Late Graft Failure (late + graft_failure)

Distribution by Scientific Domains


Selected Abstracts


De Novo Donor-Specific Antibody at the Time of Kidney Transplant Biopsy Associates with Microvascular Pathology and Late Graft Failure

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2009
L. G. Hidalgo
We studied whether de novo donor-specific antibodies (DSA) in sera from patients undergoing kidney transplant biopsies associate with specific histologic lesions in the biopsy and prognosis. DSA were assessed in 145 patients at the time of biopsy between 7 days to 31 years posttransplant. DSA was detected in 54 patients (37%), of which 32 represented de novo DSA. De novo DSA was more frequent in patients having late biopsies (34%) versus early biopsies (4%), and was usually either against class II alone or class I and II but rarely against class I alone. Microcirculation inflammation (glomerulitis, capillaritis) and damage (glomuerulopathy, capillary basement membrane multilayering), and C4d staining were associated with de novo DSA. However, the degree of scarring, arterial fibrosis and tubulo-interstitial inflammation did not correlate with the presence of de novo DSA. De novo DSA correlated with reduced graft survival after the biopsy. Thus, de novo DSA at the time of a late biopsy for clinical indication is primarily against class II, and associates with microcirculation changes in the biopsy and subsequent graft failure. We propose careful assessment of de novo DSA, particularly against class II, be performed in all late kidney transplant biopsies. [source]


Durable remission following a third allogeneic stem cell transplantation in a patient with repeatedly relapsing SAA.

PEDIATRIC TRANSPLANTATION, Issue 3 2007
The importance of stroma cells for sustained engraftment?
Abstract:, Diagnosis of acquired AATP which finally progressed to SAA was established in an eight-yr-old boy. PBSCT from an HLA-identical unrelated donor using high numbers of CD34+ selected stem cells was performed and resulted in complete remission for almost two yr. However, SAA reoccurred with 100% donor hematopoiesis and was reversed by a second CD 34+ selected PBSCT from the same donor. Declining blood cell counts after an interval of two yr indicated second relapse. Chimerism analysis in PB and BM aspirates revealed a small autologous cell population of 4,12% and 2,11%, respectively. Finally, a third transplantation with unmanipulated BM from the same donor resulted in sustained remission with 100% donor hematopoiesis. The patient is in complete remission for more than five yr following the third SCT. Late graft failure or late graft rejection known to occur after transplantation of highly purified CD34+ cells, or even graft exhaustion caused by stromal dysfunction due to the underlying disease necessitated a third transplantation. Regardless of the cause of relapse, transplantation of unmanipulated BM instead of highly purified PBSCTs led to a permanent and stable engraftment in a third attempt after two previous PBSCTs. [source]


Retransplantation for late liver graft failure: Predictors of mortality

LIVER TRANSPLANTATION, Issue 2 2000
Marcelo Facciuto
As patient survival after orthotopic liver transplantation (OLT) improves, late complications, including late graft failure, more commonly occur and retransplantation (re-OLT) is required more often. Survival after re-OLT is poorer than after primary OLT, and given the organ shortage, it is essential that we optimize our use of scarce donor livers. We sought to identify variables that predict poor outcome after late re-OLT. Among adults who underwent OLT between September 1989 and October 1997, we identified transplant recipients who survived greater than 6 months (n = 964) and analyzed those who required late re-OLT (,6 months after primary OLT). We recorded the indication for the initial OLT and interval from OLT to re-OLT. We also analyzed data collected at the time of re-OLT, including age, sex, indications for primary OLT and re-OLT, United Network for Organ Sharing status, preoperative laboratory values (white blood cells, platelets, hemoglobin, albumin, bilirubin, creatinine, and prothrombin time), Child-Pugh-Turcotte score, number of rejection episodes before re-OLT, and interval between OLT and re-OLT. In addition, we analyzed surgical factors (including procedure performed and use of packed red blood cells, fresh frozen plasma, and platelets), postoperative immunosuppression, and donor factors (age, ischemic time). Forty-eight patients (5%) underwent late re-OLT at a median of 557 days (range, 195 to 2,559 days) post-OLT. Survival rates after re-OLT at 90 days, 1 year, and 5 years were 71%, 60%, and 42%, respectively. Patients surviving 90 days or greater after re-OLT had an 85% chance of surviving to 1 year. Sepsis was the leading cause of death (15 of 25 deaths; 60%). Recipient age older than 50 years (P = .04), preoperative creatinine level greater than 2 mg/dL (P = .004), and use of intraoperative blood products (packed red blood cells, P = .001; fresh frozen plasma, P = .002; platelets, P = .004) had significant impacts on survival. Late re-OLT was associated with increased mortality. Careful patient selection, with particular attention to recipient age and renal function, may help improve results and optimize our use of scarce donor livers. [source]


Etiology of Late Free Flap Failures Occurring After Hospital Discharge,

THE LARYNGOSCOPE, Issue 11 2007
Mark K. Wax MD
Abstract Objectives: Vascular compromise of free flaps most commonly occurs in the immediate postoperative period in association with failure of the microvascular anastomosis. Rarely do flaps fail in the late postoperative period. It is not well understood why free flaps can fail after 7 postoperative days. We undertook a case review series to assess possible causes of late free flap failure. Study Design: Retrospective review at two tertiary referral centers: Oregon Health Sciences University and University of Alabama at Birmingham. Methods: A review of 1,530 flaps performed in 1,592 patients between 1998 and 2006 were evaluated to identify late flap failure. Late flap failure was defined as failure occurring after postoperative day 7 or on follow-up visits after hospital discharge. A prospective database with the following variables was examined: age, medical comorbidities, postreconstructive complications (fistula or infection), hematoma, seroma, previous surgery, radiation therapy, intraoperative findings at the time of debridement, nutrition, and, possibly, etiologies. Results: A total of 13 patients with late graft failure were identified in this study population of 1,530 (less than 1%) flaps; 6 radial forearm fasciocutaneous flaps, 2 rectus abdominis myocutaneous flaps, 4 fibular flaps, and 1 latissimus dorsi myocutaneous flap underwent late failure. The time to necrosis was a median of 21 (range, 7,90) days. Etiology was believed to possibly be pressure on the pedicle in the postoperative period in four patients (no sign of local wound issues at the pedicle), infection (abscess formation) in three patients, and regrowth of residual tumor in six patients. Loss occurring within 1 month was more common in radial forearm flaps and was presented in the context of a normal appearing wound at the anastomotic site, as opposed to loss occurring after 1 month, which happened more commonly in fibula flaps secondary to recurrence. Conclusion: Although late free flap failure is rare, local factors such as infection and possibly pressure on the pedicle can be contributing factors. Patients presenting with late flap failure should be evaluated for residual tumor growth. [source]