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NDT Advance Access originally published online on December 29, 2005
Nephrology Dialysis Transplantation 2006 21(4):975-978; doi:10.1093/ndt/gfi345
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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

Pulse pressure and inhibition of renin–angiotensin system in chronic kidney disease

Debasish Banerjee1, Stephan Brincat1, Helen Gregson1, Gabriel Contreras2, Chris Streather1, David Oliveira1 and Stephen Nelson1

1 Department of Renal Medicine and Transplantation, St George's Hospital Medical School, London, UK and 2 Division of Nephrology, University of Miami, Miami, FL, USA

Correspondence and offprint requests to: Debasish Banerjee, MD, MRCP, Consultant Nephrologist and Honorary Senior Lecturer, Renal Medicine and Transplantation, St George's Hospital, Blackshaw Road, London SW17 0QT, UK. Email: Debasish.Banerjee{at}stgeorges.nhs.uk

Background. Elevated pulse pressure (PP) is an indicator of poor outcome in hypertensives in the general population and on haemodialysis. The prognostic value of PP in pre-dialysis patients with chronic kidney disease (CKD) stages 4/5 and its interaction with renin–angiotensin system (RAS) inhibitors is unknown.

Methods. This retrospective study of 349 patients from the pre-dialysis clinic analysed the effect association of PP and RAS inhibition on adverse outcomes in CKD stages 4/5. Primary endpoints were a composite of death or dialysis.

Results. At baseline, 349 patients (63% males, 34% diabetics) were aged 60±0.8 years (mean±SEM) with systolic blood pressure (SBP) 149±1.3 mmHg, diastolic BP (DBP) 83±0.7 mmHg, PP 66± 1.0 mmHg, creatinine 442±16 µmol/l and haemoglobin 10.7±0.1 g/dl. Patients were followed up for 297±19 days and 93% took one to seven (2.45±0.07) antihypertensives. At presentation, the adverse outcome group had higher SBP (151±1.5 vs 145±2.4 mmHg; P<0.05), proportion of diabetes (39% vs 23%; P<0.05) and creatinine (478±22 vs 354±11 µmol/l; P<0.05), but lower haemoglobin (10.6±0.1 vs 11.2±0.2 g/dl; P<0.05). PP increased with age (r2: 0.4; P<0.0001). PP >80 mmHg was associated with adverse outcome (Kaplan–Meier survival analysis, log-rank test P<0.05). In a model of proportional hazards regression, adjusted for age, baseline creatinine, diabetes and haemoglobin, elevated PP was associated with poorer outcome (hazards ratio: 1.09; 95% confidence interval: 1.01–1.18; P<0.05) and angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker use was beneficial (hazards ratio: 0.73; 95% confidence interval: 0.53–0.99; P<0.05).

Conclusions. The study demonstrates that elevated PP indicates high risk of death or dialysis and the benefit of blockade of the RAS is independent of the baseline PP in patients with CKD stages 4/5.

Keywords: chronic kidney disease; pulse pressure; renin–angiotensin system; hypertension; ACE inhibitors; renal failure


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