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KIDNEY TRANSPLANT

Q.772. Discuss hyperuricemia and gout in renal transplant recipients?

 KIDNEY TRANSPLANT

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Renal transplantation- Allograft


Q.772. Discuss hyperuricemia and gout in renal transplant recipients?


A. Dcreased uric a. excretion can occur after R.Tx., esp. é of Csp. to prevent graft Rj.. Impaired urate excretionhyperuricemia & not uncommonly to gouty arthritis,  wch’s often difficult to ttt due to CKD & interaction of gout medications (e.g. colchicine, NSAIDs, allopurinol) & Tx. medication (e.g. Csp, Aza., diuretics). A.Smtic hyperuricemia shd not be ttt.ed in organ Tx. recipient. Colchicine & Csp both inhibit p-glycoprotein action, so for Ac. gout flare ttt in Tx. recipient receiving Csp or another p-glycoprotein inhibitor, colch. shd be limited to a single oral dose of 0.6 mg & not repeated for at least 3 d.. For gout flare prox: a colch. dose of 0.3 mg/d. or E.O.D. (according to R. func.) cn be given. In either case, careful monitoring for colchicine-induced myoneuropathy & blood cytopenias shd be under-taken to mitigate sequale of excessive colchicine levels. Alternative approaches: short-term NSAID & supplementation of the baseline corticosteroid dose most Tx. recipients receive. Slow (10-14 d.) rather than rapid tapering of steroids to baseline dose is recommended to avoid rebound gout flares. Long-term s. urate-lowering in Tx. recip. needs to be undertaken é special care.

XOI. (allopurinol & febuxostat) shd be avoided in ptn.s treated é Aza., because Aza metabolism involves conversion of 6-mercaptopurine to 6-thiouric acid in a reaction catalyzed by xanthine oxidase. Accumulation of 6-mercaptopurine can severe bone marrow toxicity é setting of co-administration of Aza. & XOI. Replacement of Aza é MMF (doesn’t affect xanthine oxidase activity) for graft protection presents a suitable option if gout ttt needs use of a XOI.  Allopurinol titration is strongly recommended, esp. é R.I. & diuretic use in Tx. reciep. If recommendations é allopurinol restriction occur to Cr. cl. are followed, goal: (<6.0 mg/dL) s. urate is often not achieved or maintained, and use of 👉febuxostat (no dose adj. is needed if Cr.cl. >30 mL/min) should be considered. In Tx. recipient é N. or near normal R. func. use of a uricosuric ag. may be considered, esp. where benzbromarone is available. Losartan 👉is the only uricosuric ARB👈 & may serve as a useful adjunctive agent in gouty recipient.

Q.773. How to evaluate erythrocytosis following renal transplantation (PTE)?

A. Diagnostic evaluation incl. U/S of native & transplant kidney & assessment of urine cytology. This’s to exclude underlying renal carcinoma. If these studies are suspicious for malignancy, further evaluation is performed. Ptn é P.H. of HBV or HCV infection who’re at incr. risk for hepatocellular carcinoma, we also obtain a liver U/S & a fetoprotein to screen for hepatocellular carcinoma.

Both ACEI/ARBs effectively ttt PTE. Start é an ARB,e.g losartan 50 mg/d., as it’s associated é 👈fewer S.E. thn ACEI. Dose increase to 100 mg/d. if no response obs. within 4 w. or B.P. remains raised. If adequate lowering of Hct is not seen after another 4 w., losartan may be replaced é enalapril, 10-20 mg/d, or another ACEI. Continue therapy for PTE indefinitely since relapse of erythrocytosis is common, the majority of R.Tx. recipients are hypertensive, and these drugs may slow the rate of progressive R. dysfunction.Treatment goal is HB. < 17.5 g/dL if ptn is normotensive. Phlebotomy shd be done if H.B. cannot be lowered é medications.

Q.774. How to evaluate hypertension after renal transplantation?

A. Incidence of posttransplant H.T.: 80% of R.Tx. recipients. PostTx. H.T. occur due to recip. or donor f.s, to im/m. medications such as CNI & steroids, or to RAS, wch can occur in up to 20 % of R.Tx. Recip.. Post Tx. RAS is important to identify because it’s a correctable form of H.T. Risk f. incl.: [Difficulties in harvesting & operative techniques, atherosclerotic dis., CMV infc. & delayed allograft function]. Persistent uncontrolled H.T., flash P.O. & Ac. rise in B.P.  are common features.  Arteriography is the preferred diagnostic modality but Doppler U/S., CT angio-, or MR arteriography may be used to diagnose RAS.

However, use of gadolinium during MR imaging has been strongly linked to nephrongenic systemic fibrosis among ptn
é moderate to severe R. disease. Gadolinium-based imaging should be avoided, if possible, é estimated GFR<30 mL/min. There’s no consensus among experts concerning the decision to use gadolinium among ptn. é GFR between 30-60 mL/min. Goal B.P. is 130/80 mmHg in ptn without D.M. or proteinuria & 125/75 mmHg in those é diabetes or proteinuria.  All classes of anti-H.T. ag. may be used é certain caveats. The dihydropyridine CCB : diltiazem, nitrendipine & verapamil 🠋 metabo-lism of Csp, tcrol., Siros. & evrol, and shd be avoided if possible. However, nifedipine, amlodipine & felodipine do not affect metabolism of Csp, tcrol., Siros. & evrol. If possible, ACEI & ARBs shd be avoided initially in order to avoid confusion in interpretation of a rise in s. cr. tht may sugg. Ac. Rj. or hyperkalemia.  

Q.775. What parathyroid & mineral metabolic errors can occur after R.Tx. ?

A. CKD is associated é cascade of events tht adversely affect mineral metabolism. Successful R.Tx. reverses many of these abn. in mineral & bone metabolism, although the degree of improvement is frequently incomplete. Persistent hyper-parathyroidism with or without hypercalcemia may be obs. after R.Tx.. Surgery is required for refractory cases.

Osteopenia & osteonecrosis: two mj. osseous complications of R.Tx., believed to be caused by multiple f., incl.:[ Persistent uremia- induced abn. in Ca+ homeo-stasis & acquired defects in mineral metabolism induced by im/m. drugs.] . Measures to prevent & treat post.Tx. bone dis. incl.: {Minimizing glucocorticoids, providing supplemental Ca+, ttt. vit. D def. & encouraging wt bearing-exercise. Antiresorptive agents such as bisphosphonates shd also be considered}.

Q.776. How to manage post-transplant D.M. in R.Tx. recipients (PTDM)?

A. Post-transplant D.M. occ. in 25 % of ptns in é first three y. after R.T.x. Its development is ass. é incr. recipient age >40-45 y., obesity, African-American or Hispanic ancestry, HCV infc. & CNI & Steroids. Dev. of PTDM is associated é significant infectious & CVS morbidity as well as increase M.R.. Management begins pre-Tx é screening for impaired glucose tolerance, PTDM risk assessment & counseling. Im/m. plans shd consider individual's risk for PTDM risk, wch shd be weighed agnst concerns for Rj.. Post-Tx., ptn. shd undergo regular screening for PTDM. Aggressive attention to other CVS risk f. help reduce increase M.R. sn é impaired glucose tolerance . Finally, adjustment in im/m.improve glucose tolerance. A stepwise for management of PTDM: starting é non-pharmacologic thpy, foll. by oral monothpy, oral combination therapy, then insulin as long as no metabolic decompensation needs earlier insulin thpy. With oral therapy, we usually initiate oral thpy é glipizide 5 mg/d.👈& then advance to 10 mg twice/d. as necessary to maintain HbA1c at 👉< 7 %. If this’s insufficient, consideration can be given to adding 👉 sitagliptin, as tolerated. Insulin therapy started if there’s metabolic decompensation, adverse S.E. é oral therapy, or HbA1c consistently >7 %. In addition, many ptns will require institution of insulin, esp. é FBS >200 mg/dL. We cn use multiple ag. and/or multiple-dose intensive insulin or insulin-pump thpy.