title: Type 2 diabetes strengthens the association between pulse pressure and chronic kidney disease: the AusDiab study.
abstract: OBJECTIVE
  Chronic kidney disease (CKD) is a serious disorder with significant public health impact. Identification of factors associated with risk of progression of kidney disease may help in earlier intervention in high-risk groups. We investigated whether brachial pulse pressure (PP) was associated with 5-year changes in estimated glomerular filtration rate (eGFR) and incident CKD and whether type 2 diabetes modified these associations.
  
  
  METHODS
  In the population-based Australian Diabetes, Obesity and Lifestyle Study (AusDiab) 5554 individuals (5.8% with type 2 diabetes) who took part in the 5-year follow-up and had no CKD or microalbuminuria at baseline were included.
  
  
  RESULTS
  After adjusting for baseline age, sex, eGFR and use of blood pressure-lowering medication, each baseline SD higher PP was associated with a decline in eGFR of 0.32 ml/min (P=0.006) and an odds ratio (OR) for CKD of 1.29 [95% confidence interval (CI) 1.09-1.53] in individuals without type 2 diabetes. In individuals with type 2 diabetes, eGFR declined by 1.10 ml/min (P=0.011) and the OR for incident CKD was 1.94 (1.14-3.29). Similar associations with eGFR decline were observed with systolic blood pressure and incident CKD in individuals without type 2 diabetes. In individuals with type 2 diabetes, higher systolic blood pressure was only significantly associated with eGFR decline if the diastolic blood pressure was 70 mmHg or less (P for interaction between systolic and diastolic blood pressure: 0.033).
  
  
  CONCLUSIONS
  PP is an important risk factor for eGFR decline and incident CKD over a 5-year period, especially in individuals with type 2 diabetes.
authors.affiliation: Department of Epidemiology and Biostatistics and the EMGO Institute for Health and Care Research, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. Katja.vandenHurk@VUmc.nl
authors.forename: Katja
authors.initials: K
authors.lastname: van den Hurk
authors.forename: Dianna J
authors.initials: DJ
authors.lastname: Magliano
authors.forename: Marjan
authors.initials: M
authors.lastname: Alssema
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schlaich
authors.forename: Robert C
authors.initials: RC
authors.lastname: Atkins
authors.forename: Anne T
authors.initials: AT
authors.lastname: Reutens
authors.forename: Giel
authors.initials: G
authors.lastname: Nijpels
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Dekker
authors.forename: Jonathan E
authors.initials: JE
authors.lastname: Shaw
mesh_terms: D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D005919:Glomerular Filtration Rate; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D011674:Pulse