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Chronobiology International
The Journal of Biological and Medical Rhythm Research
Volume 26, 2009 - Issue 6
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Research Papers

DO RESTLESS LEGS SYNDROME (RLS) AND PERIODIC LIMB MOVEMENTS OF SLEEP (PLMS) PLAY A ROLE IN NOCTURNAL HYPERTENSION AND INCREASED CARDIOVASCULAR RISK OF RENALLY IMPAIRED PATIENTS?

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Pages 1206-1221 | Received 20 Mar 2009, Accepted 14 May 2009, Published online: 06 Oct 2009
 

Abstract

Hypertension can cause or promote renal failure and is related to cardiovascular mortality, the major cause of death in patients with renal impairment. Changes in the circadian BP pattern, particularly the blunting or reversal of the nocturnal decline in BP, are common in chronic renal failure. These changes in turn are among the major determinants of left ventricular hypertrophy. Using a chronobiological approach, it is possible to obtain better insight into the reciprocal relationship between hypertension, renal disease, and increased cardiovascular risk of renal patients. Disruption of the normal circadian rhythm of rest/activity may be hypothesized to underlie the high cardiovascular morbidity and mortality of such patients. Epidemiological studies reveal that hemodialysis patients experience poor subjective sleep quality and insomnia and, in comparison to healthy persons, are more likely to show shorter sleep duration and lower sleep efficiency. Sleep apnea may be present and is usually investigated in these patients; however, the prevalence of restless legs syndrome (RLS), which is high in dialysis patients and which has been associated with increased risk for cardiovascular disease in the general population, could also play a role in the pathogenesis of sleep-time hypertension in renal patients. Careful assessment of sleep quality, in particular, diagnostic screening for RLS and periodic limb movements (PLM) in renal patients, is highly recommended. In renal failure, attention to sleep quality and related perturbations of the sleep/wake cycle may help prevent the occurrence and progression of cardiovascular disease. (Author correspondence: [email protected])

ACKNOWLEDGMENTS

The authors wish to express their gratitude to Prof. Elio Lugaresi, University of Bologna, for his critical revision of the manuscript of this article, and to Mr. Mauro Pasin, University of Ferrara, who gave his invaluable technical assistance in the preparation of the paper. The authors report no conflicts of interest, and are alone responsible for the writing of this article.

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