Plasma Neutrophil Gelatinase-Associated Lipocalin Associates with New-Onset Chronic Kidney Disease in the General Population
Arno R. Bourgonje,
Amaal E. Abdulle,
Martin F. Bourgonje,
Lyanne M. Kieneker,
Sacha la Bastide-van Gemert,
Sanne J. Gordijn,
Clara Hidden,
Tom Nilsen,
Ron T. Gansevoort,
Douwe J. Mulder,
Robin P. F. Dullaart,
Martin H. de Borst,
Stephan J. L. Bakker,
Harry van Goor
Affiliations
Arno R. Bourgonje
Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Amaal E. Abdulle
Department of Internal Medicine, Division of Vascular Medicine, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Martin F. Bourgonje
Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Lyanne M. Kieneker
Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Sacha la Bastide-van Gemert
Department of Epidemiology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Sanne J. Gordijn
Department of Gynecology and Obstetrics, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Clara Hidden
Gentian AS, 1596 Moss, Norway
Tom Nilsen
Gentian AS, 1596 Moss, Norway
Ron T. Gansevoort
Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Douwe J. Mulder
Department of Internal Medicine, Division of Vascular Medicine, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Robin P. F. Dullaart
Department of Internal Medicine, Division of Endocrinology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Martin H. de Borst
Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Stephan J. L. Bakker
Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Harry van Goor
Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands
Circulating levels of neutrophil gelatinase-associated lipocalin (NGAL) have been associated with acute kidney injury and the severity and progression of chronic kidney disease (CKD). This study investigated its potential utility as a biomarker for the risk of new-onset CKD in a population-based cohort study. Individuals without CKD at baseline (n = 4660) who participated in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) prospective population-based cohort study in the Netherlands were included. Baseline plasma NGAL concentrations were investigated for their associations with new-onset CKD, defined as a composite outcome of an estimated glomerular filtration rate (eGFR) 2, urinary albumin excretion (UAE) > 30 mg/24-h, or both. Mean (±SD) plasma NGAL concentrations were 104.0 (±34.7) μg/L and median eGFR was 96 [IQR: 85.3–105.8] mL/min/1.73 m2. After median follow-up of 8.3 [IQR: 7.8–8.9] years, 467 participants developed new-onset CKD. Plasma NGAL concentrations were significantly associated with an increased risk of new-onset CKD (hazard ratio [HR] per doubling 1.35 [95% CI: 1.11–1.63], p = 0.002), even after adjustment for potentially confounding factors (1.37 [1.09–1.73], p = 0.007) except baseline eGFR (1.09 [0.86–1.37], p = 0.490). In secondary analyses, plasma NGAL concentrations were significantly associated with new-onset CKD as defined by eGFR 2 alone (adjusted HR per doubling 2.54 [1.69–3.80], p p = 0.828), also when UAE > 30 mg/24-h was set as individual outcome (1.05 [0.82–1.35], p = 0.705). Higher plasma NGAL concentrations are associated with an increased risk of developing CKD in the general population. This association is dependent on renal function, and mainly driven by new-onset CKD as defined by renal function decline.
