There is limited information regarding the incidence and features of post-transplant diabetes mellitus (PTDM) in pediatric renal transplant recipients. We noted a recent increased frequency of PTDM and reviewed charts of children who underwent renal transplantation from 1 September 1986 to 31 August 1999 to characterize the risk factors and natural history of PTDM. Sixteen children were identified with PTDM, and were each matched with two transplanted controls who did not develop PTDM. Clinical presentation varied from asymptomatic hyperglycemia to hyperosmolar dehydration or diabetic ketoacidosis. The mean time from transplantation to PTDM presentation was 1.2 years (range 1 day to 6.2 years). Significant risk factors for PTDM included: first degree family history of type 2 DM [odds ratio (OR) 23.9]; second degree family history of type 2 DM (OR 5.8); tacrolimus use (OR 9.1 versus cyclosporin); and hyperglycemia in the 2 weeks immediately after transplantation (OR 4.7). Seven of eight children with persistent PTDM continue to receive insulin. Patients with persistent PTDM had later onset disease (mean 1.9 years) compared to those with transient PTDM (0.3 years), suggesting different pathophysiologic processes. We suggest that all children undergoing renal transplantation be screened routinely for PTDM after transplantation, and that such patients may benefit from the avoidance of tacrolimus, as it may cause permanent beta-cell injury.
"In particular, although it provides a lower rejection rate, tacrolimus also results in an increased risk of NODAT compared with ciclosporin (31,56). In one study, tacrolimus had an odds ratio of 9.1 for development of NODAT compared with ciclosporin (57). In renal transplantation, two different strategies have been investigated, namely corticosteroid withdrawal and CNI minimization, which are discussed below. "
[Show abstract][Hide abstract] ABSTRACT: Solid organ transplantation has transformed the lives of many children and adults by providing
treatment for patients with organ failure who would have otherwise succumbed to their disease. The
first successful transplant in 1954 was a kidney transplant between identical twins, which
circumvented the problem of rejection from MHC incompatibility. Further progress in solid organ
transplantation was enabled by the discovery of immunosuppressive agents such as corticosteroids and
azathioprine in the 1950s and ciclosporin in 1970. Today, solid organ transplantation is a
conventional treatment with improved patient and allograft survival rates. However, the challenge
that lies ahead is to extend allograft survival time while simultaneously reducing the side effects
of immunosuppression. This is particularly important for children who have irreversible organ
failure and may require multiple transplants. Pediatric transplant teams also need to improve
patient quality of life at a time of physical, emotional and psychosocial development. This review
will elaborate on the long-term outcomes of children after kidney, liver, heart, lung and intestinal
transplantation. As mortality rates after transplantation have declined, there has emerged an
increased focus on reducing longer-term morbidity with improved outcomes in optimizing
cardiovascular risk, renal impairment, growth and quality of life. Data were obtained from a review
of the literature and particularly from national registries and databases such as the North American
Pediatric Renal Trials and Collaborative Studies for the kidney, SPLIT for liver, International
Society for Heart and Lung Transplantation and UNOS for intestinal transplantation.
"However, information on the incidence and risk factors for diabetic ketoacidosis (diabetic ketoacidosis) after solid organ transplantation has been limited to single-center reports. [1-4] There are even fewer reports on hyperglycemic hyperosmolar syndrome (hyperglycemic hyperosmolar syndrome, previously called nonketotic hyperosomolar coma) after renal transplantation. [5,6] Recently, post-transplant diabetes mellitus has been associated with tacrolimus use in renal transplant recipients with hepatitis C antibody positivity,  although this experience is not universal. "
[Show abstract][Hide abstract] ABSTRACT: Background
The incidence and risk factors for diabetic ketoacidosis (diabetic ketoacidosis) and hyperglycemic hyperosmolar syndrome (hyperglycemic hyperosmolar syndrome, previously called non-ketotic hyperosmolar coma) have not been reported in a national population of renal transplant (renal transplantation) recipients.
We performed a historical cohort study of 39,628 renal transplantation recipients in the United States Renal Data System between 1 July 1994 and 30 June 1998, followed until 31 Dec 1999. Outcomes were hospitalizations for a primary diagnosis of diabetic ketoacidosis (ICD-9 code 250.1x) and hyperglycemic hyperosmolar syndrome (code 250.2x). Cox Regression analysis was used to calculate adjusted hazard ratios for time to hospitalization for diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome.
The incidence of diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome were 33.2/1000 person years (PY) and 2.7/1000 PY respectively for recipients with a prior diagnosis of diabetes mellitus (DM), and 2.0/1000 PY and 1.1/1000 PY in patients without DM. In Cox Regression analysis, African Americans (AHR, 2.71, 95 %CI, 1.96–3.75), females, recipients of cadaver kidneys, patients age 33–44 (vs. >55), more recent year of transplant, and patients with maintenance TAC (tacrolimus, vs. cyclosporine) had significantly higher risk of diabetic ketoacidosis. However, the rate of diabetic ketoacidosis decreased more over time in TAC users than overall. Risk factors for hyperglycemic hyperosmolar syndrome were similar except for the significance of positive recipient hepatitis C serology and non-significance of female gender. Both diabetic ketoacidosis (AHR, 2.44, 95% CI, 2.10–2.85, p < 0.0001) and hyperglycemic hyperosmolar syndrome (AHR 1.87, 95% CI, 1.22–2.88, p = 0.004) were independently associated with increased mortality.
We conclude that diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome were associated with increased risk of mortality and were not uncommon after renal transplantation. High-risk groups were identified.
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