title: Central venous pressure and impaired renal function in patients with acute heart failure.
abstract: OBJECTIVE
  To determine the relationship between central venous pressure (CVP) and renal function in patients with acute heart failure (AHF) presenting to the emergency department.
  
  
  RESULTS
  Central venous pressure was determined non-invasively using compression sonography in 140 patients with AHF at presentation. Worsening renal function (WRF) was defined as an increase in serum creatinine ≥ 0.3 mg/dL during hospitalization. In the study cohort [age 77 ± 12 years, B-type natriuretic peptide 1862 ± 1564 pg/mL, left ventricular ejection fraction 40 ± 15%, estimated glomerular filtration rate (eGFR) 58 ± 28 mL/min, and CVP 13.2 ± 6.9 cmH(2)O], 51 patients (36%) developed WRF. No significant association between CVP at presentation or discharge and concomitant eGFR (r = 0.005, P = 0.419 and r = 0.013, P = 0.313, respectively) was observed. However, in patients with systolic blood pressure (SBP) <110 mmHg and concomitant high CVP (>15 cmH(2)O), eGFR was significantly lower at presentation and discharge (29 ± 17 vs. 47 ± 19 mL/min/1.73 m(2), P = 0.039 and 26 ± 10 vs. 53 ± 26 mL/min/1.73 m(2), P = 0.013, respectively). Central venous pressure at presentation and at discharge did not differ between patients with or without in-hospital WRF (12.6 ± 7.2 vs. 13.5 ± 6.7 cmH(2)O, P = 0.503 and 7.4 ± 6.5 vs. 7.7 ± 5.7 cmH(2)O, P = 0.799, respectively) (receiver-operating characteristic analysis 0.543, P = 0.401 and 0.531, P = 0.625, respectively). However, patients with CVP in the lowest tertile (<10 cmH(2)O) at presentation were more likely to develop WRF within the first 24 h than patients with CVP in the highest tertile (>15 cmH(2)O) (18 vs. 4%, P = 0.046).
  
  
  CONCLUSIONS
  In AHF, combined low SBP and high CVP predispose to lower eGFR. However, lower CVP may also be associated with short-term WRF. The pathophysiology of WRF and the role of CVP seem to be more complex than previously thought.
authors.affiliation: Department of Angiology, University Hospital, Basel, Switzerland.
authors.forename: Heiko
authors.initials: H
authors.lastname: Uthoff
authors.forename: Tobias
authors.initials: T
authors.lastname: Breidthardt
authors.forename: Theresia
authors.initials: T
authors.lastname: Klima
authors.forename: Markus
authors.initials: M
authors.lastname: Aschwanden
authors.forename: Nisha
authors.initials: N
authors.lastname: Arenja
authors.forename: Thenral
authors.initials: T
authors.lastname: Socrates
authors.forename: Corinna
authors.initials: C
authors.lastname: Heinisch
authors.forename: Markus
authors.initials: M
authors.lastname: Noveanu
authors.forename: Barbara
authors.initials: B
authors.lastname: Frischknecht
authors.forename: Ulrich
authors.initials: U
authors.lastname: Baumann
authors.forename: Kurt A
authors.initials: KA
authors.lastname: Jaeger
authors.forename: Christian
authors.initials: C
authors.lastname: Mueller
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D002496:Central Venous Pressure / Q000502:physiology*; D004636:Emergency Service, Hospital; D005260:Female; D005919:Glomerular Filtration Rate; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D051437:Renal Insufficiency / Q000503:physiopathology*