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NDT Advance Access originally published online on October 12, 2005
Nephrology Dialysis Transplantation 2006 21(2):402-410; doi:10.1093/ndt/gfi187
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Original Articles: Clinical Nephrology

Diagnostic potential of circulating natriuretic peptides in chronic kidney disease

Patrick B. Mark1,2, Graham A. Stewart2,4, Ron T. Gansevoort2,5, Colin J. Petrie3, Theresa A. McDonagh3,6, Henry J. Dargie2,3, R. Stuart C. Rodger1 and Alan G. Jardine1,2

1 Renal Unit, University of Glasgow, 2 Division of Cardiovascular and Medical Sciences, 3 Department of Cardiology, Western Infirmary, Glasgow, UK, 4 Department of Nephrology, Ninewells Hospital, Dundee, UK, 5 Clinical Pharmacology, University Medical Center, Groningen, The Netherlands and 6 Department of Cardiology, National Heart and Lung Institute, Royal Brompton Hospital, London, UK

Correspondence and offprint requests to: Dr Patrick Mark, Renal Unit, Western Infirmary, Glasgow G11 6NT, UK. Email: p.mark{at}clinmed.gla.ac.uk

Background. Measurement of natriuretic peptides, particularly brain natriuretic peptide (BNP) is an established method for the diagnosis of cardiovascular disorders, chiefly left ventricular (LV) dysfunction. The influence of renal function on the diagnostic utility of natriuretic peptides is unclear.

Methods. We performed a cross-sectional study of 296 patients with renal disease but no history of cardiac disease using echocardiography to assess LV mass and function. Circulating levels of atrial natriuretic peptide (ANP) and BNP were also measured.

Results. The incidence of LV hypertrophy increased with progressive renal dysfunction; from 39% in patients with near-normal renal function, to 80% in renal transplant patients. There was a negative correlation between both ANP and BNP, and glomerular filtration rate (GFR) (ANP: r = –0.28, P<0.001; BNP: r = –0.40, P<0.001). Serum ANP and BNP had sensitivity and specificity for LV hypertrophy of 39.9%, 87.4% (ANP) and 61.4%, 67.6% (BNP) respectively. Sensitivity and specificity for LV dysfunction was 77.2%, 32.4% (ANP) and 71.8%, 40.0% (BNP). Significant confounders in determining serum ANP were haemoglobin, beta blockade and albumin, while serum BNP levels were significantly confounded by GFR, albumin, haemoglobin, beta blockade and age.

Conclusions. Across a spectrum of renal dysfunction, GFR is a more important determinant of serum BNP than ventricular function, and several factors are predictors of natriuretic peptide levels. In chronic kidney disease, the use of natriuretic peptides to diagnose LV hypertrophy must be interpreted in light of these other factors. The use of these peptides in renal dysfunction to diagnose LV dysfunction may be of limited value.

Keywords: atrial natriuretic peptide; brain natriuretic peptide; cardiomyopathy; chronic renal failure; left ventricular hypertrophy


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