Kamar N, Mariat C, Delahousse M, et al.. Diabetes mellitus after kidney transplantation: A French multicentre observational study. Nephrol Dial Transplant 22: 1986

Hôpital Foch, Lutetia Parisorum, Île-de-France, France
Nephrology Dialysis Transplantation (Impact Factor: 3.58). 07/2007; 22(7):1986-93. DOI: 10.1093/ndt/gfm011
Source: PubMed


New-onset diabetes mellitus (NODM)-a common complication of kidney transplantation-is associated with increases in graft loss, morbidity and mortality.
This is a purely observational study of 527 patients taking a calcineurin inhibitor (CNI), based on data collected at a single routine visit 6-24 months after kidney transplantation. Diabetes was defined according to ADA/WHO guidelines.
The mean age of the patients was 47.2 years and 61.1% were men; 49.5% were receiving cyclosporine microemulsion (CsA-ME) and 50.5% tacrolimus (Tac). NODM developed in 7.0% after a median interval of 1.6 months. In CsA-ME-treated patients, the unadjusted cumulative risks of NODM were 5.5% and 8.4% at 1- and 2-year post-transplantation, while in Tac-treated patients, the risks were respectively 17.4% and 21%. Four independent risk factors (RFs) were identified by multivariate analysis: maximum lifetime body mass index>25 [odds ratio (OR)=5.1], pre-transplantation impaired fasting glucose (OR=4.7), hepatitis C status (OR=4.7) and Tac vs CsA-ME treatment (OR=3.0).
NODM is associated with certain RFs present prior to kidney transplantation, and with treatment with Tac as opposed to CsA-ME.

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Available from: Pierre Yves Benhamou
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    • "However, large clinical trials did not reveal any increase in the incidence of posttransplantation diabetes among patients who were treated with SIR and a lower risk of NODAT if compared to cyclosporine and tacrolimus [20], and sirolimus could prevent the development of NODAT in kidney transplant recipients [41]. Recent observations, however, reported that the addition of rapamycin to tacrolimus [20] or to cyclosporine [49] [52] could increase the risk of NODAT. The rationale of our conversion protocol was developed on two basis: first, in a recent pilot study, we have showed that among 45 kidney transplant recipients treated with de novo therapy with sirolimus, no patients developed a NODAT during a mean follow up of 3.4 years [53]; moreover, kidney transplant recipients with type 2 diabetes as a cause of end-stage renal disease were successfully treated with sirolimus without worsening of their metabolic parameters [54]. "
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    ABSTRACT: New-onset diabetes mellitus after transplantation (NODAT) may complicate 2-50% of kidney transplantation, and it is associated with reduced graft and patient survivals. In this retrospective study, we applied a conversion protocol to sirolimus in a cohort of kidney transplant recipients with NODAT. Among 344 kidney transplant recipients, 29 patients developed a NODAT (6.6%) and continued with a reduced dose of calcineurin inhibitors (CNI) (8 patients, Group A) or were converted to sirolimus (SIR) (21 patients, Group B). NODAT resolved in 37.5% and in 80% patients in Group A and Group B, respectively. In Group A, patient and graft survivals were 100% and 75%, respectively, not significantly different from Group B (83.4% and 68%, resp., P = 0.847). Graft function improved after conversion to sirolimus therapy: serum creatinine was 1.8 ± 0.7 mg/dL at the time of conversion and 1.6 ± 0.4 mg/dL five years after conversion to sirolimus therapy (P < 0.05), while in the group of patients remaining with a reduced dose of CNI, serum creatinine was 1.7 ± 0.6 mg/dL at the time of conversion and 1.65 ± 0.6 mg/dL at five-year followup (P = 0.732). This study demonstrated that the conversion from CNI to SIR in patients could improve significantly the metabolic parameters of patients with NODAT, without increasing the risk of acute graft rejection.
    Full-text · Article · May 2013 · Clinical and Developmental Immunology
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    • "The risk factors for posttransplantation diabetes are similar to those for type 2 diabetes (Markell, 2004; González-Posada at al., 2004; Kamar et al., 2007). Hypertension (38-89%) is common, as is drug-induced diabetes (24%), exacerbated by the use of corticosteroids. "

    Full-text · Chapter · Sep 2011
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    • "The adverse impact of HCV on survival after kidney transplantation has been linked to liver dysfunction. Furthermore, a positive anti-HCV serology in kidney-transplant patients has been implicated in the development of de novo glomerulopathy [19], an increased incidence of serious infections [20], and new-onset diabetes mellitus [21]. In addition, in kidney-transplant patients, the use of alpha-interferon (αIFN) to treat HCV infection has been associated with (i) a poor response to antiviral therapy and (ii) the occurrence of a high rate of acute rejection, that is, up to 50% in some series [22, 23]. "
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    ABSTRACT: Hepatitis C virus (HCV) infection is a blood-borne infection and its prevalence used to be elevated in hemodialysis (HD) patients. Its main mode of contamination relies on nosocomial transmission. HCV infection is frequently associated in HD patients with normal liver enzymes whereas liver histology can display some degree of HCV-related lesions. The assessment of HCV-related lesions, even in HD dialysis patients, can be done via noninvasive tests. After kidney transplantation, HCV-related lesions can worsen; however, in this setting antiviral treatment harbors the risk of acute rejection. Therefore, it is recommended to implement antiviral treatment while the patient is receiving dialysis therapy. In this setting, the rate of viral clearance is usually high. In case of sustained virological response, no relapse occurs after kidney transplantation, despite heavy immunosuppression.
    Full-text · Article · Sep 2010 · Hepatitis research and treatment
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