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OBJECTIVE Chronic exposure to calcineurin inhibitors and corticosteroids poses renal transplant recipients (RTR) at high risk for development of new-onset diabetes after transplantation (NODAT). Pancreatic β-cell dysfunction may be crucial to the pathophysiology of NODAT and specific markers for β-cell dysfunction may have additive value for predicting(More)
OBJECTIVEdChronic exposure to calcineurin inhibitors and corticosteroids poses renal transplant recipients (RTR) at high risk for development of new-onset diabetes after transplan-tation (NODAT). Pancreatic b-cell dysfunction may be crucial to the pathophysiology of NODAT and specific markers for b-cell dysfunction may have additive value for predicting(More)
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