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PubMed2004

Analysis of the cardiovascular risk profile in stable kidney transplant recipients after 50% cyclosporine reduction.

BACKGROUND: Long-term use of cyclosporine (CsA) contributes to post-transplant cardiovascular disease (CVD). Hence, a reduction in CsA dosage in kidney transplant recipients (KTR) may improve long-term outcomes. We analyzed the effects of 50% CsA dose reduction on the CVD risk profile in stable KTR. METHOD: Thirty-one KTR on a regimen of CsA, prednisone and mycophenolate mofetil (MMF) were studied. Patients were randomized to either a) continue their previously determined CsA dose (control group, n = 15) or b) lower their CsA dose by 50% (CsA reduction group, n = 16). Renal function, blood pressure, lipid profile, plasma homocysteine (HCY), C-reactive protein (CRP), fibrinogen, and uric acid were compared at baseline and at 6 months. RESULTS: At 6 months, there was a significant improvement in allograft function, systolic blood pressure, number of anti-hypertensive medications and serum uric acid levels in the CsA reduction group. No significant decrease in plasma HCY, CRP, fibrinogen or improvement in lipid profile was found. In contrast, in the Control group, there was a significant increase in HCY, uric acid, and triglycerides. No acute rejection occurred in either group. CONCLUSIONS: A greater reduction in CsA dose could further improve CVD risk profiles, although this may increase the risk of acute or subclinical rejection.

Adult↗

PubMed1997

Late renal allograft failure secondary to thrombotic microangiopathy associated with disseminated malignancy.

A renal transplant recipient with a remote history of end-stage renal disease due to postpartum hemolytic-uremic syndrome (HUS) presented with acute renal failure after having stable renal allograft function for 9 years. A diagnosis of thrombotic microangiopathy was made based on clinical and histologic findings at renal biopsy. She was treated conservatively, never regaining graft function and ultimately succumbing from her overwhelming tumor load approximately 6 months following diagnosis of her malignancy. To our knowledge, this is the first report of thrombotic microangiopathy associated with disseminated malignancy resulting in renal allograft failure.

Acute Kidney Injury↗

PubMed1984

Glomerulonephritis in renal allografts: results of 18 years of transplantations.

The analysis of 1282 renal transplantations revealed 13 cases of allograft glomerulonephritis (GN). Membranous GN was detected in seven patients, and mesangiocapillary GN type 1, IgA GN and focal segmental glomerulosclerosis in two patients each. The transplantation material included 13 patients with post-transplant nephrotic syndrome (NS), in 9 of whom it was evidently caused by GN. NS was the most common clinical sign of allograft GN. In addition, one patient developed low-grade proteinuria and one hematuria. In one case no signs of GN were detected at the time of graft biopsy. Loss of allograft function was associated with additional severe rejection changes. Five patients are living with a functioning graft, four have been started on hemodialysis and four have died form non-renal causes. It is concluded that NS is rare after renal transplantation and that it is most often caused by allograft GN. The prognosis of the graft is determined by co-existing rejection.

Adolescent↗

PubMed1994

Mechanisms of acquired thymic unresponsiveness to renal allografts. Thymic recognition of immunodominant allo-MHC peptides induces peripheral T cell anergy.

We have recently shown that a single intrathymic injection of synthetic 25mer peptides, representing full sequences of the hypervariable domain of RT1.BuB (4 peptides) and RT1.Du beta (4 peptides) WF class II MHC molecules, 48 hr before transplantation induces donor-specific unresponsiveness to WF rat renal allografts in adult LEW recipients. The induction of unresponsiveness was abrogated by the recipient's thymectomy within the first week after intrathymic injection. Peripheral T cells of long-term survivors exhibited antigen-specific hyporesponsiveness in the LEW x WF MLR. Studies on the mechanisms of induction of acquired thymic unresponsiveness to alloantigen in vivo and in vitro are now reported. First, since we have previously demonstrated in LEW responders that only 4 of the 8 synthetic 25mer peptides, 2 RT1.Du beta and 2 RT1.Bu beta sequences, were immunogenic in vitro and in vivo, we compared the tolerogenicity of the immunogenic versus the nonimmunogenic peptides. While LEW rats intrathymically injected with the nonimmunogenic peptides acutely rejected their renal allografts within 6-10 days, animals injected with the immunogenic peptides did not reject their grafts and are surviving > 100 days with normal allograft function. In vitro studies established that peripheral T cells from intrathymically tolerized animals exhibited antigen-specific hyporesponsiveness in the LEW x WF MLR starting as early as 1 week posttransplant. Immunohistological evaluation of renal allografts from intrathymically tolerized animals 1 week postengraftment showed marked reduction in mononuclear cell infiltrates with no evidence of tubulitis, and marked reduction in intragraft staining for activation and inflammatory cytokines and alloantibodies, as compared with acutely rejecting controls. Systemic administration of 1000 U of rIL-2 daily for 5 days starting on the day of transplantation abrogated the tolerogenic effect of intrathymic MHC allopeptides. Injection of 100 micrograms of a single immunogenic peptide, RT1.Du beta 2 (residues 20-44), into the thymus of responder LEW rats 48 hrs before immunization with RT1.Du beta 2 effected significant reduction of in vitro proliferation of primed lymphocytes to RT1.Du beta 2, an effect that was abrogated by addition of rIL-2 in vitro. In contrast, thymectomy beyond 2 weeks and administration of rIL-2 at 4-6 weeks after transplantation failed to cause rejection. These observations indicate that thymic recognition of immunodominant class II MHC allopeptides leads to peripheral T cell anergy that mediates the induction phase of systemic unresponsiveness to renal allografts. The maintenance phase appears to be mediated by dense anergy or clonal deletion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Kidney transplantation in diabetic patients using cyclosporine. Five-year follow-up.

OBJECTIVE: To review our center's experience with kidney transplantation in diabetic recipients; specifically, to compare long-term (5-year) patient and graft survival rates between diabetic and nondiabetic recipients overall and according to donor source using cyclosporine-based immunosuppression. DESIGN: A retrospective review of all kidney transplants performed over the 7-year period from 1987 to 1993. SETTING: A large urban tertiary care referral center with a long history of kidney transplantation and care of the diabetic patient. PATIENTS: All patients receiving a kidney transplant, either alone or simultaneously with a pancreas transplant, were reviewed. MAIN OUTCOME MEASURES: Actuarial patient and graft survival, serum creatinine levels, and causes of late graft loss. RESULTS: There was no significant difference in actuarial 5-year patient or kidney graft survival between diabetic and nondiabetic recipients overall or when analyzed by donor source. There was no significant difference in mean serum creatinine levels at 5 years between diabetic and nondiabetic recipients overall or between diabetic and nondiabetic cadaveric recipients. While chronic rejection was the major cause of late graft loss in nondiabetic recipients, death with a functioning graft, principally due to cardiovascular disease, was the major cause of graft loss in diabetic recipients. CONCLUSIONS: With cyclosporine-based immunosuppression, diabetic kidney transplant recipients have 5-year patient and graft survival rates and allograft function comparable to nondiabetic recipients. Given the high mortality of diabetic patients receiving dialysis, kidney transplantation is the treatment of choice for end-stage diabetic renal disease.

Actuarial Analysis↗

PubMed1996

Impact of donor/recipient size matching on outcomes in renal transplantation.

Interest in nonimmunologic factors affecting longterm graft survival has focused on adequacy of nephron dosing. Body surface are (BSA) is a reliable surrogate for nephron mass. In a retrospective study of 378 primary recipients of paired kidneys from 189 cadaveric donors, we assessed the impact of matching donor and recipient BSA on outcome over 7 years. BSA of donors was 1.82 +/- 0.26 m2. Initially, paired recipients of kidneys from a single donor were divided into two groups. Group 1 included the recipient with the larger BSA of the pair (1.97 +/- 0.17 m2), while group 2 consisted of smaller BSA recipients (1.69 +/- 0.19 m2). Although early function was better in group 2 patients, graft survival at 1 year (77% vs. 79%) and 5 years (54% vs. 55%) was identical between groups, as were most recent serum creatinine levels (2.0 +/- 0.1 vs. 2.1 +/- 0.1 mg/dl). A second analysis divided patients with a functioning allograft at discharge from initial transplant hospitalization (n = 345) into three groups based solely on donor to recipient BSA ratio: the ratio of group A (n = 30) was < or = 0.8, that of group B (n = 255) was between 0.81 and 1.19, and that of group C (n = 51) was > or = 1.2. Graft survival and kidney function over 5 years did not differ among groups. In multivariate analysis of 17 variables, donor:recipient BSA, independent of other risk factors, did not affect risk allograft loss. These data indicate that including nephron mass as a criterion for cadaveric organ allocation is unlikely to improve long-term results in renal transplantation.

Adult↗

PubMed2006

The older living kidney donor: Part of the solution to the organ shortage.

BACKGROUND: Strategies to increase kidney transplantation are urgently needed. METHODS: We studied all (n = 73,073) first kidney-only transplant recipients in the United States between 1995 and 2003 to determine the incidence and outcomes of living donor transplantation as a function of donor age. Because 90% of living donors were <55 years, we defined older living donors as > or =55 years. Factors associated with transplantation from older living donors and the association of living donor age with allograft function and survival were determined. RESULTS: Recipients of older age, female gender, white race, and preemptive transplants had higher odds of older living donor transplantation. Older living donor transplantation was more likely from spousal donors rather than blood relatives, and more likely when a husband was the donor. The glomerular filtration rate (GFR) one year after transplantation decreased with increasing donor age (P < 0.001). Graft survival from living donors > or =55 years was 85% and 76% at three and five years (compared to 89% and 82% with living donors <55 years, and 82% and 73% with deceased donors <55 years). In a multivariate model, the risk of graft loss with living donors 55-64 years was similar to that with deceased donors <55 years, while recipients from living donors 65-69 years (HR = 1.3, 95% CI: 1.1-1.7) and >70 years (HR = 1.7, 95% CI: 1.1-2.6) had a higher relative risk of graft loss. CONCLUSIONS: Outcomes are excellent with living donors <65 years. Expanded use of older living donors may help meet the demand for transplantation.

Adolescent↗

PubMed1994

Late renal allograft failure secondary to thrombotic microangiopathy-human immunodeficiency virus nephropathy.

The case of a renal transplant recipient with a known history of iv drug abuse but unknown human immunodeficiency virus (HIV) status who presents after having a stable renal allograft function for 4 yr, with acute/subacute advanced renal failure, nephrotic syndrome, and hypertension, as well as clinical and histologic findings of thrombotic microangiopathy, is reported. He was subsequently found to have a positive serology for HIV-1 with a low CD4 count but no clinical manifestations of the acquired immunodeficiency syndrome. He was treated conservatively with zidovudine (AZT). The patient never regained graft function and was ultimately discharged from the hospital on maintenance dialytic therapy. This is, to our knowledge, the first report of thrombotic microangiopathy in an HIV-1-infected patient presenting late in the course as acute/subacute renal allograft failure.

AIDS-Associated Nephropathy↗

PubMed1992

Evaluation of factors contributing to mortality in pediatric renal transplant recipients.

From 1969 to 1985, 303 renal allografts (290 cadaveric) were placed in 215 pediatric recipients. A review of actuarial recipient and allograft survival 2 years posttransplant showed good results in patients over 6 years of age (greater than 90% for patients, about 70% for allografts) but less satisfactory results in younger patients (75% for patients, about 45% for allografts). Thirty-nine patients died. Loss of allograft function preceded death in 67% of cases and was due to rejection (61%), renal vascular thrombosis (35%), and recurrence of original disease (4%). On retrospective analysis, 13 deaths might have been preventable with current diagnostic and therapeutic modalities. Allograft dysfunction from thrombosis occurs at a higher frequency in the young child and may be confused with rejection. Treatment of rejection without biopsy, overagressive treatment of a chronically failing graft, and failure to withdraw immunosuppressive therapy in face of infection are poorly tolerated in the very young recipient and are prominent causes of preventable mortality. Transplant nephrectomy and repeated attempts at transplantation are poorly tolerated in very young patients. Patient survival is very dependent on the success of the initial allograft in children.

Age Factors↗

PubMedDate not supplied

Mechanical support for acutely failed heart or lung grafts.

Heart and lung allograft dysfunction continues to be a problem in thoracic transplantation. Although medical therapy is often sufficient to restore allograft function, occasionally more invasive means are required. Mechanical assist devices, inhaled nitric oxide (iNO), and extracorporeal membrane oxygenation (ECMO) have been used with a modest degree of success in cases of refractory heart, lung, and heart-lung allograft failure. Allograft failure secondary to pulmonary hypertension often responds to iNO concentrations between 5 and 70 ppm without major toxicity. More severe cases may require mechanical assist devices or ECMO and carry higher risks of complications such as bleeding, neurological injury, and death. Utilization of and weaning from these interventions require intensive monitoring. Randomized, prospective studies are not ethically feasible, but case reports and patient series indicate the usefulness of mechanical circulatory support, iNO, and ECMO. This review focuses on the indications, complications, and patient survival rates associated with these modalities.

Assisted Circulation↗

PubMed1996

Late pancreas allograft rejection. Preliminary experience with factors predisposing to rejection.

A case series of 31 cadaveric pancreas transplant recipients who were insulin-independent at least for one year was analyzed for the factors predisposing to late acute rejection (> 12 months posttransplant). Sixty-two pancreas transplants were performed in 61 patients, of whom 53 had functioning allografts 3 months posttransplant; 31 of these had a follow-up > 12 months. Twenty had no evidence of late rejection, whereas 11 had evidence of acute rejection after 12 months. All patients received quadruple induction immunosuppression. No demographic or clinical factors-including donor age, organ cold time, HLA mismatch, age, sex, or race-could distinguish the late acute rejection group. The presence of acute rejection in the first year posttransplant was similar in the late rejectors (21 episodes in 9 of 11 patients) compared with patients without late rejection (31 episodes in 16 of 20 patients). Antilymphocyte induction therapy type had no influence, but the amount of immunosuppression with prednisone and cyclosporine (CsA) at 3 months posttransplant was significantly lower in those patients who experienced late rejection. After the first year posttransplant, CsA 12-hr trough levels were significantly lower in late rejection months (121 +/- 7 ng/ml) compared with each patient's own stable months (183 +/- 5 ng/ml, P < 0.0001). Neither prednisone nor azathioprine dosages differed between teh two groups after the first year posttransplant. Our preliminary results suggest that early under immunosuppression with prednisone and CsA in the first year and 12-hr trough CsA levels less than approximately 180 ng/ml after the first year posttransplant predispose to late pancreatic rejection.

Adult↗

PubMed1998

Treatment of fibrosing cholestatic hepatitis with lamivudine.

Fibrosing cholestatic hepatitis is a histological variant of hepatitis B virus infection with a high rate of mortality. We describe a patient who acquired acute hepatitis B virus infection 8 months after renal transplantation. Clinical features of rapidly progressive liver failure, indicated by prolonged prothrombin time (57 seconds) and increased bilirubin (40.4 mg/dL) and ammonia (129 mumol/L) concentrations, were accompanied by an extremely high serum HBV DNA level (2.153 x 10(6) pg/mL). Liver biopsy specimen showed fibrosing cholestatic hepatitis with widespread balloon degeneration of hepatocytes, focal hepatocyte loss, bile stasis, periportal fibrosis, mild lymphocytic infiltration, and strongly positive immunohistochemical staining for hepatitis B surface antigen (HBsAg) and hepatitis B core antigen. Lamivudine therapy suppressed HBV DNA to < 10 pg/mL within 4 weeks, which was followed by gradual recovery of liver function from a state of hepatic precoma. Twenty-four months after the onset of hepatitis, the patient had normal prothrombin time and bilirubin, transaminase, and albumin levels. She remained HBsAg positive and hepatitis B e antigen negative. Renal allograft function was stable, with a creatinine level of 1.52 mg/dL. HBV DNA remained suppressed after 22 months of lamivudine therapy. Our experience shows that fibrosing cholestatic hepatitis and liver failure caused by HBV infection can be successfully treated with lamivudine.

Adult↗

PubMed2003

Chronic rejection of murine cardiac allografts discordant at the H13 minor histocompatibility antigen correlates with the generation of the H13-specific CD8+ cytotoxic T cells.

BACKGROUND: Minor histocompatibility antigen (mHag) discordances have been shown to play a critical role in graft-versus-host disease after bone marrow transplantation. However, the role of mHag in rejection of solid-organ allografts remains unknown. Therefore, the goal of this study was to define the role of a single mHag discordance derived from the polymorphic H13 allele in the development of cardiac allograft rejection in mice. The H13a and H13b alleles encode for the SSVVGVWYL (SVL9) and SSVIGVWYL (SIL9) mHag bound to the H2Db molecule, respectively. METHODS: C56BL/10SnJ (H13a) cardiac allografts were transplanted into congenic B10.CE-H13b Aw(30NX)/Sn (H13b) mice. Allograft function was monitored daily and rejection was defined by cessation of heart beat. Rejection was confirmed histologically. The phenotypic and functional characteristics of the graft-infiltrating cells were analyzed by in situ and in vitro staining with H13a-specific tetramers and by chromium-51 (51Cr)-release assay, respectively. RESULTS: Sixty-five percent of H13-incompatible allografts were rejected in 37.0+/-14.5 days. Sixty-eight percent of the H13a allografts transplanted into H13a-sensitized mice were rejected earlier, in 27.6+/-15.9 days. Rejected allografts showed histopathologic signs of chronic rejection with diffuse mononuclear cell infiltration, concentric intimal hyperplasia, and fibrosis. Both CD8+ (87%) and CD4+ (13%) T cells were observed in rejected allografts. In addition, 60% of the graft-infiltrating CD8+ T cells recognized a H2Db/SVL9 tetramer. Graft-infiltrating CD8+ T cells showed a significant H2Db-restricted, SVL9-specific cytotoxic activity. CONCLUSIONS: A single mHag discordance, as demonstrated with H13 disparity, results in the pathogenesis of chronic rejection of major histocompatibility complex-matched vascularized solid-organ allograft.

Animals↗

PubMed2000

A calcineurin inhibitor-sparing regimen with sirolimus, mycophenolate mofetil, and anti-CD25 mAb provides effective immunosuppression in kidney transplant recipients with delayed or impaired graft function.

Delayed graft function (DGF) after renal transplantation is a significant risk factor for early acute rejection and graft loss. Sirolimus (SRL) can be administered in the setting of DGF without exacerbating the impaired renal function after transplantation. We examined a calcineurin-sparing regimen using SRL during the early post-operative period in renal transplant patients with delayed or impaired graft function. A retrospective review of 14 consecutive kidney transplant recipients with delayed or impaired graft function who received SRL was performed. The immunosuppressive regimen consisted of daclizumab induction (2 mg/kg), SRL (5-15 mg load followed by 2 5 mg daily maintenance therapy), corticosteroids, and mycophenolate mofetil (MMF, 1.5-3 g/d). Patients were monitored for allograft function, acute rejection, graft survival, thrombocytopenia, and leukopenia. Serum levels of SRL were determined by high-performance liquid chromatography performed at an independent commercial laboratory. Donors were cadaveric in 13 cases and living related in one. The duration of follow-up was 0.5-5.2 months. Nine patients required hemodialysis after transplantation. The mean time to initiation of calcineurin inhibitors was 21 +/- 13 d. Average serum creatinine levels at the initiation of SRL and at 1 month after transplantation were 8.4 +/- 2.7 and 2.1 +/- 1.2 mg/dL, respectively. There were 2 patients (14%) who experienced acute rejection within the first month after transplantation -1 with type I (steroid therapy) and 1 with type II (anti-thymocyte therapy). Serum levels of SRL were initially undetectable in the 2 patients with acute rejection. No grafts were lost during the period of follow-up. Three patients developed thrombocytopenia (platelets < 100 x 10(9)) and no patients developed leukopenia. The combination of SRL with anti-CD25 mAb, MMF, and corticosteroids appears to provide effective non-nephrotoxic immunosuppression for kidney transplantation without the need for a lymphocyte-depleting regimen. However, it is important to monitor serum SRL levels to determine the optimal dosing regimen. Furthermore, long-term follow-up of these patients will be helpful to determine whether improved immunosuppression can be achieved with a fully calcineurin-sparing regimen using SRL.

Adult↗

PubMed1984

The enhancing and sensitizing effects of donor blood components, including dendritic cells, in a rat renal allograft model.

In the DA-to-Lewis renal allograft model, donor whole blood enhanced renal allograft survival (14.5 +/- 7.6 days versus 6.9 +/- 0.6 days in controls [P less than 0.01]). The effect of individual cell components given in numbers equivalent to those present in the enhancing volumes of donor whole blood was studied. Immunization with donor red cells alone produced greater enhancement than that produced by whole blood (36.14 +/- 19.5 days [P less than 0.01]). B lymphocytes also enhanced allograft survival (16.0 +/- 3.9 days [P less than 0.01]). Although slight enhancement was observed with platelets (8.5 +/- 0.6 days) and 10(5) dendritic cells (8.4 +/- 0.5 days), in terms of allograft function dendritic cell immunization produced evidence of dose-dependent accelerated rejection. A similar finding was obtained with donor T cell immunization. Donor plasma had no effect. We conclude that, although donor blood has an overall enhancing effect on renal allograft survival in this model, the sensitizing and enhancing effects can be ascribed to individual types of cells.

Animals↗

PubMed1998

Results of transplantation for acute and chronic hepatic allograft rejection.

BACKGROUND/PURPOSE: Transplantation for rejection is a requirement in liver transplant recipients when allograft failure is imminent. The authors evaluated the outcome of these children and their allografts. METHODS: The medical records of 129 children who received a liver transplant were reviewed retrospectively. Twelve children required transplantation for biopsy-proven rejection--10 chronic and two acute. Overall patient and graft survival were compared with children receiving primary liver transplants. The current allograft function of the patients undergoing transplants was also reviewed. Statistical significance was determined by Fisher's Exact test. RESULTS: Twelve children received at least one retransplant for biopsy-proven rejection. Graft survival at 1 year was 58% (v 79% for primary transplants) and patient survival was 83% (vs 89%). Two allografts were lost because of primary allograft nonfunction. Three additional allografts were lost-two to recurrent rejection and one to hepatic artery thrombosis. Two patients who lost a second transplant to rejection required a total of seven transplants to treat rejection. Two children died, one of primary nonfunction and one of adenovirus pneumonia. The 10 surviving patients all have excellent graft function (total bilirubin, 0.74 +/- 0.38, aspartate aminotransferase, 40 +/- 22). CONCLUSION: These data suggest that transplantation for rejection can be accomplished safely with a patient survival rate comparable to primary liver transplantation; however, graft loss is excessive and underscores the need for more adequate immunosuppression.

Adolescent↗

PubMed1983

Vibration sensory threshold: a guide to adequacy of dialysis?

The vibration sensory threshold (VST) is an easy non-invasive reproducible and sensitive bedside test of peripheral nerve function. It is impaired in pre-dialysis uraemic patients with no clinical evidence of peripheral neuropathy; tends to deteriorate during the first year of dialysis after which it remains relatively constant, and returns towards normal within one week of kidney allograft function. It is unrelated to type of dialysis, acetylator status, average serum creatinine values or serum aluminium. VST may be a valuable monitor of the adequacy of dialysis.

Female↗

PubMed1997

Endothelial activation and development of coronary artery disease in transplanted human hearts.

CONTEXT: The development of coronary artery disease in heart transplants is often associated with graft failure. Early detection of allografts prone to develop this disease is essential to institute new therapeutic approaches that could prolong allograft function. OBJECTIVE: To determine if early activation of arterial/arteriolar endothelium predicts the development of coronary artery disease, graft failure, or both in transplanted human hearts. DESIGN: Prospective cohort study. SETTING: Heart Transplant Center. PARTICIPANTS: A total of 121 consecutive adult cardiac allograft recipients who received transplants between 1988 and 1995 and were followed up through 1996. MAIN OUTCOME MEASURES: Development of coronary artery disease and graft failure. METHODS: Immunocytochemistry was performed on serial endomyocardial biopsy specimens to evaluate endothelial activation markers (intercellular adhesion molecule-1 and histocompatibility antigen HLA-DR) in arteries and arterioles. The presence and progression of coronary artery disease was evaluated by annual coronary angiograms with side-by-side comparisons. RESULTS: None of the 121 donor hearts showed arterial/arteriolar endothelial activation before transplantation. Arterial/arteriolar endothelial activation was present in 78 and absent in 43 of 121 allografts during the first 3 months after transplantation. The time of appearance and the proportion of biopsy specimens showing endothelial activation during these first 3 months were significantly associated with the risk of developing coronary artery disease, the progression of the disease, and the time required to develop the disease (P<.001). Significantly more patients with arterial/arteriolar endothelial activation died or received a second transplant (P<.001). CONCLUSIONS: Activation of arterial/arteriolar endothelium in transplanted human hearts predicts development of coronary artery disease and increased risk of graft failure.

Adult↗