Q.679. Give the D.D. of Post- T.x. infection?
KIDNEY TRANSPLANT
II. Infection
Q.679. Give the D.D. of Post- T.x. infection?
A. Post-T.x. infection:
I. 0-1 m.: Conven. nosocomial
infection:[HSV- Candida Albicans - onset of
(HBV/HCV)].
II. 1-6 m.: (Opportunestic”
non-conventional” infections):
·
Viral:[C.M.V.- E.B.V.- H.Z.V.(varicella zoster
v.)]: Antiviral: 3-6 m. & SMX/TMP 🠊 6-12
m.
·
Bacterial: [T.B.- Pneumonia- wound & catheter infection].
·
Fungal: [P.J. (Pneumocystis Jerovecii.)-
Cryptococcosis- Aspergillosis].
·
Parasitic: [Toxoplasmosis-Leishmania- Strongloidosis].
III. >6 m.: [CMV. Chorioretinitis & Colitis – P.K.
papilloma v.] 🠊 Risk 🠟gradually, ptn. either: (i)
Good allog. function🠊 No need for
more im/m. & rare opp-ortunistic infc..
(ii) Poor allog. function 🠊 Risky due to accumulative im/m. 🠊 So, Long-term Prox. é SMX/TMP. is warranted.
Q.680. What harm can CMV cause to the renal allograft? And what
harm can B.K.V
cause to the renal allograft?
A. CMV & renal allograft:
1) A.T.N.
2) Allog. dysfunction.
3) Decreased R. perfusion.
4) R.A.S. 👍
Other organs : [hepatitis-pneumonitis- chorioretinitis
(after 6 m)- meningeo-encephalitis-
oesphageal ulceration- colitis- G.I. bleeding]. (see also Q. Q.686).
B.K.V & the renal
allograft:
- ✌ :{Tubulointerstitial nephritis + ureteral stenosis. }.
Q.681. What
are the general💢 policies of organ donors
with HCV?
A.Due to high prevalence of HCV
among recipient of organs fr. anti-HCV +ve donors, several organ procurement
organizations hs a policy of testing all cadaver organ donors for
anti-HCV & restricting use of organs fr. anti-HCV +ve
donors to life-saving Tx.
(heart, liver, or lung). Similar
policies were recommended by U.S. Public Health Service Inter-Agency
Guidelines. A
complete moratorium on Tx. of organs fr. anti-HCV +ve donors into kidney recipient
may not be appropriate for the following:
1) Wide prevalence of liver dis. & HCV infc. after org.
Tx. fr. anti-HCV+ve donors
2) Abs.
of definitive evidence
of a detrimental effect on ptn. survival.
3) The
current shortage of cadaver
kidney.
4) The
constantly growing waiting
list for organ Tx.
Short-term data on outcomes é anti-HCV+ve recipient of
kidney from anti-HCV +ve donors as well as evid. tht mixed infection. (HCV infection é more thn one HCV-genotype) don’t adversely
affect
survival among ESRD ptn justify further study of strategy of
allocating kid. fr. anti-HCV +ve organ donors to anti-HCV +ve Tx candidates. A better
alternative seems to be a policy of Tx. Kidney from anti-HCV+ve donors to only HCV RNA+ve recipient, which’s consistent
é 2008
KDIGO guidelines. Preliminary data from
Tx. centers in Spain demonstrated no differences in liver dis. & ptn.
survival between HCV RNA +ve recipient of kidney from anti-HCV +ve
donors & anti-HCV +ve recip. of
kidney from anti-HCV-ve donors. Data from a survey include: 147 of 245 R.Tx. centers in U.S.
indicated tht: 49
% of these centers use HCV sero+ve
donors .
Q.682.What is the effect of pre-transplantation
anti-HCV status on post-transplantation clinical outcome?
A. Anti-HCV +ve ptns before Tx. have a
significant increase risk of post-Tx. liver dis.. CAH & its sequelae are
the principal forms of liver involvement. Also, unusual form of liver dis. é severe cholestasis & rapidly
progressive liver failure has been described in a few ptns. é HCV infection who undergo R.Tx.. This
condition, termed fibrosing cholestatic hepatitis, is ch.ch. by prominent
cholestasis & extensive fibrosis.
Overall, post-Tx. liver disease is an important clinical
problem since 11-49 % of
R.Tx. recip. are anti-HCV+ve. Studies from New England Organ Bank have shown that relative
risk of post-Tx. liver disease was 5.0 for recip. é anti-HCV prior to
Tx.. In add., a survey of rel. studies has revealed: post-Tx. liver dis. occ. in
19-64% of recipient é anti-HCV comp. to
only 1-30%
among recipient without anti-HCV .
R.Tx. in ptn.
previously infected é HCV is associated é incr. viral proliferation🠞1.8-30.3-fold increase in viral titer. An🠉viral titer, however, may not be
associated é increase risk of post-Tx. liver dis.. Among HCV RNA ptn,
titer of HCV RNA was no different among ptn.s with & without
postTx. liver dis.. Furthermore, post-Tx. viral load was similar in ptn.s
é mild hist. changes on liver biopsy or ch. changes, and
there ws no ass. between transaminase patterns & viral load level.
These data suggest: f. other thn viral load determine risk of liver dis.
among Tx. recipient é HCV infec..
Liver inj. progression of may be slower in ptn who undergo R.Tx.
as compared to those on waiting list. This was shown in retrospective analysis
of liver
biopsies obtained before & after R.Tx. among 31 HCV+ve ptn & comp. to
biopsies of 13 HCV-ptn who remained on waiting list . In general, ptns on
waiting list were more likely to have progression of liver fibrosis (62 vs 23
% among those who were Tx.). Although studies consistently show 🠉risk of post-tx. liver
dis. é anti-HCV +ve, conflicting results surround the
question: whether this’s associated é 🠟survival. 3
studies failed to detect significant differences in survival between recip. with & without anti-HCV
prior to Tx..
In contrast, several
studies hv shown “lower
survival” é pre-Tx. evid. of HCV infection : Data
fr. New England Organ Bank: recipient é preTx. anti-HCV hd a 3.3-fold higher risk of
death & a 9.9-fold higher risk of death due
to sepsis . A retrospective study from France evaluated 500
HBV-ve ptn é R.F. who underwent Tx.; survival & causes of death
post-Tx. were comp. among anti-HCV +ve & -ve ptn. : HCV infection was associated. é a significant 🠉in M.R..The🠉M.R. was principally due to liver
dis. & sepsis. To assess effects of HCV on outcomes
post-Tx., a 2005 meta-analysis ws performed: Hepatic cancer & cirrhosis were significant more
frequent causes of death é anti-HCV A.B.
Q.683. What
is the impact of HCV genotype on survival after R.Tx.?
A.
There’re limited data concerning the impact of
different HCV genotypes on survival after Tx. Data fr. New England
Organ Bank revealed: patient survival did not vary significantly with
genotype .
Q.684. What
is the effect of HCV infection upon survival with dialysis or
renal transplantation?
A. Despite pres. of anti-HCV A.B. at
time of R.Tx. may be ass. éincr. risk
of death, it’s not yet known whether survival incr. é RRT é DX. oré Tx. Some
studies suggest: R.Tx. 🠊better survival thn DX among anti-HCV +ve ptn.: A New England Organ Bank
study evaluated risk of death with or without anti-HCV A.B. in R.Tx. waiting
list & either did or didn’t receive R. allog. . Tx. was associated é. enhanced survival comp. to continued DX..Relative
risk of death was similar
between those with & without anti-HCV A.B.. Thus, Tx. resulted in a long-term
survival benefit é anti-HCV +ve. Similar findings were noted in another
rep. comp. survival among anti-HCV +ve ptn. who underwent R.Tx. é anti-HCV +ve individuals who were
acceptable for Tx. but hd not yet undergone the procedure. Outcomes were
assessed in ptns é
at least 2
y. of follow-up. Despite similar co-morbid C.P., ptns in whom R.Tx. hd bn
performed hd a lower
M.R. thn those remaining on DX.
So, the possible detrimental
effect of Tx. on the course of HCV infc. does not outweigh its long-term beneficial
effect on survival in ESRD. Thus, anti-HCV +ve status alone should not👆be considered C.I. for R.Tx. Liver damage (determined by hist. severity) is a strong predictor of liver
failure & death
after Tx..As a result, in anti-HCV +ve ptn. without evidence of
liver disease & in abs. of definite
studies demonstrating worse outcomes after R.TX., we suggest: such ptn. should be
allowed to make an informed
choice of staying on DX or undergoing Tx.. However, Tx. recip. can have
hist. evidenceof liver dis. in abs. of🠉s.
ALT.
So, there should be policy to perform liver
biopsies on all anti-HCV +ve ptns awaiting R.Tx. for histopth.
evaluation. In ptn. é histological evid. of liver dis., decision to proceed é R.Tx. shouldd be made
cautiously, since im/m.🠞🠉viral replication & exacerbate liver dis..
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