Background: Vasopressin plays an important role in maintaining volume homeostasis. However, recent studies suggest that vasopressin also may play a detrimental role in the progression of chronic kidney disease. It therefore is of interest to identify factors that influence vasopressin concentration, particularly modifiable ones.
Study Design: Cross-sectional analyses.
Setting & Participants: Data used are from participants in a large general-population cohort study (Prevention of Renal and Vascular Endstage Disease [PREVEND]). Patients with a missing copeptin value (n = 888), nonfasting blood sample (n = 495), missing or assumed incorrect 24-hour urine collection (n = 388), or heart failure (n = 20) were excluded, leaving 6,801 participants for analysis.
Factor: Identification of lifestyle-and diet-related factors that are associated with copeptin concentration.
Outcomes: Copeptin concentration as surrogate for vasopressin.
Measurements: Copeptin was measured by an immunoluminometric assay as a surrogate for vasopressin. Associations were assessed in uni- and multivariable linear regression analyses.
Results: Median copeptin concentration was 4.7 (IQR, 2.9-7.6) pmol/L. When copeptin was studied as a dependent variable, the final stepwise backward model revealed associations with higher copeptin concentrations for lower 24-hour urine volume (P <0.001), higher sodium excretion (P <0.001), higher systolic blood pressure (P <0.001), current smoking (P <0.001), higher alcohol use (P <0.001), higher urea excretion (P = 0.003), lower potassium excretion (P = 0.002), use of glucose-lowering drugs (P = 0.02), higher body mass index (P <0.001), and higher plasma glucose level (P <0.001). No associations with copeptin concentration were found for C-reactive protein or use of diuretics or nondiuretic antihypertensives.
Limitations: The cross-sectional study design does not allow firm conclusions on cause-effect relationships.
Conclusions: Important lifestyle-and diet-related factors associated with copeptin concentration are current smoking, alcohol use, protein and potassium intake, and particularly fluid and sodium intake. These data form a rationale to investigate whether intervening on these factors results in a lower vasopressin concentration with concomitant beneficial renal effects. (C) 2015 by the National Kidney Foundation, Inc.
- general population cohort
- fluid intake
- sodium intake
- modifiable factor
- kidney disease progression
- URINARY ALBUMIN EXCRETION
- PLASMA VASOPRESSIN
- SURROGATE MARKER