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Complications of Transplantation

COVID-19 and solid organ transplant (SOT).

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COVID-19 poses new challenges for individual SOT candidates & transplant recipients (TR), as well as the process of SOT. There’s currently a theoretical risk of transmitting SARS-CoV-2 (virus responsible of COVID-19) from an organ donor to TR based upon detection of viral RNA particles in organs that can be transplanted (eg, lung, heart, kidney, intestine), despite donor-derived infection has not been observed to date. Owing to this risk with possibility of transmitting SARS-CoV-2 to health care providers, all solid organ donor and TR should be screened for COVID-19 by history, chest imaging & microbiologic testing. Post-tx, SOT recipients may be at increased risk for acquisition of COVID-19 as they’re immunocompromised (im/m) and have frequent contact with health care system, although this link has not been studied. Clinical pivture of COVID-19 in SOT recipients are variable and similar to that seen in non-im/m ptns. However, fever appears to be less common. Whether disease course is more severe is not known.  


﴾﴾ V. Complications of Transplantation.  ﴿﴿

Q.739. How to evaluate anemia in a renal transplant recipient?

A. Anemia: a common finding before & after R.Tx. It’s most often rel. to: [iron def., graft Rj or dysfunction, Epo deficiency, viral infection, im/m. & infc. Prox.] Evaluation of anemic R.Tx recip. incl.: assessment for causes of anemia shared é non-Tx. ptn. & for more sp. causes tht may be unique to R.Tx.. To exclude  non-renal causes of anemia , evaluation shd incl.:[RBCs indices, Retics., s. iron, TIBC ,% TSAT, s. ferritin & bld in stool]. However, inflmm.Øêê TSAT & incr. ferritin, obscuring diagnostic utility of these tests. Initial assessment shd incl. a review of potential causative medications & P.H. of bld loss/hemolysis. Prior to ESA thpy, ensure ironrepletion: F{s. ferritin> 200 ng/mL & TSAT >20 %}. If ptn. is iron deficient, give i.v. iron. Because of lower expense & ability to give larger dose, we cn use INFeD brand of iron dextran as iron infusion of choice. We prefer not to use Dexferrum brand of iron dextran (higher m.w.) due to a higher incid. of adverse effects.  We us. give 25 mg test dose in 50 mL of N.S. i.v., é precautions for ttt of anaphylactic reaction. If tolerated, give 1000 mg by slow i.v. infusion. This’s us. done dur. initial Tx. hospitalization stay. This cn be repeated as necess-ary in an outpatient infusion center to maintain HB > 10 g/dL, s. ferritin > 200 ng/mL & TSAT>20 %. Alternatively, we cn give ferumoxytol (Feraheme) as 510 mg rapid inj. at visits (separated by at least 3-8  d.). If ptn is allergic to iron dextran, we give ferumoxytol (Feraheme) as two 510 mg rapid inj. about one w. apart. Alternatively, give Na ferric gluconate cx: 250 mg on 4 different occasions, us. weekly/4 w., or iron sucrose 300 mg IV over 2 h. on 3 separate occasions, separat-ed by 14 d. Adv. of iron sucroseü : unlike iron dextran, No fatal anaphylactic reactions, but are more expensive & less convenient thn a single iron dextran.


Persistent anemia: assess iron status /8-12 w.. Oral iron hs bn inadequate to replace or keep adequate iron stores & may bind7é im/m., (e.g. MMF). We do not use ESA in the immediate Tx. period. With CKD anemia occ. > 3 m. post Tx in iron-replete ptn.Øinitiate Epoa. Ptn. shd be apprised A of risks ofÖ: {Stroke, thrombotic events & incr. risk of recurrent cancer} prior to ESA. In U.S., Medicare guidelines mandate CKD ptn receive ESA in a physician's office, wch’s inconvenient for the ptn..  Instead of Epo a., an alternative is to use darbepoetin alfa (Aranesp) because of its longer half-life tht may permit less frequent doses. Depo. carries the same risks as other ESAs. Initiate Depo. 0.45 mcg/kg S.Q, wch’s given once/w.. However, Depo. is more expensive.

Q.740. What causes elevation of the lipid profile in R.T.x.?              B

A. Csp. (replace é tacrolimus), Sirolimus & Steroid therapy.

Q.741. How can u suspect R.V.T.?      ž ž

A. { Abrupt  anuria. + Loin pain. +é LDH + Doppler  evidence =  R.V.T.}.

Q.742. When should the diagnosis of T.M.A. be suspected?

A.  The constellation of (3 high+2 Low) :       { B + A }

1. Incr. s. cr.

2. Incr. LDH.

3. Incr. Schistocytes in blood film.

4. Low HB.

5. Low platelet count.            

Q.743. What is the D.D.? How to solve this problem?  {Ñ}

A.   T.M.A. cn be mistaken é :  

1. Lab”. changes       …. us. ”mild”.

2. Sirolimus & thymoglobulin toxicity:Ø [Anemia + thrombocytopenia].

A. R. biopsyØ {Endothelial dge + arterial microangiopathy} é T.M.A.,…. prognosis is poor.

Q.744. How to treat this problem?   

A.  T.M.A. cn be caused by:       B

     1. A.P.A  ð Pph + anticoacgulants.

     2. C.N.I.  ð Change the drug.

     3. Recurrence of the original dis. (esp. non-Drr. HUS.) ð Pph.

Q.745. What are the causes of post R.Tx. R.A.S?

A.  Post R.Tx. RAS   Ø        B

1. Surgical trauma.  

2. Atherosclerosis.   

3. CMV.

Dgx: similar to general population. As Sn & Sm of COVID-19 may be subtle in TR and disease progression can be rapid, some physicians hv a lower threshold for evaluating & testing TR. Approach to management (eg, antivirals, supportive care) is also similar to general population, although careful attention should be paid to possibility drug-drug interactions & effects on the im/m regimen. Adjustments to im/m protocol should be individualized, based according to disease severity, specific regimen used, type of organ transplant, time post-tx, and risk of acute allograft rejection. Some organ TR recover without reduction in im/m. that carries the risk of rejection & immune reconstitution. Conversely, continued im/m. may enhance the risk of uncontrolled infection.