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COMPLICATIONS OF PEDIATRIC RENAL TRANSPLANTATION

Recent progress in im/m therapy and the post-Tx management have led to improving both graft and recipient survivalin pediatric kidney transplantation.

 

COMPLICATIONS OF PEDIATRIC RENAL TRANSPLANTATION

 

Abbreviations:

o   Ac Rj: acute rejection

o   ACR:  Acute cellular rejection

o   AKI: acute kidney injury

o   AMR: acute antibody-mediated

o   CNI: Calcineurin inhibitor

o   CIN: Calcineurin inhibitor nephrotoxicity

o   CAI: Chronic allograft injury

o   Csp: Cyclosporine.

o   CVS: cardiovascular disease.

o   DM: diabetes mellitus

o   DGF: delayed graft function

o   FSGS: focal segmental glomerulosclerosis.

o   aHUS: atypical hemolytic uremic syndrome

o   HT: hypertension,

o   im/m: immunosuppressive.

o   KTx: Kidney transplantation.

o   MPGN: membranoproliferative glomerulonephritis.

o   SCr: serum creatinine

o   Tac: Tacrolimus

o   TR: transplant recipients.

o   Tx: transplantation

o   PNp: pyelonephritis

 

Recent progress in im/m therapy and the post-Tx management have led to improving both graft and ptn survival in pediatric KTx TR. However, long-term benefits have been limited by the sequelae related to im/m, rejection, and recurrence of the original kidney disease. Several complications of KTx appear as graft dysfunction. Etiology of kidney graft dysfunction will be varied with the timing after Tx. The timing periods can be categorized as:

o   immediate (0-one week post-operative),

o   Early (1-12 weeks post-operative),

o   Late acute (after 3 mo), & late chronic (years).  

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Etiology of DGF (immediate renal failure that persists after Tx) include:

o   Post-ischemic AKI, thrombosed renal artery/vein,

o   Urologic sequelae (i.e., urine leak or obstructive uropathy) &

o   Hyperacute Rj, rare.

Ptns with initial graft function who develop early kidney insufficiency (i.e., 1-12 weeks post-Tx), the major causes of graft dysfunction include:

o   Ac graft Rj,

o   Ac Rj toxicity,

o   Obstructive uropathy

o   Infectious episodes,

o   Fluid deprivation and hypovolemia, &

o   Recurrence of the native disease.

Kidney allograft dysfunction acutely observed > 3 mo after Tx is mostly due to:

o   Ac allograft Rj,

o   CNI toxicity,

o   Obstructive uropathy

o   Hypovolemic states, PNp, &

o   Recurrence/de novo native renal disease.

Slowly progressing renal diseases that observed over years post- KTx most commonly induced by:

o   Viral infection,

o   Chronic allograft injury,

o   CNI nephrotoxicity,

o   HT nephrosclerotic kidney disease, &

o   Recurrent or de novo renal disease.

Etiology of DGF that seen after KTx may include:

o   Hyperacute Rj.  

o   Post-ischemic AKI,

o   Renal artery/vein thrombosis,

o   Urinary leakage or obstructive uropathy,

 

o   Etiology of graft dysfunction from 1 to 12 weeks post- KTx include:

1.    CIN,

2.    Ac Rj,

3.    Obstructive uropathy

4.    Infectious episodes,

5.    Hypovolemic states, &

6.    Recurrence of the original disease.

o   Causes of graft dysfunction that develop acutely > 3 mo after Tx include:

1.    Ac Rj,

2.    CIN,

3.    urinary obstruction,

4.    hypovolemia, &

5.    Recurrent and de novo kidney disease.

o   Causes of allograft dysfunction that slowly developed over years include:

1.    CAI

2.    CIN,

3.    HT nephrosclerotic kidney disease,

4.    Viral infection, &

5.    Recurrent or de novo renal disease.

pediatric renal transplantation an overview and update pediatric renal transplantation pdf paediatric renal transplantation guidelines pediatric renal transplant protocol pediatric renal transplant rejection

Ac Rj can be expected with an acute rise in the SCr level and can be confirmed histologically via allograft biopsy with the finding of AMR & ACR. So, SCr should be regularly monitored for the early diagnosis of Ac Rj.  

Despite that CAI (chronic allograft injury) is the most commonly observed etiology of graft loss after the 1st y after Tx, its underlying background still uncertain. The diagnosis can be expected via:

o   Slowly elevated SCr,

o   Rising proteinuria, &

o   Worsened HT.  

CNI (Csp & Tac) nephrotoxicity can be seen acutely that is highly reversible after dose modification, or may be progressing to CKD that is usually irreversible.  

In pediatrics KTx, recurrent native kidney diseases inducing allograft loss can be observed in 5-15 % of ptns. Primary pediatric native kidney disease with a high rate of recurrence rate in the kidney allograft may include:

o   FSGS,

o   MPGN,

o   Primary hyperoxaluria

o   Genetic types of aHUS.  

Other complications that can be observed with pediatric kidney TR may include HT, CVS disease, infection, cancer, DM, anemia, and surgical sequelae (e.g., urological and vascular sequelae). These can be contributing to allograft injury/dysfunction.

pediatric renal transplantation an overview and update pediatric renal transplantation pdf paediatric renal transplantation guidelines pediatric renal transplant protocol pediatric renal transplant rejection


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Recent progress in im/m therapy and the post-Tx management have led to improving both graft and recipient survivalin pediatric kidney transplantation.
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