Q.756.What else? How to treat?

 KIDNEY TRANSPLANT

Q.756.What else? How to treat?  

A. IV. Osteoporosis: = {Reduction of bone density>2.5 S.D. below sex matched, using DEXA[Dual Energy X-ray Analysis]}.

Bone Loss occurs mostly é 1^st 6 m. due to: 🠞

o   Bone cell apoptosis.

o   Inhibition of sex hormone (m. & F.).

o   Steroids-induced inhibition of “Osteoblastogenesis”.

o   Dcr. “G.I. Ca+”abs. &“incr Ca+” urinary excretion.

o   Others: [Vit.D. def.- Csp A- Hyperpara.- Po4 depletion].

**  ttt. & prevention:

v 🠟🠟 Steroid dose.

v Wt bearing, inexpensive.

v No smoking, No alcohol.      🚭

v Vit. D.: 800 i.u. v.D2/d, Cacitrol é GFR <30ml/min.

v Bisphosphonate: prevent Bone density loss.

v Denosumab:(Prolia): an A.B. directed agnst  f. (RANKL) involved in formation of cells tht break down bone. It improves bone mineral density&🠟postmenopaus-al fracture inosteoporotic♀, given as an inj. s.c. once/6 m. Alth. well tolerated, S.E. : [skin infec. (cellulitis)- eczema- Hypo Ca+]. As it’s a new drug & there’re nolong-term safety data, denosumab is us. reserved for ptn.s intolerant of or unresponsive to other therapies. It shd not be given to hypocalcemic ptn.s  until corrected.To monitor resp.: measurement of bone mineral density (DEXA) or lab. tests tht indicate bone turnover (New bone formation & breakdownrate) cn be used.

Q.757.A 49 y. old T.x. female, experienced osteoporotic changes, how to D.D. Post T.x. from post-menopausal?

A. Post-menopausal O.P.🠊[Sex hormone deficiency- incr. osteoclasticacti-vity & accelerated bone breakdown- “ DEXA” predicts fracture risk- common site: appendicular bone.].    زيادة الهدم

On the other hand, Post T.x. “O.P” 🠊 [Dcr. osteoblastic activity- reduced bone synthesis- background of R. osteodystrophy – site: Vertebral bone]. ضعف البناء

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N.B.: Bone dis. in CKD: Majority of fractures occur. in early of CKD (stages 1-3) are mostly due to osteoporosis and Not metabolic bone dis. e.g. {hyperpara., osteomalacia, or adynamic bone dis.} (CKD-MBD components). Before assign-ning a Dgx. of osteoporosis it’s important to rule outosteomalacia (by measuring s.25[OH]2 D.) & hyperparathyroidism. Alth. both CKD-MBD & osteopor-osis are ass. é dcr. bone strength that can result in fractures, the pathophysiology is different. Osteoporosis is limited to a skeletal disorder ch.ch. by comp-romised bone strength (due to impairments in bone quality and/or bone mineral density) that predisposes to an increase risk of fracture. CKD-MBD, on the other hand, is defined as a systemic diso. of mineral & bone metabolism due to CKD, which manifests as either one or a combination of the foll.:{Vsc. or soft tissue calcification, abn. of Ca+, P+, PTH or vit. D mtab., or abn. in bone turnover, mineralization, vol., linear growth, or strength}. (Medscape).

Q.758.What else?

A.V. C.V.S.: Death é functioning graft🠊 the most common cause of early & late graft loss.     

               * Pathogenesis: 

v  [H.T. + Anemia + Fluid overload🠊L.V.H.].

v  [HyperPo4 + Hyperpara.🠊Vascular calcification].

v  [♂+ Smoking+ Old age+ D.M + obesity+ homocystinemia🠊Atherosclerosis].

Q.759.What else? How to treat?

VI. H.T.🠊due to:[Steroids- weightt gain- CNIs- Allog. dysfunction-Native kid. dis.-RAS].                    * ttt:

I. Non pharmacological: Wt. reduction-Na+ restriction-Alcohol abstinence – Exercise 🚲 Reduce CNI dose].      🚲

II. Drugs: Acc. to JNC [Joint National Committee é detection, prevention, ttt., & evaluation of H.T.]: Start é one drug, 🠝dose, use diuretic to enhance others: 

1)   B.B.: Cheap, CAD - 🠞hyperkalemia.

2)   Loop d.:Potentiate others- hypervolemia🠞: Hypovolemia- hyperuricemia- 🠝s. cr., use cautiously early post T.x. , [thiazides] 🠞cheap.🠞hypovolemia- hyperurecemia- 🠝s.cr. use low dose HCTZ: 12.5mg.

3)   ACE/ARB.:Dcrease Prot.- beneficial C.V. effects- ? Slow allograft dysfunction progression.: 🠝k+,🠝s.Cr.- use cautiously early post T.X.- useful é D.M. & é Prot.

4)   CCB.: Well tolerated- Graft👆 protective effect esp. é CNIs.:[Leg edema-Diltiazem & verapamil🠞 Dcrease CNI metabolism 🠊🠝toxicity. 👎

Q.760. What else? How to treat?

VII. Hyperlipidemia🠞Hypercholesterolemia & hypertriglyceridemia: Causes: ] [Steroids- CNIs (Csp more than Tcrol.)- Sirolimus].

Hyperlipidemia🠞Poor graft outcome. So, ttt:[Wt. control-  physical 🚲 activity-Diet. -minimize steroids. - switch Csp. to tcrol].          

-N.B. Csp: 🠟 Statin mtb. 🠞Statin toxicity & rhbdomyolysis, wch augmented by concomitant use of cytochrome P 450 inhibitors like Diltiazem… So, use Prava-statin & fluvastatin: [Low dose statin – avoid 👆 P 450 inhibitors  – avoid 👆  fibrates- check C.K. &L.F.T] .

Q.761.What else? How to treat?

VIII. Post-Tx cancer. Causes of incr. incidence:

1)   Uncontrolled proliferation of oncogenic viruses. (im/m).

2)   Inhbition of the “normal tumor surveillance” mechanisms. (im/m).

3)   Csp]🠝TGFB]Tumor promoting effect. (im/m).

4)   Iry R. dis.: [Analgesic abuse-HBV-HCV] or to ESRDmilieu. (acquired R. cyst).

N.B.:

      The most important f. incr. cancer risk] Cumulative effect of im/m. %

      The most important Single item in cancer prevention]🠋🠋 excess im/m.

   Sirolimus ♠§♠] has anti-neoplastic effect.    👍

Q.762.What kind of relation exists between viral infection& cancer?

v  HBV. ] Hepatocelluler carcinoma.

v  HCV. ] Hepatocelluler carcinoma.

v  Human Herpes v. 8]Kaposi sarcoma.

v  Epstein-Barr v.]Squamous cell carcinoma é  anogenital area & mouth.

Q.763.What are the most common types of cancer in R. Tx.?

A.The most common types are: 👌

(1) Vulva(Ano-genital)]45% (squamouscell carcinoma due: Ep.-Barr v.)

(2) Kaposi sarcoma] 26% (Human Herpes virus 8).   

(3) All lymphomas] 10%.

Q.764.What is the position of PTLD in the aforementioned types of cancer?

A. PTLD 🠞 One of the most fearful complications of T.x., occur early é high morbidity & mortality, mostly at 1^st24 m. é incidence of 1-5%, majority  Non-Hodgkin’s lymphoma & most are recipient of B-cell origin.    👽👽

* Risk f. include:   

1.    EBV (+ve) donor & EBV (–ve) recipient.

2.    CMV (+ve) donor & CMV (–ve) recipient.

3.    Pediatric recipient (mostly EBV–ve).

4.    Aggressive im/m. esp. Okt3/polyclonals.

* Pathogenesis: Infection transformation of B-cell by EBV.]Polyclonalproli-feration.… [Extranodal, G.I. tract, CNS] ]more common than non- T.x.  ptn.