Background: The incidence of new-onset diabetes after initiation of hemodialysis (NODAD) and its impact on survival is not known. Methods: We used data from the United States Renal Data System (USRDS) from January 2000 to December 2001, with at least 3 years of follow-up for this study. Patients aged 18–80 years were included. NODAD was defined as two Medicare institutional claims for diabetes in patients with no history of diabetes prior to starting hemodialysis (HD). Incidence (per 1,000 patient-years), prevalence (%) and hazard ratios for mortality in patients with NODAD were calculated. Results: There were 59,340 incident patients with no history of diabetes prior to starting HD, of which 3,853 met criteria for NODAD. The overall incidence and prevalence of NODAD were 20 per 1,000 patient-years and 7.6%, respectively. In a cohort of 444 patients without diabetes and documented glycosylated hemoglobin A1c, <6% prior to starting HD (from January 2005 and March 2006), at a mean follow-up of 4.7 ± 2.6 months, 6.8% developed NODAD defined by two Medicare claims for diabetes after initiation of HD. NODAD was associated with a significantly increased risk of death as compared to non-diabetes patients (hazard ratio 1.20, 95% confidence interval 1.14–1.25). Conclusion: The USRDS showed a high incidence of NODAD, associated with significantly higher mortality compared to those who did not develop NODAD. The mechanism of NODAD needs to be explored further in experimental and clinical studies.
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
metatarsal and phalangeal aplasia or hypoplasia. The hands and/or feet appear split into 2 halves with aplasia (failure of development) of the phalanx, metacarpal, and/ or metatarsal bones of one or more fingers and/or toes as well as hypoplasia (underdevelopment) of the phalanges, metacarpals, and metatarsals (the bones leading up to the toes) [Duijf et al., 2003]. SHFM is inherited as an autosomal dominant, recessive, or X-linked entity, with a prevalence of 1 per 90,000 live births, and its clinical severity varies from patient to patient as well as between the limbs of the same patient ( Fig. 1 A, B) [Duijf et al., 2003;Elliott and Evans, 2006].
SHFM ClassificationTwelve different types of SHFM have been mapped to different human chromosomes, including SHFM1 located in 7q21 (OMIM 183600) [
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.