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KIDNEY TRANSPLANT

Q. 716. What are other types of rejection?


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.

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

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.


 KIDNEY TRANSPLANT

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Acute Vascular rejection

Q. 716. What are other types of rejection?    

A. Other types include:  👌

v Hyperacute Rj. 🠊Occur due to presence of “preformed recipient A.B.” reacting é endothelial surface of allograft, mainly occur é recurrent blood TX & pregnancy.

v Accelerated Ac. Rj. 🠊2-5 d. (us. Humoral immune).

v Ac. CNI. toxicity (Csp.&Tcrol.)🠊Afferent G. V.C.🠊Ac. Reversible decrease é GFR.

Q. 717. What is the difference between AMR/AHR & ACR? What is the difference in treatment?

A.AMR/AHR (Ac. A.B. mediated Rj. /Ac. humoral Rj.)🠊[🠝3 d.- Donor reactive A.B.- Neutrophil polymorph in G. & peri-tub. Cpll.- C4 st. é peritub. cpll.- No tubulitis.]     

*   While ACR (Ac. cell. Rj.)🠊[🠝 5 d.+ tubulitis لازم ] + Abs. of :

1)   Donor reactive A.B.

2)   C4 d. st. é peritub. Cpll.

3)   Neutrophil polymorph é G. & peritubuer. cpll.

A.  While ttt. of  ACR 🠊[Steroids] mainly, AMR/AHR ttt. é 🠊[ Pph.+ Steroids+ I.G.]  is mandatory.  

Q. 718. How can CNI.s be toxic? How to treat?

A.  Ac. CNI.s🠊Affer. G.V.C🠊Pre-renal Reversible 🠋GFR & 🠝 s. Cr..                                                                      It’s us. dose-dependent & Responds to dose reduction. 

Q. 719. So, How can you differentiate between Ac. CNI.s & Ac. Rj.?

A.   …..     Both can Co-exist ! ولكن  !  ,

But:  Pointers to Ac. CNI.s🠊  👌

1)   Sn. of extra-renal toxicity.  e.g.  severe tremors.  

2)   Moderate rise in s.Cr.<25 % over baseline.

3)   High trough level of Csp> 350 ng/ml & Tacro>15 ng/ml.

***  While, in Ac. Rj. 🠊    

 1. Low drug level, e.g.< 150 ng/ml.

 2. Rapid Non-Plateau rise in s. Cr.

Q.720.Then, how to consider a final decision in this problem? ž👆

A.   Renal Biopsy, esp. in a high risk ptn. i.e.:  👌

1)   Previous graft rejection.             

2)   Highly sensitized ptn. (blood. T.X. & pregnancy).                         

3)   High risk of early recurrence of the Iry disease e.g. FSGS.

Q.721. How to D.D. ACR. (Ac. cellular Rj.) from Ac. allergic interstitial nephritis?

A. Both have.:🠊{1. Eosinophilia.   2. Mononuclear cell infiltration. }, but,

- Ac. allergic interstitial nephritis 🠊[fever + Rash.] after ingestion of a new drug.

-While, ACR.🠊Endothelialitis.(Polyoma virus) should be considered in D.D.

Q.722. What is late acute rejection? Mention the accused factors?

A. Late Ac. Rj. = Rj. >6 m., post Tx.

Etiology: Like early acute Rj.: [Shock, ACEI, UT. Ob. & NSAID. ].

Q.723. What is new in ABO desensitization programs in renal transplantation?

A. Poor outcomes combined é improvement in results using DDA limited ABOI T.x. in U.S. in the past. However, an extreme lack of available deceased donor encouraged investigation é Dsz for ABOI/LDA in Japan🠊successful long-term  results combined é subsequent successful short-term results fr. U.S. have renewed interest in this procedure.

-[Pph, immunoadsorption, IVIG., rabbit ATG, anti-IL-2 receptor A.B.- splenectomy, anti-CD20 (Rituximab)]or a combination therapy, all  have been tried, but it’s unclear which strategy is more effective or cost effective. While a variety of protocols seem to be effective in allowing successful T.x. across blood group barrier, much work remains to determine the optimal protocols.

Q.724. As regard HLA sensitization (Ssz) what are the types & importance of anti-HLA antibodies?

A. ESRD ptn. tht are sensitized to HLA Ag via bld products, pregnancy, or prior T.x. us. hs A.B. directed agnst deceased donor & potential living donor kid. Assays that define Ssz detect 🠊A.B. agnst broad spectrum of potential donors, while crossmatch (Crossm) identifies 🠊A.B. agnst a specific donor. Depending upon assay, different types of A.B. & their clinical relevance can be identified. Ig.G vs.M: Ig.G A.B. detected by Ssz or crossm are considered to reflect true Ssz agnst HLA Ag., while IgM are Not considered typical response.

T vs. B cell: A.B. detected agnst T cells have been considered to represent true anti-HLA Ssz agst class I. Ag. By comparison, T cell -ve, B cell +ve crossm results have been considered to represent HLA class II A.B. of less significance.   C. fixing vs non fixing: A.B. tht must fix C. to produce a +ve assay are considered cytotoxic & of clinical importance. A.B. detected by means independent of C. fixation, e.g. flow cytometry, may detect other A.B. that may not be cytotoxic & of unclear clinical significance. While data suggest: +ve flow crossm is associated é 🠝risk of Rj. & 🠟graft survival, +ve predictive value of this assay is likely dependent upon whether or not donor A.B. are present and, if so, whether A.B. is able to fix C.  Most assays detect pres. of A.B. but not the precise HLA specificity. Assays to identify sp. HLA Ag. targeted require more time to perform & can only be undertaken in settings such as LDA, when time constraints are not an issue. T.x. shd Not 👆proceed é evid. of +ve crossm 2ndry to cytotoxic IgG anti-HLA AB.

Q.725. What are the desensitization protocols (Dsz) available?

A. Two protocols are used to desensitize potential recip. é preformed HLA A.B.:

Dsz cn be used for a potential recipient of a LDA é defined HLA/DSA against donor to🠋specific A.B.. It can also be used for an individual on the DDA waiting list broadly sensitized to HLA Ag. (PRA30%) é repeated +ve crossm. One method uses high dose IVIG & the other uses low dose IVIG & Pph in a protocol identical to that described for ABOI Tx.. Monitoring for AMR post-Tx. consists of: 👌

*      (1) Lab. Evaluation.

*      (2) Monitoring DSA titers.            

*      (3) Protocol biopsies.

I. High dose” IVIG (HiiV): Adv. incl.:{ability to desensitize ptn on DDA waiting list & potential LDA recip.. It’s much less resource intense & less expensive thn low dose IVIG. Ptn on HDX. cn receive monthly IVIG while undergoing Dx. ttt.}.

Disadv. incl.:[lack of experience in either ABOI or é high titer HLA DSA. Crossm monitoring & monitoring of post-Tx. DSAs for 3 w. is limited to the less sensitive NIH-CDC assay 2ndry to interfere of high d. IVIG é other more sensitive assays]. Using less sensitive NIH-CDC for crossm screening rather more sensitive 👉AHG- assay, one could infer tht recipient in HiiV will be more sensitized (false –ve crossm) & thus at higher risk of Rj. comp. to low dose IVIG, using AHG assay. HiiV” S.E.:🠊[hd, fever, msc. pain, S.O.B. & chest discomfort ]. ttt.: by using products é osmolality mimicking tht of plasma. Giving iso-osmolar IVIG dur. DX allows for simultaneous correction of vol. issues. Keeping individual guidelines for rate of infusion shd be foll. to 🠋 complications of high osmotic load, wch. cn be avoided by using 👉[Non-sucrose based, isoosmolar product].

II. Low dose IVIG (Lodiv): Adv.:[documented use é high titer anti-HLA A.B. é Dsz & successful Tx. é DSA titers of up to 1:256]. Although high titer DSA can respond to Lodiv, numerous preTx. sessions us. required to get🠊adequate low titer+ numerous post-Tx. sessions to limit rise of DSA titers 🠋AMR. As é ABOI protocol, No. of preTx. Pph sessions usually estimated based on initial A.B. titer. Using Lodiv, the more sensitive AHG crossm cn be used prior Tx., which help detect pres. of preformed A.B. missed using NIH assay. After Tx., it’s possible to follow crossm & DSA by several assays, rather thn only by NIH assay.


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