Q.709. DescrIbe the “Banff ✽ System”?
Solid-organ transplant (SOT) TR are immunocompromised and may be at higher risk for severe COVID-19 disease as compared to general population. Two large observational studies of SOT recipients with COVID-19, about 80-90 % of ptns required hospitalization; of those, nearly 40 % required intensive care & 30 % required mechanical ventilation. At one month, mortality (MR) exceeds > 20 %. These findings suggest: TR are at a higher risk for poor outcomes, multivariate analyses in both studies reported that age & chronic co-morbidities were the primary drivers of MR rather than immunosuppression.
KIDNEY TRANSPLANT
Acute cellular rejection
﴿﴿IV.Rejection﴾﴾
Q.709. Describe the “Banff ✽ System”?
1. Normal : A histologically normal
biopsy.
2. A.B.-med.: docum. of circul.
antidonor A.B. & C4d or allog. pathology.
* Ac.
A.B.-med. Rj.:
Type I: ATN.-like
histology (C4d+ve) é minimal inflmm.
Type II: Cpll.-glomerulitis é margination and/or thromboses (C4d+ ve).
Type III:
Arterial-transmural inflmm./fibrinoid ch. (C4d+ ve).
* Ch. active A.B.-med. Rj.:Hist.: G. double counters
and/or multilayering of peri-tub. cpll. B.M. and/or IFTA or fibrous &
intimal thicken. in arteries, (C4d +ve).
3. Borderline: Susp. for Ac. T cell-med. Rj. (tubulitis foci é no intimal
arteritis ).
4. T-cell med. Rj.:
* Ac. T cell med. Rj.:
Type IA: Signif. interstitial inflmm. (>25 % of parench. & foci moderate tubulitis).
Type IB : Signif. interstitial inflmm. (>25 % of parench. & sev. tubulitis).
Type IIA:
Mild/moderate arteritis.
Type IIB : Sev. arteritis, wch’s ass. é >25 % loss of luminal area.
Type III : Transmural arteritis and/or arterial fibrinoid alter. & necrosis of medial s.m. cells occ. in ass. é lymphocytic inflmm. of the vessel .
* Ch. active T-cell-med. Rj.= ch. arteriolopathy: [Arterial intimal fibrosis + mononuclear cell infilt + fibrosis + form. of neo-intima].
5. Interst.
fibrosis & tub. atrophy, without any sp. etiology = CAN.:
I. Mild interst. fibrosis & tub. atrophy (<25 % of
cortical area).
II. Moderate interst. fibrosis & tub. atrophy (25-50 % of
cortical area).
III. Sev. interst. fibrosis & tub.
atrophy (>50 % of
cortical area).
6. Others: Not due: Ac. and/or
ch. Rj: e.g.[Ch.
H.T., CNI.s toxicity & viral infc.].
Q.710. How can you diagnose acute renal allograft rejection? 👉
A. Incidence of Ac. R.
allograft Rj. (U.S.R.
Data System)= 10
%. It’s
us. present
é Ac. rise in s. Cr., sugg. underlying R. allg. dysfunction. &
us. aSm.tic. Monitoring for Ac. rj. relies principally
upon repeated measurement of s. cr.. Monitoring schedule varies by Tx. centers. Ac. Rj.
is def. as {Ac. deterioration in allg. function determined by raised s. Cr.,
ass. é sp. path.
changes in graft biopsy}.
The two principal histologic forms of Rj.: Ac. cellular Rj. & Ac. A.B.-mediated Rj..
Banff system
provides diagnostic categories for path. Rj. criteria (see Q. 44).
Ac. R. allograft Rj. must be distinguished fr. other causes of Ac. rise in
s. Cr. and/or similar
histologic findings on R. biopsy.
Subclinical Rj.:={histologic evidence of Ac. Rj. but without
rise in s. cr.}. Natural history of subclinical Rj. is unclear.
Although the data are not clear, clinical biopsies in high
risk ptn. shd be performed for Ac. rejection.
Q.711.What is the D.D. of renal allograft dysfunction?
A. Causes vary é time post T.x. & periods classified into four stages:
I. Immediate
(0-1 w.
post-surgery).
II. Early (1- 12 w. post s.).
III. Late acute (> 3 m.).
IV. Late chronic (y.s).
The best approach is to consider: [pre-renal, postrenal & intrinsic renal].
R.F. persisting after T.x., called delayed graft function
(DGF). The
principal underlying causes of kidney allog. dysfunction immediately
after T.x. incl.: [Post-isch. ATN.,
vol. depletion, thrombosis of R. a. or v. & postrenal
causes ].
Ptn. é initial graft function dev.
R.I. (1-12 w. post-T.x.), major
causes🠞 CNI toxicity, Ac. allog. Rj., urinary obstruction,
infc., hypovolemia & recurrent dis]. Ac. allograft dysfunction development>3 m. after T.x. is most
commonly due to: [CNI toxicity, Ac. allog. Rj., urinary obstruction, vol. depletion, recurrent
dis. & de novo R. disease.].
Slowly progressive R. disease occur
over years after R.Tx. (often é persistent
Prot.) most commonly results fr. [CAN (ch. allog. Np.), CNI nephrotoxicity, H.T.
nephron-sclerosis, viral infections & recurrent or de novo
renal disease].
Q.712. Describe different situations in
the early post-Tx. period?
A. “Allograft
function” may be:
Excellent : é Good
urine output + Rapid fall in s. Cr. 😃✓
SGF: s. cr. > 3 mg/dl é No need for DX. 😑
DGF: failure to function immediately + need
for DX. é 1st week. 😌
Q.713.What are the risk factors of DGF? What are the possible causes inducing DGF?👉
A. Risk
f. for DGF 🠞{Deceased donor- old age-
incr. cold/warm isch. time + Recipient f. [old
age- incr. H.DX. period – greater HLA mis-matching-Higher P.R.A. (Panel Reactive Ag.).]}.
A. Causes of DGF:
i.
Pre-renal 🠞[Hypovolemia
– Hypotension- R.V.T.].
ii.
Post-renal 🠞U.T. obstruction.
iii.
Renal 🠞[Isch. ATN. (most common)-HyperAc. Rj.- accelerated Ac.
on top of ATN- CNIs toxicity.].
N.B.
[MMF. &
Tcrol.] 🠞Drr.🠞Hypovolemia 🠞Early
post-TX . graft dysfunction.
Q.714.What causes ischemic damage to deceased
donated kidney?
A. [Shock syndrome-Toxic drugs- Brain surgery- Trauma
renal vessels - Prolonged storage (cold time)-Pulsatile perfusion injury] +
+ Recipient factors (🠉warm time & trauma renal
vessels).
Q. 715. How to ameliorate DGF? How to treat?
A. To ameliorate DGF: 👉
1) Adjust “hemodynamic” status.
2) Meticulate “surgical“ procedures.
3) Rapid transport of the harvest graft.
4) Optimum preservation solution.
A. ttt.: “Biopsy”
within 3-5 d.🠞Rejection: R ✎
1)
Mild/mod.
cellular 🠞Pulse Steroids.
2)
Severe cellular🠞Pulse & or OKT3/ thymoglobulin.
3) Ac. A.B.-mediated 🠞[Pulse + Pph + MMF +Tacrolimus ].
“Intra-operative Thymoglobulin”🠞Shorter duration
of DGF/evid. based.
COMMENTS