allograft dysfunction

allograft dysfunction

Persistent suboptimal function of an organ system after transplantation (e.g., kidney, liver, lung), which is conceptually related to problems with vascular supply and urinary flow, as well as medical or immune related issues.
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The paradox is that these organs from extended criteria donors, are most susceptible to the consequences of preservation related injury (early allograft dysfunction, primary non-function, acute rejection) and thus, impacting negatively the post-operative outcomes after transplantation and the quality of life of the patients.
Reviews have suggested that the development of alloantibodies and polyomavirus (BKV)--related allograft dysfunction are important mechanisms of late-onset graft loss (6, 7).
The current core networks (sub-thematic areas) are interstitial lung diseases, cystic fibrosis, pulmonary hypertension, primary ciliary dyskinesia, non-CF bronchiectasis, alpha1-antitrypsin deficiency, mesothelioma, chronic lung allograft dysfunction, and other rare lung diseases.
Furthermore, acute kidney injury is a frequent complication of LDLT patients and is a significant risk factor of increased early- and late-term mortality.[5] In addition, postoperative allograft dysfunction, postreperfusion syndrome, intra-abdominal or gastrointestinal bleeding, pulmonary or infectious complications, sepsis, biliary tract complications including biliary stenosis or leakage, major vascular complications including isolated or combined hepatic artery, portal vein and hepatic vein thrombosis or stenosis, and multiple-organ failure, are the independent risk factors of increased early- and late-term mortality after LDLT.
Histological examination of allograft tissue remains the gold standard for the diagnosis of allograft dysfunction (3).
(16) assessed miRNA expressions related to chronic allograft dysfunction in urine samples in parallel to allograft tissues.
In addition to protocol biopsies, 24 out of 41 patients underwent for-cause biopsies for allograft dysfunction at some point during the 5 years of follow-up.
Chronic tacrolimus toxicity was defined as histologic evidence of CNI toxicity (IF/TA and arteriolar hyalinosis by Banff classification) and worsening allograft dysfunction [9, 10].
He underwent workup for allograft dysfunction, which included a normal renal transplant ultrasound; negative testing for DSA, BK virus, and CMV; review of blood tacrolimus levels; and maintenance of blood pressure control.
The elevation of bilirubin level on posttransplantation day 4 could not be explained with inadequate size of the graft liver but rather was a presentation of early allograft dysfunction (EAD) [12].
Even though macrovesicular steatosis is a recognized risk factor for primary nonfunction and early allograft dysfunction (EAD) [14-21], the extent of the postoperative impairment remains disputed.
(31) The proposed staging of clinical AMR (allograft dysfunction, defined as "alterations in pulmonary physiology, gas exchange properties, radiologic features, or deteriorating functional performance," which may be asymptomatic) is summarized in Table 4.