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



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

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

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

A. {Abrupt  anuria. +Loin pain. +🠉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) :         { 👌 + }

1. Incr. s. Cr.

2. Incr. LDH.

3. Incr. Schistocytes in blood film.

4. Low H.B.

5. Low platelet count.

Q.743.What is the D.D.? How to solve this problem?  😎 😎

A.   T.M.A. can be mistaken é :  

1. Lab”. changes       …. usually ”mild”.

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

A. R. biopsy 🠞{Endothelial damage+arterial microangiopathy} é T.M.A.,…. prognosis is poor.

Q.744. How to treat this problem?   

A.  T.M.A. can be caused by:     👌

     1. A.P.A🠞Pph + anticoacgulants.

     2. C.N.I. 🠞 Change the drug.

     3. Recurrence of the original disease (esp. non-Drr. HUS.) 🠞Pph.

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

A. Post R.Tx. RAS        👌

1. Surgical trauma.    2. Atherosclerosis.      3.CMV.

Q.746How can u evaluate the late allograft loss?

A. Late Allograft loss:

I. 50% 🠞 of ptn die é functioning graft. 

II. 50%🠞 Ch. allograft dysfunction & failure:

                        (1) 30-40 % 🠞 CAN. (Ch. allograft Np.) :

                                a. True CAN: ch. Rj. (im/m. inj.).

                                                    b. CAN of mixedorigin (fibrosis/tub. atrophy).

                       (2) 10-20% 🠞 Others: 

o   Recurrent  dis.

o   De Novo dis.

o   Ch. CNI toxicity.

Q.747Define CAN?     😎

A.CAN is the most common (after death) cause of allograft loss. It’s defined by “Halloran as a [State of impaired renal allograft function, 3 m. at least post Tx., independent of : 1. Ac Rj. 2. Drug  toxicity. 3. Recurrent dis.. 4. De Novo dis., & é typical features é R. biopsy.].

Q.748Describe its C.P.?       

A. C.P.: { H.T. +Proteinuria +🠝 S.cr. + P.H. of Ac Rj.}.

Q.749.Describe the biopsy findings?       

AActually not unique for CAN, but u can find:    👌

1)   Atrophy & fibrosis of the tubulointerstitium. (T/I).

2)   Fibrointimal thickening of the arterial wall. (B.V.).  

3)   Ch. T.x. glomerulopaty:     

*      Double contour/thickening é cpll. wall.

*      Segmental sclerosis.

*      Damaged mesangium.

Q.750.What is the pathogenesis of CAN?     

A. Pathogenesis of CAN:

(A) Allograft -dependent:      👌

·         Rejection.

·         Poor compliance.

·         H.L.A. mismatching.

  (B) Allograft -independent:   

o   CNI toxicity.

o   Ischemic damage.              

o   Inadequate nephron mass.

o   Donor kid. disease. (H.T., age related).

o   H.T., Hyperlipidemia, proteinuria.

Q.751.How to manage CAN  ?

A. CAN is ttt. accordingly:  {RAS : ttt , H.T.: ttt. , Hyperlipidemia: ttt., CNI : reduce or replace é MMF, Sirolimus}.

Q.752How to improve R. allograft survival?         👍

1)  🠝Living donor (related & non-related).

2)   Donor from deceased Younger donor.

3)   Better donor preparation.

4)   Faster matching & T.x.  

5)   Prevention & ttt. of Ac. Rj.

6)   High quality medical care : H.T., Dyslipidemia.

7)   Pre-emptive T.x.

8)   Zero mismatching.

9)   Reduce cold ischemic time.

10) Reduce CNI toxicity.

11)ACEI/ARBs: few physician encouraging them. 

12)Nephron dosing: Sex & BMI.

Q.753.What medical problems that can be seen in R.T.x.? How to deal with them?

A. I. Hyperphosphatemia🠊due hyperphosphaturia, due to:

*      Glucocorticoids.

*      Low vit. D.🠊 Po4 wasting.

*      Residual hyperparathyroidism.

    ***    ttt.

v  Po4 supplementation.

v  Vit. D. analogue           

v  High Po4 diet (low fat dairy products).

Q.754What else?  How to treat?

A. II. Gout: Hyperurecemia, mostly due:  Csp  Impair renal urate clearance é 80 % of ptn., only 7% of them develop gout

* ttt.:

1)   High dose steroids.

2)   Low-dose colchicine, to avoid colchicine-induced neuromyopathy.

3)   Allopurinolor uricosuric drug, Probenecid, to prevent gouty attacks (only effective é GFR>30 ml/min.).

4)   Switch Csp to Tacolimusé recurrent gout.     

* N.B. {Reduce Aza dose (75%) é concomitant use of Allopurinol( Allo. inhibit metabolism of Aza 🠞 Serious leucopenia, or better to switch to MMF}.    💀👽💀

Q.755.What else? How to treat?

A.III. Osteonecrosis  (avascular necrosis)🠞= The most 👆serious bone complication é T.x., due to [Steroid thpy], common site🠞Hip. Dgx.🠞MRI.

*ttt.:  [Rest – Joint Replacement – Osteotomy].