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ACUTE ALLOGRAFT REJECTION

Acute kidney allograft Rj is a fundamental cause of allograft dysfunction. Certain allografts cannot resume function even after maximal anti-Rj therap

Clinical features & diagnosis of acute renal allograft rejection

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o   List of abbreviations:

o   Rj: Rejection.

o   PRA: Panel reactive antibody,

o   HLA: human leukocyte antigen,

o   DGF: delayed graft function,

o   AKI: acute kidney injury,  

o   dd-cf DNA: Plasma donor-derived cell-free DNA,

o   TCMR: acute T cell-mediated (cellular) rejection.

o   ABM: antibody-mediated rejection,

o   CMV: cytomegalovirus,

o   im/m: immunosuppression,

o   DSAs: Donor specific antibodies,

o   ABOi: ABO-incompatible,

o   KTx: Kidney transplantation,

o   TR: Transplant recipients,

o   SCr: serum creatinine,

o   DD: differential diagnosis,

o   GN: Glomerulonephritis,

o   PTLD: posttransplant lymphoproliferative disease.  

o   IF/TA: interstitial fibrosis/tubular atrophy.

 

Acute kidney allograft Rj is a fundamental cause of allograft dysfunction. Certain allografts cannot resume function even after maximal anti-Rj therapy. Furthermore, in recovering TR, acute Rj episodes may reflected negatively on the long-term allograft survival.

 acute allograft rejection kidney acute allograft rejection diagnosis allograft acute rejection symptoms acute rejection allograft dysfunction acute graft rejection antibodies acute graft rejection signs and symptoms acute rejection and allograft loss what is graft rejection what causes graft rejection acute rejection graft definition acute renal allograft rejection guidelines acute renal transplant rejection pathophysiology acute graft rejection ultrasound treatment of acute renal allograft rejection with okt3 monoclonal antibody

Acute kidney allograft Rj can be defined as a sudden decline in allograft function that can be reflected as specific pathological alterations in the graft tissues. There are 2 major histological types of acute Rj, acute T cell-mediated (cellular) Rj (TCMR) and active ABMR. Both ABMR & acute TCMR may co-exist simultaneously in the allograft tissues. Moreover, subclinical Rj can be defined as the finding of histological evidence of acute Rj on biopsy specimen without associated rise in the SCr.

 

Risk factors triggering the evolution of acute Rj may include:

1)    DGF.

2)    HLA mismatching,

3)    paediatric TR,

4)    African American ethnicity,

5)    Pre-sensitization (i.e., finding of DSAs or elevated PRA),

6)    Incompatible blood grouping,

7)    Extended cold ischemic time, &

Furthermore, ptns with a previous attack of Rj, TR receiving a 2nd or more tx, and those nonadherent to his/her medications are at increasing risk for acute Rj. Acute Rj episodes are generally complicated with a decline in the long-term allograft longevity, despite not all Rj episodes exerting the same effect on the long-term allograft function. Considering the significant decline in the acute Rj incidence rates along the last decade, there has not been associated advantages in the long-term allograft longevity. Most attacks of acute Rj observed within the 1st 6 mo post Tx, with so many episodes seen early post-operative. Rj after 12 mo is typically attributed to non-compliance or aggressively reduced im/m. Most ptns having acute Rj episodes can be presented with no symptoms. However, occasional manifestations can be seen e.g., pyrexia, malaise, oliguria, and allograft pain and/or tenderness. HT is also a commonly seen finding.