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Pancreas-kidney transplantation

Almost 3/4th of pancreatic Tx in the US are proceeded as a SPK Tx, with the observed remainder reported as either sequential PAK or PTA

 

Pancreas-kidney transplantation in DM: Pancreatic allograft rejection

 



Abbreviations:

 

o   AB: antibodies.

o   Ac Rj: acute rejection.

o   ACR: acute cellular rejection.

o   AMR: antibody-mediated rejection.

o   CyA: Cyclosporine.

o   DCD: deceased-donor.

o   GC: Glucocorticoids.

o   im/m: Immunosuppression.

o   IVIG: immune globulin.

o   KTx: kidney transplant.

o   PAK: pancreas after kidney.

o   Prd: Prednisone.

o   PTA: pancreas transplants alone. 

o   PE: plasmapheresis.

o   rATG: rabbit Antithymocyte globulin.

o   Rtx: Rituximab.

o   SAB: single-antigen bead.

o   Sms: Symptoms.

o   SPK: simultaneous pancreas-kidney.

o   Tac:  Tacrolimus 

o   TR: transplant recipient.

o   TR: Transplant recipients

o   FBS: fasting plasma glucose.

o   Tx: transplantation.

o   US: Ultrasound.

o   DCAL: death-censored allograft loss.

 

Almost 3/4th of pancreatic Tx in the US are proceeded as a SPK Tx, with the observed remainder reported as either sequential PAK or PTA. Pancreatic  allograft Rj remains a crucial clinical challenge and is the primary cause of pancreatic DCAL after 3 mo post-Tx. Ptns with pancreas allograft Rj are mostly asymptomatic, despite some ptns present with mild allograft tenderness and/or fever. Other less commonly clinical manifestations of Ac Rj may include painful abdomen, distension (typically induced by ileus), or a bowel functional alterations. Lastly, the primary tools of monitoring ptns with allograft Rj is lab testing.  

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Pancreatic allograft Rj should be suspected with either the aforementioned clinical criteria or with lab study alterations (raised s. lipase and/or amylase levels). The subsequent approach can be followed:

o   PAK or PTA seen with abdominal Sms or presenting within 6 weeks post-Tx, > abdominopelvic US+CT imaging with oral contrast to assess postsurgical sequelae & intra-abdominal infections. If either pancreatic US or CT imaging show an intra-abdominal abnormality explaining the rise in pancreatic enzymes, then > appropriate antibiotics + follow up s. lipase & amylase. Ptns may need pancreatic graft biopsy with lack of lipase and/or amylase lowering.  

o   PAK or PTA with no intra-abdominal alterations on either US or CT images, or ptns presenting without abdominal Sms and presenting > 6 weeks post-Tx, recommended approach rely primarily on blood Tac (or CyA) levels:

1)    If Tac (or CyA) level is above the therapeutic range > reduce im/m & monitor Tac (or CyA) level until returned to an accepted range. If lipase/amylase normalizes with the im/m decline, pancreas allograft Rj is unlikely, and enzymatic rise can be attributed to Tac (or CyA) toxicity at supra-therapeutic range. Otherwise, pancreatic allograft biopsy should be proceeded.

2)    If Tac (or CyA) levels are within or below the therapeutic level, proceed to > pancreatic allograft biopsy.

SPK Tx presenting with a new rise in s. lipase and/or amylase and a new rise in SCr > renal biopsy to diagnose possible combined kidney/pancreas graft Rj. If kidney allograft biopsy showed > Ac Rj in SPK TR, we treat for Ac Rj without the need for pancreatic biopsy.  

The gold standard for Dgx of pancreatic Rj is > pancreas biopsy that is the only accurate tool for grading Rj intensity & DD between ACR, AMR, and other causes of graft inflammation & injury. Generally, we ttt most ptns with Ac Rj on biopsy irrespective to injurious chronicity or magnitude of graft dysfunction. However, with abnormal graft function (e.g., raised FBS, lowered C-peptide, or HB A1c >7 %) and histologically reduced pancreatic islets, some clinicans would not treat for Ac Rj. Therapy for Ac Rj relied primarily upon the type & intensity of Rj on biopsy:

1)    ACR therapy according to magnitude of inflammation per Banff classification:

o   Borderline ACR: augment maintenance im/m for the coming 2-3 mo + pulse IV GC, followed by tapered oral Prd.  

o   ACR grade I, II, or III > rATG-TG > methylprednisolone as pre-medication prior to the 1st 2-3 doses of rATG-TG, followed by a tapered oral Prd. Do not give high-dose pulse GC with rATG-TG. Augment also maintenance im/m.  

2)    AMR: 3-5 sessions PE followed by VIG, add also anti-B cell e.g., Rtx Plus augmented maintenance im/m.  

3)    Mixed AMR/ACR: rATG-TG + 3 sessions PE & IVIG, followed by low dose Rtx.  

In case of difficult pancreas biopsy, decision for empirical therapy of Rj is usually relying on a case-by-case consideration. Empirical therapy for ACR can be considered if the likelihood of Ac Rj is high. Moreover, we can treat AMR with detected de novo DSAs or rising DSA as compared to pret-Tx level in the setting of allograft malfunction.

 

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