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KIDNEY TRANSPLANT

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.

v Leeaphorn N, Thongprayoon C, Chon WJ, et al. Outcomes of kidney retransplantation after graft loss as a result of BK virus nephropathy in the era of newer immunosuppressant agents. Am J Transplant 2020; 20: 1334.   

v Kates OS, Haydel BM, Florman SS, et al. COVID-19 in solid organ transplant: A multi-center cohort study. Clin Infect Dis 2020.

                                   

                                     

 

KIDNEY TRANSPLANT

Acute cellular rejection 

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 ﴿﴿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.


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