantation from the same donor and compared patient and transplant kidney survival as well as function with caliper‐matched living‐donor renal transplantations from the Austrian dialysis and transplant registry. Overall, 22 tolerant and 20 control patients were included (median observation period 10 years [range 11 months to 26 years]). In the tolerant group, no renal allograft loss was reported, whereas 3 were lost in the control group. Median creatinine levels were 85 μmol/l (interquartile range [IQR] 72‐99) in the tolerant cohort and 118 μmol/l (IQR 99‐143) in the control group. Mixed linear‐model showed around 29% lower average creatinine levels throughout follow‐up in the tolerant group (P < .01). Our data clearly show stable renal graft function without long‐term immunosuppression for many years, suggesting permanent donor‐specific tolerance. Thus sequential transplantation might be an alternative approach for future studies targeting tolerance induction in renal allograft recipients.     

Kidney allograft failure in the steroid‐free immunosuppression era: A matched case‐control study

We studied the causes and predictors of death‐censored kidney allograft failure among 1670 kidney recipients transplanted at our center in the corticosteroid‐free maintenance immunosuppression era. As of January 1, 2012, we identified 137 recipients with allograft failure; 130 of them (cases) were matched 1‐1 for recipient age, calendar year of transplant, and donor type with 130 recipients with functioning grafts (controls). Median time to allograft failure was 29 months (interquartile range: 18‐51). Physician‐validated and biopsy‐confirmed categories of allograft failure were as follows: acute rejection (21%), glomerular disease (19%), transplant glomerulopathy (13%), interstitial fibrosis tubular atrophy (10%), and polyomavirus‐associated nephropathy (7%). Graft failures were attributed to medical conditions in 21% and remained unresolved in 9%. Donor race, donor age, human leukocyte antigen mismatches, serum creatinine, urinary protein, acute cellular rejection, acute antibody‐mediated rejection, BK viremia, and CMV viremia were associated with allograft failure. Independent predictors of allograft failure were acute cellular rejection (odds ratio: 18.31, 95% confidence interval: 5.28‐63.45) and urine protein ≥1 g/d within the first year post‐transplantation (5.85, 2.37‐14.45). Serum creatinine ≤1.5 mg/dL within the first year post‐transplantation reduced the odds (0.29, 0.13‐0.64) of allograft failure. Our study has identified modifiable risk factors to reduce the burden of allograft failure.     

Association of prevalent vascular disease with allograft failure and mortality in live‐donor kidney transplant recipients – a retrospective cohort study

Limited data exist regarding the impact of prevalent vascular disease after live‐donor kidney transplantation. We aimed to determine the associations between the number of prevalent vascular diseases, allograft, and patient outcomes following live‐donor transplantation. This cohort study used data from the Australia and New Zealand Dialysis and Transplant Registry. Rates between recipients of live‐donor kidney transplants ± prevalent vascular disease prior to transplantation were calculated. The associations between vascular disease, allograft failure, and all‐cause mortality were assessed using Cox regression modeling. Kaplan–Meier proportions were used to calculate all‐cause mortality and death with a function graft stratified by vascular disease burden. Of 4742 live‐donor recipients, 428 (9%) and 84 (2%) had prevalent vascular disease at 1 and ≥2 sites, respectively. Compared to recipients without vascular disease, the respective adjusted hazard ratios (95% confidence intervals) for patients with vascular disease at 1 and ≥2 sites were 1.78 (1.41–2.25) and 3.02 (2.03–4.50) for all‐cause mortality; and 1.54 (1.26–1.88) and 2.28 (1.54–3.38) for allograft failure. All‐cause mortality in recipients with vascular disease at 0, 1 and ≥2 sites was 0.028 (0.025, 0.031), 0.090 (0.073, 0.106) and 0.247 (0.196, 0.282) over the first 5‐year post‐transplant. There was an incremental association between the number of prevalent vascular disease sites and risk of allograft failure and all‐cause mortality in live‐donor kidney transplant recipients.     

Microvasculature partial endothelial mesenchymal transition in early posttransplant biopsy with acute tubular necrosis identifies poor recovery renal allografts

Acute tubular necrosis (ATN), a frequent histopathological feature in the early post–renal transplant biopsy, affects long‐term graft function. Appropriate markers to identify patients at risk of no or incomplete recovery after delayed graft function are lacking. In this study, we first included 41 renal transplant patients whose biopsy for cause during the first month after transplantation showed ATN lesions. Using partial microvasculature endothelial (fascin, vimentin) and tubular epithelial (vimentin) to mesenchymal transition markers, detected by immunohistochemistry, we found a significant association between partial endothelial to mesenchymal transition and poor graft function recovery (Spearman's rho = ?0.55, P = .0005). Transforming growth factor–β1 was strongly expressed in these phenotypic changed endothelial cells. Extent of ATN was also correlated with short‐ and long‐term graft dysfunction. However, the association of extensive ATN with long‐term graft dysfunction (24 months posttransplant) was observed only in patients with partial endothelial to mesenchymal transition marker expression in their grafts (Spearman's rho = ?0.64, P = .003), but not in those without. The association of partial endothelial to mesenchymal transition with worse renal graft outcome was confirmed on 34 other early biopsies with ATN from a second transplant center. Our results suggest that endothelial cell activation at the early phase of renal transplantation plays a detrimental role.     

Liver transplantation arrests and reverses muscle wasting

Muscle wasting, sarcopenia, is common in advanced cirrhosis and predicts adverse outcomes while awaiting and following liver transplantation. Frequent post‐transplant worsening of sarcopenia has attracted recent interest. It is unknown whether this serious problem is an expected metabolic consequence of transplantation or results from confounding conditions such as recurrent allograft liver disease or avoidable post‐transplant complications. To clarify this question, we studied pre‐ and post‐transplant muscle mass in a retrospective cohort of 40 patients transplanted for three diseases – alcoholic cirrhosis, non‐alcoholic steatohepatitis cirrhosis, and primary sclerosing cholangitis cirrhosis – in whom allograft disease recurrence was monitored and excluded, and who lacked common post‐transplant muscle wasting complications such as sepsis, renal failure, ischemia, and cholestasis. We measured skeletal muscle index (SMI) using computed tomography before and 12–48 months after transplant. SMI as a categorical variable significantly improved, from 18 patients above the normal cutoff pre‐transplant to 28 post‐transplant (p = 0.008). SMI increases were greatest in patients with the lowest pre‐transplant SMI (p < 0.01). As a continuous variable, mean SMI remained stable, with a non‐significant trend toward improvement. We conclude that after liver transplantation sarcopenia does not progress but is arrested and frequently improves in the absence of confounding conditions.     

Early loss of peritubular capillaries after kidney transplantation

Inflammation, interstitial fibrosis (IF), and tubular atrophy (TA) precede chronic transplant dysfunction, which is a major cause of renal allograft loss. There is an association between IF/TA and loss of peritubular capillaries (PTCs) in advanced renal disease, but whether PTC loss occurs in an early stage of chronic transplant dysfunction is unknown. Here, we studied PTC number, IF/TA, inflammation, and renal function in 48 patients who underwent protocol biopsies. Compared with before transplantation, there was a statistically significant loss of PTCs by 3 months after transplantation. Fewer PTCs in the 3-month biopsy correlated with high IF/TA and inflammation scores and predicted lower renal function at 1 year. Predictors of PTC loss during the first 3 months after transplantation included donor type, rejection, donor age, and the number of PTCs at the time of implantation. In conclusion, PTC loss occurs during the first 3 months after renal transplantation, associates with increased IF and TA, and predicts reduced renal function.     

Subclinical Inflammation and Chronic Renal Allograft Injury in a Randomized Trial on Steroid Avoidance in Pediatric Kidney Transplantation

Steroid avoidance is safe and effective in children receiving kidney transplants in terms of graft function and survival, but the effects on allograft histology are unknown. In this multicenter trial, 130 pediatric renal transplant recipients were randomized to steroid‐free (SF; n = 60) or steroid‐based (SB; n = 70) immunosuppression, and underwent renal allograft biopsies at the time of graft dysfunction and per protocol at implantation and 6, 12 and 24 months after transplantation. Clinical follow‐up was 3 years posttransplant. Subclinical acute rejection was present in 10.6% SF versus 11.3% SB biopsies at 6 months (p = 0.91), 0% SF versus 4.3% SB biopsies at 1 year (p = 0.21) and 0% versus 4.8% at 2 years (p = 0.20). Clinical acute rejection was present in 13.3% SF and 11.4% SB patients by 1 year (p = 0.74) and in 16.7% SF and 17.1% SB patients by 3 years (p = 0.94) after transplantation. The cumulative incidence of antibody‐mediated rejection was 6.7% in SF and 2.9% in SB by 3 years after transplantation (p = 0.30). There was a significant increase in chronic histological damage over time (p < 0.001), without difference between SF and SB patients. Smaller recipient size and higher donor age were the main risk factors for chronic histological injury in posttransplant biopsies.     

Chronic allograft nephropathy--biopsy findings and outcome.

BACKGROUND: Chronic allograft nephropathy (CAN) is a composite term for various types of damage to a kidney transplant. We wanted to analyse its components in relation to baseline biopsy findings, transplant function, and outcome. METHODS: Among renal transplantations performed from 1985 to 1997, 156 were identified where allograft biopsies had been obtained on clinical indication 6 months after transplantation or later, baseline biopsies were available in each case and the patient's original disease was known. Time after transplantation was median 2.2 years (range 0.5-13). The biopsies were reviewed and the Banff 1997 CAN score obtained. RESULTS: All but one late biopsy showed some CAN grade, 48% grade II, and 7.5% grade III. Acute tubulointerstitial rejection was seen in 9% but vascular rejection in only 3%. Arterial wall thickening was present in 66% of the late biopsies, correlated with donor age and its presence at baseline but also with time after transplantation. The Banff CAN score and serum creatinine level were both independent predictors of further graft survival, relative risk 0.35 (confidence interval 0.15-0.82, P=0.015) for CAN grade I vs III and 0.30 (0.14-0.67, P=0.003) for serum creatinine <170 vs >250 micromol/l. Presence of arterial wall thickening had no prognostic impact. CONCLUSION: The CAN grade is predictive of further graft survival independently of the serum creatinine level. Interstitial fibrosis and tubular atrophy are more prominent features of chronic graft damage than vascular rejection. Unspecific arterial wall thickening is partly dependent on baseline conditions and lacks prognostic impact in this late stage.     

Machine perfusion of donor kidneys may reduce graft rejection

Recent evidence suggests that hypothermic machine perfusion of donor kidneys reduces delayed graft function (DGF). This study addresses the effect of machine perfusion (MP) on allograft rejection in the United States. We assembled a retrospective cohort of patients undergoing kidney‐alone transplants in the UNOS database from June 30, 2004 to May 31, 2017. DGF was defined as dialysis requirement in the first week post‐transplant; graft rejection was defined at 6 months and 1 year. Multivariable logistic regression adjusted for recipient and donor factors evaluated the effect of MP on DGF and graft rejection. Records for 79 300 kidney transplants meeting inclusion criteria were abstracted, 42% of which underwent MP. MP kidneys came from older donors, were more likely to have been obtained following donation after cardiac death, and had longer cold ischemic times. Rates of DGF and rejection were similar between MP and static storage kidneys. Following adjustment, recipients of MP kidneys were less likely to experience rejection at 1 year (OR 0.91 [95% CI 0.86‐0.97] P = .002), but not at 6 months post‐transplantation (OR 0.94 [0.88‐1.02] P = .07). This effect persisted following adjustment for cold ischemic time. This study adds to the accumulating evidence demonstrating improved outcomes following MP of kidneys. We encourage protocolized consideration of MP for kidney grafts.     

Histologically proven non‐alcoholic fatty liver disease and clinically related factors in recipients after liver transplantation

Non‐alcoholic fatty liver disease (NAFLD) affects a substantial proportion of the world population, and its prevalence has been increasing. The study was aimed at evaluating the prevalence and peri‐transplant risk factors for post‐liver transplantation (LT) NAFLD. A retrospective review was performed for adult recipients who underwent late protocol biopsy (>1 yr after LT) between August 2010 and December 2012. Hepatic steatosis was reviewed and graded by hepatopathologists, and the peri‐transplant factors were analyzed for relationships to histologically proven NAFLD. Total 166 biopsies had been performed in 156 recipients. NAFLD was present in 27.1% at a mean period of 35.4 months between LT and biopsy, moderate and severe steatosis (≥33%) consisted of 28.9%. In multivariate analysis, pre‐LT alcoholic cirrhosis (odds ratio [OR] 8.031, p = 0.003), obesity at biopsy (OR 3.873, p = 0.001), and preexisting donor graft steatosis (OR 3.147, p = 0.022) were significant risk factors for post‐LT NAFLD. In conclusion, NAFLD represented a considerable portion of recipients, but this prevalence was not higher than those for general population. Three risk factors were significantly related to post‐LT NAFLD, and recipients with those factors should be monitored for NAFLD. Furthermore, possible progression to non‐alcoholic steatohepatitis (NASH) or fibrosis and metabolic syndrome should be considered in future studies.     

“White‐Out” After Lung Transplantation: A Multicenter Cohort Description of Late Acute Graft Failure

Graft failure represents a leading cause of mortality after organ transplantation. Acute late‐onset graft failure has not been widely reported. The authors describe the demographics, CT imaging–pathology findings, and treatment of patients presenting with the latter. A retrospective review was performed of lung transplant recipients at two large‐volume centers. Acute late‐onset graft failure was defined as sudden onset of bilateral infiltrates with an oxygenation index <200 without identifiable cause or concurrent extrapulmonary organ failure. Laboratory, bronchoalveolar lavage (BAL), radiology, and histology results were assessed. Between 2005 and 2016, 21 patients were identified. Median survival was 19 (IQR 13–36) days post onset. Twelve patients (57%) required intensive care support at onset, 12 (57%) required mechanical ventilation, and 6 (29%) were placed on extracorporeal life support. Blood and BAL analysis revealed elevated neutrophilia, with CT demonstrating diffuse ground‐glass opacities. Transbronchial biopsy samples revealed acute fibrinoid organizing pneumonia (AFOP), organizing pneumonia, and diffuse alveolar damage (DAD). Assessment of explanted lungs confirmed AFOP and DAD but also identified obliterative bronchiolitis. Patients surviving to discharge without redo transplantation (n = 2) subsequently developed restrictive allograft syndrome. This study describes acute late‐onset graft failure in lung allograft recipients, without known cause, which is associated with a dismal prognosis.     

No impact of disseminated intravascular coagulation in kidney donors on long‐term kidney transplantation outcome: A multicenter propensity‐matched study

The diagnosis of disseminated intravascular coagulation (DIC) is often considered to be a contraindication to organ donation. The aim of this study was to evaluate the impact of DIC+ donors on kidney recipient (KR) evolution. We identified 169 KRs with DIC+ donation after brain death donors between January 1996 and December 2012 in 6 French transplant centers. Individuals were matched using propensity scores to 338 recipients with DIC? donors according to donor age and sex, whether expanded criteria for the donor existed, graft year, and transplantation center. After kidney transplantation, delayed graft function was observed in 28.1% of DIC+ KRs and in 22.8% of DIC? KRs (NS). Renal allograft survival at 1, 5, and 10 years was 94.5%, 89.3%, and 73.9% and 96.2%, 90.8%, and 81.3% in DIC+ KRs and DIC? KRs, respectively (NS). The median estimated glomerular filtration rate (eGFR) was similar between DIC+ and DIC? KRs at 3 months, 1 year, and 10 years: 45.9 vs 48.1 mL/min, 42.1 vs 43.1 mL/min, and 33.9 vs 38.1 mL/min, respectively. Delayed calcineurin inhibitor introduction or induction had no impact on delayed graft function rate or eGFR evolution at 10 years after transplantation in DIC+ KRs. Donor DIC did not seem to affect initial outcome, long‐term graft function, or allograft survival.     

Liver transplantation for hepatitis C virus (HCV) non‐viremic recipients with HCV viremic donors

In the context of organ shortage, the opioid epidemic, and effective direct‐acting antiviral (DAA) therapy for hepatitis C virus (HCV), more HCV‐infected donor organs may be used for liver transplantation. Current data regarding outcomes after donor‐derived HCV in previously non‐viremic liver transplant recipients are limited. Clinical data for adult liver transplant recipients with donor‐derived HCV infection from March 2017 to January 2018 at our institution were extracted from the medical record. Ten patients received livers from donors known to be infected with HCV based on positive nucleic acid testing. Seven had a prior diagnosis of HCV and were treated before liver transplantation. All recipients were non‐viremic at the time of transplantation. All 10 recipients derived hepatitis C infection from their donor and achieved sustained virologic response at 12 weeks posttreatment with DAA‐based regimens, with a median time from transplant to treatment initiation of 43 days (IQR 20–59). There have been no instances of graft loss or death, with median follow‐up of 380 days (IQR 263–434) posttransplant. Transplantation of HCV‐viremic livers into non‐viremic recipients results in acceptable short‐term outcomes. Such strategies may be used to expand the donor pool and increase access to liver transplantation.     

Allograft biopsy findings in patients with small bowel transplantation

In this study, we sought to determine the incidence of post‐transplant complications including acute cellular rejection (ACR), infection, and post‐transplant lymphoproliferative disease (PTLD) in mucosal allograft biopsies in patients with small bowel transplant at our institution. We retrospectively reviewed pathology reports from 5675 small bowel allograft biopsies from 99 patients and analyzed the following: indications for biopsy, frequency and grade of ACR, the presence of infectious agents, results of workup for potential PTLD, results of C4d immunohistochemistry (IHC), features of chronic mucosal injury, and findings in concurrent native bowel biopsies. Findings from 42 allograft resection specimens were also correlated with prior biopsy findings. Indeterminate, mild, moderate, and severe ACR were seen in 276 (4.9%), 409 (7.2%), 100 (1.8%), and 207 (3.6%) of biopsies, respectively. Although ACR may show histologic overlap with mycophenolate mofetil toxicity, we found the analysis of concurrent native bowel biopsies to be helpful in this distinction. Adenovirus was the most common infectious agent seen (11%), and we routinely performed adenovirus IHC on biopsies. Eighteen patients (18%) developed PTLD, 83% of which were EBV associated, but only 28% of PTLD cases were diagnosed on mucosal allograft biopsies. C4d IHC did not correlate with the presence of donor‐specific antibodies in limited cases.     

Impact of glucose metabolism abnormalities on histopathological changes in kidney transplant protocol biopsies

The impact of post‐transplant diabetes (PTDM) on kidney transplant histopathology has been poorly described. We examined the association of glucose metabolism abnormalities on the progression of histopathological changes in serial protocol biopsies. Helsinki University Hospital kidney transplant recipients during 2004–2006 were followed up. Patients with pre‐existing diabetes or 2‐h oral glucose tolerance test (OGTT) performed at 3 months, and protocol biopsies taken at 0 and 12 months were analyzed (n = 76). Diabetes was defined according to WHO/ADA. Histology was analyzed with chronic allograft damage index (CADI). Altogether 32 patients had pre‐existing diabetes. In OGTT at 3 months, four showed PTDM, eight impaired glucose tolerance (IGT), two impaired fasting glucose, and 30 normal glucose tolerance. Patients with impaired glucose metabolism were older (P = 0.005), received grafts from older donors (P = 0.04), and had reduced renal function at 12 months (P = 0.003). In patients with IGT or PTDM, 2‐h postload glucose values in OGTT correlated with CADI at 12 months (R = 0.84, P = 0.001) and with the change in CADI score between 0 and 12 months (R = 0.67, P = 0.025). Graft survival was reduced in patients with pre‐existing diabetes (P = 0.01). Glucose abnormalities were associated with the progression of histopathological changes, especially in patients with already compromised kidneys, supporting the harmful role of PTDM to the kidney allograft.     

Transmission of breast cancer by a single multiorgan donor to 4 transplant recipients

We report 4 cases of breast cancer transmission to transplant recipients from a single organ donor that occurred years after donation. The diagnosis of breast cancer was occult at the time of donation. All of the recipients developed a histologically similar type of breast cancer within 16 months to 6 years after transplantation. Three out of 4 recipients died as a result of widely metastasized disease. One of the recipients survived after transplant nephrectomy followed by cessation of immunosuppression and chemotherapy. This extraordinary case points out the often fatal consequences of donor‐derived breast cancer and suggests that removal of the donor organ and restoration of immunity can induce complete remission.     

Short‐term kidney transplant outcomes among African American recipients do not predict long‐term outcomes: donor pair analysis

Keith D, Patrie JT. Short‐term kidney transplant outcomes among African‐American recipients do not predict long‐term outcomes: donor pair analysis.
Clin Transplant 2011: 25: 69–76. © 2010 John Wiley & Sons A/S. Abstract: African American (AA) renal transplant recipients have poorer graft survival compared to other racial and ethic groups. This study was undertaken to determine whether pre‐transplant factors and events occurring in the first six months post‐transplant were predictive of the poorer long‐term outcomes in AA recipients. To control for kidney quality, a paired analysis of deceased donor kidneys in which one donor kidney was transplanted into an adult AA recipient and the other was transplanted into an adult Caucasian was undertaken. Cox proportional hazard modeling was used to determine the impact of outcome variables at six months. Outcomes at six months among the paired recipients were very similar for graft and patient survival, and estimated glomerular filtration rate (GFR). Less than 10% of difference in long‐term outcomes was explained by differences in the pre‐transplant covariates and events in the first six months. Causes of graft failure after six months revealed a two to three times higher rate of chronic allograft nephropathy (CAN) and late acute rejection among AA. In conclusion, early outcomes after kidney transplant did not predict the poor long‐term graft survival among AA, and AA recipients appear to be more prone to graft loss because of CAN and late acute rejection.