CKD after non-renal SOT is commonly observed. Almost 15 % of these ptns ultimately develop stage 4/5 CKD post-Tx.
Kidney function in non-kidney solid organ transplantation
Abbreviations:
o
CKD: Chronic kidney
disease.
o
ESRD: end-stage
renal disease.
o
CNI: Calcineurin
inhibitor.
o
Post-tx: post-transplantation.
o
AKI: Acute kidney
injury.
o
SOT: Solid organ
transplantation.
o
US: Ultrasonography.
o
KTx: kidney
transplantation.
o
TR: transplant recipients.
o
OPTN: Organ
Procurement and Transplant Network.
o
SRTR: Scientific
Registry of Transplant Recipients.
o
im/m: immunosuppression.
o
TORi: Target of
rapamycin inhibitors.
o
CyA: Cyclosporine.
o
MMF: Mycophenolate mofetil.
o
Tac: Tacrolimus.
o
SRL: Sirolimus.
o
Pred: Prednisone.
o
VC: vasoconstriction.
CKD after non-renal SOT is commonly observed. Almost 15 % of these ptns
ultimately develop stage 4/5 CKD post-Tx.
Pre-operative assessment of renal function in
non-renal SOT candidate should include
the possibility of reversal and the chance of development of ESRD. This assessment of kidney function starts
with a full-detailed history with thorough physical examination, an accurate testing
of renal profile, complete urine analysis, and renal imaging (US). Despite that kidney biopsy may be occasionally
indicated, there’s no evidence that tissue biopsy is more predictive of post-Tx
kidney survival than SCr alone. Further approaches
are currently depending upon the associated clinical progress and the specific
non-renal solid organ deterioration. CNI therapy has been included as a crucial cause of
post-Tx CKD in non-renal solid organ TR.
The augmented risk of CKD in this cohort has been also observed with:
o
Pre-Tx AKI,
o
Higher age at Tx,
o
Female gender,
o
pre-Tx HT
& DM,
o
African-American ethnicity,
o
HCV infection
o
Type of Tx organ,
o
surgical approach.
The reported incidence of ESRD necessitating
some type of RRT in non-renal SOT was as follows:
o
3-10 % in liver TR,
o
0-20 % in heart TR,
o
5-15 % in lung TR, &
o
3 % in heart/lung
TR.
There’re scanty data about islet cell &
intestinal Tx.
Alleviation of the risk of nephrotoxicity incidence post-Tx should focus on the modification of the
possible risk factors that are commonly observed with all risky ptns to CKD and
those entirely related to the Tx subset. In
non-renal SOT
TR with advanced CKD considered
healthy enough for receiving a subsequent KTx,
the risk of death or exclusion from waiting list while awaiting a donated graft
is highly increased. A suggested recommendation is the timely referral of
potential candidates for KTx, early consideration
of live-donor KTx, and a lower threshold including
of non-standard-criteria deceased-donor kidney allograft.
Choice
of CNI & CNI sparing regimen:
The choice of im/m
protocol, including CNI, is usually
tailored by the primary Tx clinicians and is
usually relying upon the assessment of efficacy and the potential toxicity. CyA-induced nephrotoxicity
can be alleviated by dose declining coupled with adding MMF, leading to better long-term kidney function.
From the kidney function point of view, there’re single-center case series,
registry analyses, and multicenter reports showing the benefit of Tac over CyA
in both converting and de novo settings in heart as well as liver TR. Tac seems
to induce less renal VC as
compared to CyA that may partially
explaining the typical, short-term decline in SCr seen
with conversion from CyA. In agree
with this notice, vast majority of non-kidney organ TR
in the US receive an im/m protocol comprising Tac, MMF,
& Pred
at timing of Tx. Revising the annual registry
of the OPTN & SRTR, most of TR are
remaining on a Tac-based protocol at the
1st y. post-Tx.
A commonly applied strategy in the non-renal
organ TR involving
administration of regimens that reducing, delay, or excluding CNI. TORi,
SRL &
everolimus,
particular, can be administrated in this setting. In certain non-renal organ TR, withdrawal/minimizing of CNI has
been resulting a mild improvement in renal profile, that is usually coming at
the expense of a decline in im/m efficacy
and worse ptn survival. TORi should
also be discouraged in ptns with eGFR
<40 or proteinuria as
this will induce more progression of renal dysfunction. Furthermore, TORi also have significant untoward effects
that limiting their administration. Generally, the results of the many reports have
been variable. There’re no available data concerning co-stimulation blockade
for renal-sparing in non-kidney organ
TR. Eventually, choice of an im/m. protocol has to be individualized from
one ptn to the other so that optimizing the total risk-to- benefit ratios.
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