title: Neuropeptide Y, left ventricular mass and function in patients with end stage renal disease.
abstract: OBJECTIVE
  Neuropeptide Y (NPY) is released during sympathetic stimulation and mediates the central effects of the adipostatic hormone leptin. The plasma concentration of NPY and leptin is increased in patients with end stage renal disease (ESRD), but it is unknown whether these substances are related to biochemical markers of sympathetic activity and to alterations in left ventricular (LV) mass and function in these patients.
  
  
  METHODS
  We investigated the relationship between NPY, norepinephrine (NE), leptin and echocardiographic measurements in a cross-sectional study in 198 patients with ESRD.
  
  
  RESULTS
  NPY was directly related to plasma NE and heart rate but it was largely independent of arterial pressure and of retention of metabolic waste products. NPY was significantly higher in patients with LV hypertrophy and in those with LV systolic dysfunction than in those without these alterations. Of note, NPY emerged as an independent correlate of LV mass index and of LV ejection fraction (LVEF) (both P <or= 0.002) in multiple linear regression analyses including a series of cardiovascular risk factors. Furthermore in a multiple logistic regression model patients in the top NPY tertile had a risk for LV concentric hypertrophy that was 18.10 (95% confidence interval: 5.87-55.83) times higher than in those in the first tertile (P < 0.001). Leptin was unrelated to NPY as well as to LV mass and to systolic function.
  
  
  CONCLUSIONS
  Elevated NPY is independently associated with LV concentric hypertrophy and systolic dysfunction in ESRD. It remains to be seen whether these links contribute to the high cardiovascular mortality in these patients.
authors.affiliation: CNR, Institute of Biomedicine, Epidemiology and Pathophysiology of Renal Diseases and Hypertension and Division of Nephrology, Morelli Hospital, Reggio Calabria, Italy. carmine.zoccali@tin.it
authors.forename: Carmine
authors.initials: C
authors.lastname: Zoccali
authors.forename: Francesca
authors.initials: F
authors.lastname: Mallamaci
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.forename: Francesco A
authors.initials: FA
authors.lastname: Benedetto
authors.forename: Saverio
authors.initials: S
authors.lastname: Parlongo
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Cutrupi
authors.forename: Graziella
authors.initials: G
authors.lastname: Bonanno
authors.forename: Francesco
authors.initials: F
authors.lastname: Rapisarda
authors.forename: Pasquale
authors.initials: P
authors.lastname: Fatuzzo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Seminara
authors.forename: Alessandro
authors.initials: A
authors.lastname: Cataliotti
authors.forename: Lorenzo S
authors.initials: LS
authors.lastname: Malatino
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004452:Echocardiography; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000378:metabolism* / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000378:metabolism*; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D009478:Neuropeptide Y / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D012307:Risk Factors; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000378:metabolism* / Q000473:pathology
chemical_list: D015415:Biomarkers; D020738:Leptin; D009478:Neuropeptide Y; D009638:Norepinephrine