NDT Advance Access originally published online on May 18, 2004
Nephrol Dial Transplant (2004) 19: 1682-1686
Nephrol Dial Transplant Vol. 19 No. 7 © ERA-EDTA 2004; all rights reserved
Editorial Comment
Left ventricular hypertrophy after renal transplantation: new approach to a deadly disorder
Domingo Hernández
Department of Nephrology, Research Unit, University Hospital of the Canary Islands, Research Institute Reina Sofia, La Laguna, Tenerife, Spain
Correspondence and offprint requests to: Domingo Hernández, Urbanización San Diego, 51, E-38208, La Laguna, Tenerife, Spain. Email: dhmarrero@hotmail.com
Keywords: cardiovascular mortality; left ventricular hypertrophy; renal transplantation
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Introduction
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Renal transplantation (RT) is the treatment of choice for end-stage
renal failure, but all-cause mortality is high in these patients
[1]. The cardiovascular death rate is higher than in the general
population, even after stratifying for age, gender and race.
Moreover, left ventricular hypertrophy (LVH) is extremely common
in kidney transplant recipients (5070%) and appears to
be an important determinant of survival [2]. In general, correction
of the uraemic state by RT leads to regression of LVH, but in
many patients cardiac growth persists, even in normotensive
recipients [3]. Many risk factors of volume and pressure overload
concur after RT. Additionally, other risk conditions inherent
to RT, such as immunosuppressive therapy and possibly genetic
factors, may contribute to perpetuate this complication. The
reninangiotensin system (RAS) plays an important role
in the pathogenesis of cardiac growth. Blockade of this system
by angiotensin-converting enzyme inhibitors (ACEIs)
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Clinical significance
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Pathophysiology of LVH: Role of immunosuppression
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Can diabetes influence cardiac growth?
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Role of ACE gene polymorphism
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Preventive and therapeutic options to minimize LVH
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Conclusions
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