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Transplant-Associated Hyperglycemia: A New Look at an Old Problem

Michael F. Crutchlow^*, and Roy D. Bloom

^* Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, and the Institute for Diabetes, Obesity and Metabolism, and Renal Electrolyte and Hypertension Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Address correspondence to: Dr. Roy D. Bloom, Renal Electrolyte and Hypertension Division, University of Pennsylvania, 700 Clinical Research Building, 412 Curie Boulevard, Philadelphia, PA 19104. Phone: 215-662-4643; Fax: 215-349-5703; E-mail: rdbloom{at}mail.med.upenn.edu

New-onset diabetes has long been recognized as a common complication of kidney transplantation, promoting cardiovascular disease, death, and graft failure. Studies in recent years have begun to highlight the very high posttransplantation prevalence of the prediabetic states of impaired fasting glucose and impaired glucose tolerance and the significant repercussions of these states on cardiovascular health. Therefore, the overall burden of transplant-associated hyperglycemia (TAH), which encompasses new-onset diabetes and the prediabetic states, is far greater than previously appreciated. The kidney transplant population is predisposed to insulin resistance and to additional insults of hypertension and hyperlipidemia that, together with hyperglycemia, compose the metabolic syndrome and promote atherosclerosis. When recipients with an underlying, frequently nonmodifiable predisposition to glucose dysregulation encounter transplant-specific, often modifiable, diabetogenic exposures, TAH manifests. Aggressive screening will effectively detect TAH, whereas risk factor modification, lifestyle intervention, and, when appropriate, drug therapy may decrease its impact. Topics of future investigation should include the use of emerging diabetes therapies and avenues for the prevention and reversal of TAH.

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