Patients who would benefit from higher doses are not identifiable a priori, titration for maximal anti-proteinuric effect would be a logical step during the treatment. Higher doses of ACEI and ARB seem well tolerated. Thus, this approach should be considered in patients who have not achieved optimal response for proteinuria reduction with their conventional doses of ACEI or ARB. This work was supported by a National Nature & Science Grant (no. 30830056) and a National 973 Program (no. 2006CB503904) to Dr Fan Fan Hou. All authors are in agreement with the content of the manuscript. The Authors state that there is no conflict of interest regarding

the material

discussed in the manuscript. “
“Date written: June 2008 Final submission: June 2009 Akt inhibitor No recommendations possible based on Level I or II evidence. (Suggestions are based on Level III and IV evidence) Pre-transplant weight and pre-transplant weight gain increase the risk of the development of diabetes therefore weight management strategies should be a priority for patients awaiting a kidney transplant. (Level III evidence) New-onset selleck chemical diabetes mellitus after organ transplantation (NODAT) has emerged as an increasingly important determinant of outcome and survival in transplant recipients. Its reported prevalence among renal transplant recipients varies widely because of the use of inconsistent definitions of diabetes. However, an International Consensus Expert Panel2 convened in 2003 agreed that the definition of NODAT should be in accordance with the American Diabetes Association (ADA)’s criteria for the diagnosis of diabetes mellitus,3 which specifies: 1 symptoms of diabetes mellitus plus casual plasma glucose ≥200 mg/dL. Casual is defined as any time of day. Classic symptoms include polyuria, polydipsia and unexplained weight loss, OR The

prevalence of NODAT has been Rho reported at around 20% at 1 year4 and best available data suggest that the disorder is a life-long problem for the majority of those diagnosed, not a temporary aberration driven by high-dose steroid exposure in the early post-transplant phase.5 NODAT is caused by the combination of insulin resistance and deficient insulin production.3 Non-modifiable risk factors for the development of NODAT include: age, ethnicity, family history of type 2 diabetes and HCV infection. Key modifiable risk factors the choice of immunosuppressive regimen, particularly steroid exposure and use of tacrolimus, and obesity.6–10 Diabetes mellitus has a major impact on graft and patient outcomes. It places patients at increased risk of the key causes of premature graft failure – death with function and chronic allograft dysfunction.