PMID- 18370695
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20220309
IS  - 1557-8518 (Electronic)
IS  - 1540-4196 (Linking)
VI  - 2
IP  - 4
DP  - 2004 Fall
TI  - Immunosuppression and metabolic syndrome in renal transplant recipients.
PG  - 263-73
LID - 10.1089/met.2004.2.263 [doi]
AB  - Cardiovascular disease is the major cause of death in renal transplant 
      recipients. Renal transplant recipients share the same cardiovascular risk 
      factors as the general population, including hypertension, hyperlipidemia, 
      diabetes mellitus, smoking, and positive family history. However, renal 
      transplant recipients are also exposed to transplant-specific risk factors such 
      as chronic immunosuppression. Most renal transplant recipients receive 
      combinations or permutations of immunosuppressive drugs including a calcineurin 
      inhibitor (cyclosporine or tacrolimus), a mammalian target of rapamycin (mTOR) 
      inhibitor (sirolimus), an antiproliferative drug (mycophenolate mofetil and 
      azathioprine), and corticosteroids. Cyclosporine and tacrolimus can induce 
      glucose intolerance, hypertension, and hyperlipidemia. Sirolimus can induce 
      hyperlipidemia. Corticosteroids can induce glucose intolerance, hypertension, 
      hyperlipidemia, and weight gain. Central to the development of metabolic 
      complications in renal transplant recipients is insulin resistance induced by 
      immunosuppressive drugs. Insulin resistance is considered to be the central 
      pathophysiological feature of metabolic syndrome, which is linked to increased 
      risk of cardiovascular disease and to chronic renal failure. Therefore, metabolic 
      syndrome likely contributes to cardiovascular disease and chronic renal allograft 
      dysfunction in renal transplant recipients. Treatment of metabolic complications 
      in renal transplant recipients is difficult, as conversion to an alternate 
      immunosuppressive drug may lead to introduction of new metabolic complications, 
      and as discontinuation of immunosuppressive therapy may lead to rejection. Future 
      research should focus on designing immunosuppressive regimens that have minimal 
      effects on insulin resistance and metabolic complications but that are effective 
      in preventing acute rejection and in prolonging both allograft and patient 
      survival.
FAU - Lo, Agnes
AU  - Lo A
AD  - College of Pharmacy, University of Tennessee Health Science Center, Memphis, 
      Tennessee.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Metab Syndr Relat Disord
JT  - Metabolic syndrome and related disorders
JID - 101150318
EDAT- 2008/03/29 09:00
MHDA- 2008/03/29 09:01
CRDT- 2008/03/29 09:00
PHST- 2008/03/29 09:00 [pubmed]
PHST- 2008/03/29 09:01 [medline]
PHST- 2008/03/29 09:00 [entrez]
AID - 10.1089/met.2004.2.263 [doi]
PST - ppublish
SO  - Metab Syndr Relat Disord. 2004 Fall;2(4):263-73. doi: 10.1089/met.2004.2.263.