New-onset diabetes mellitus and dyslipidemia should be monitored in this patient. Although kidney transplant recipients have improved clinical outcomes compared with patients who remain on dialysis, they require lifelong immunosuppression to prevent rejection of the transplanted kidney. In addition to increasing the risk of hypertension, infection, and certain malignancies, these medications can predispose patients to metabolic complications that should be anticipated by clinicians. Kidney transplant recipients are predisposed to new-onset diabetes after transplantation (often referred to as NODAT). Medications that promote development of NODAT include glucocorticoids, tacrolimus, and the mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus. Dyslipidemia is also a common complication posttransplantation, and commonly used immunosuppressive medications that promote dyslipidemia include cyclosporine and mTOR inhibitors. Because cardiovascular disease is the leading cause of death among kidney transplant recipients, it is important to aggressively treat modifiable cardiac risk factors, including diabetes and dyslipidemia. It is important to emphasize that many medications, including some statins, can significantly alter the pharmacokinetics of immunosuppressant medications. Clinicians should therefore never change medication regimens in kidney transplant recipients without ensuring that there will be no adverse drug interactions.

Although hypophosphatemia is commonly observed in the posttransplant period, which is due in part to residual secondary hyperparathyroidism, hyperphosphatemia is not commonly observed unless there is severely impaired allograft function.

Hyperthyroidism is not a common complication of kidney transplantation or of immunosuppressive medications typically used in kidney transplant recipients.

Many patients have residual hyperparathyroidism after transplant that can be slow to resolve; hypercalcemia is relatively commonly observed posttransplant but hypocalcemia is uncommon. Therefore, hypoparathyroidism is unlikely in this patient.