Endogenous ouabain and cardiomyopathy in dialysis patients

Authors

  • P. Stella,

    1. From the Division of Nephrology, Dialysis, and Hypertension, University ‘Vita e Salute’, San Raffaele Hospital, Milan, Italy
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  • P. Manunta,

    1. From the Division of Nephrology, Dialysis, and Hypertension, University ‘Vita e Salute’, San Raffaele Hospital, Milan, Italy
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  • F. Mallamaci,

    1. Division of Nephrology, Consiglio Nazionale della Ricerche-Istituto di Bio-Medicina, Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria, Italy
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  • M. Melandri,

    1. From the Division of Nephrology, Dialysis, and Hypertension, University ‘Vita e Salute’, San Raffaele Hospital, Milan, Italy
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  • D. Spotti,

    1. From the Division of Nephrology, Dialysis, and Hypertension, University ‘Vita e Salute’, San Raffaele Hospital, Milan, Italy
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  • G. Tripepi,

    1. Division of Nephrology, Consiglio Nazionale della Ricerche-Istituto di Bio-Medicina, Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria, Italy
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  • J. M. Hamlyn,

    1. Department of Physiology, School of Medicine, University of Maryland, Baltimore, MD, USA
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  • L. S. Malatino,

    1. Department of Internal Medicine, Catania University, Catania, Italy
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  • G. Bianchi,

    1. From the Division of Nephrology, Dialysis, and Hypertension, University ‘Vita e Salute’, San Raffaele Hospital, Milan, Italy
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  • C. Zoccali

    1. Division of Nephrology, Consiglio Nazionale della Ricerche-Istituto di Bio-Medicina, Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria, Italy
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Paolo Manunta MD, Division of Nephrology, Dialysis and Hypertension, University ‘Vita e Salute’ San Raffaele Hospital, Via Olgettina 60, 20132 Milan, Italy.
(fax: 390226432384; e-mail: manunta.paolo@hsr.it).

Abstract.

Background and methods.  Endogenous ouabain (EO) is markedly raised in patients with chronic renal failure. As high EO induces myocardial cell hypertrophy in vitro and it is associated with left ventricular hypertrophy (LVH) in essential hypertensives and in patients with heart failure we investigated the relationship between plasma EO and LV mass and geometry in 156 end-stage renal disease (ESRD) patients. EO was measured by a specific radioimmunoassay and by mass spectrometry.

Results.  On univariate analysis, plasma EO was directly related to LV mass (r = 0.26, P = 0.001) and LV end diastolic volume (r = 0.25, P = 0.002) and these relationships held true in multiple linear regression models including a series of potential confounders. Patients with eccentric LVH (n = 41, i.e. 26%) had the highest plasma levels of EO when compared to patients with other patterns of LV geometry (P = 0.001). Furthermore, plasma EO had diagnostic value for eccentric LVH because the area under the corresponding ROC curve (68%) was significantly greater (P = 0.002) than the threshold of diagnostic indifference. In this analysis, the sensitivity was 91% and the specificity was 36%. The positive predictive value was 33% but EO had a remarkably high negative predictive value (92%) for the exclusion of eccentric hypertrophy.

Conclusions.  In ESRD patients, plasma EO is independently associated with LV mass, LV volume and eccentric LVH. The results of this study are compatible with the hypothesis that EO is involved in alterations of LV mass in ESRD.

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