Chemoreflex Sensitivity in Chronic Kidney Disease

Cardiovascular Morbidity, Chronic Kidney Disease

Cardiovascular autonomic neuropathy, Chemoreflex sensitivity, Chronic kidney disease, Sudden cardiac arrest

Cardiovascular morbidity and mortality are markedly increased in chronic kidney disease (CKD) and may be explained in part by sympathetic hyperactivity. Impaired hyperoxic chemoreflex sensitivity (CHRS) has been attributed to an increased sympathetic activity. The aim of the present study is to examine whether chemosensor function is altered in patients with stage 3 and stage 4 CKD.

Impaired hyperoxic chemoreflex sensitivity (CHRS) is assessed in patients with stage 3 CKD \[glomerular filtration rate (GFR) 30-59 ml/min/1.73 m2\], in patients with stage 4 CKD \[GFR 15-29 ml/min/1.73 m2\], as well as in patients without any evidence of CKD. CHRS is measured by determination of the venous partial pressure of oxygen and the heart rate before and after deactivation of the chemoreceptors by inhalation of pure oxygen. The difference in the R-R intervals before and after inhalation divided by the difference in the oxygen pressures is calculated as the CHRS. A CHRS below 3.0 ms/mmHg is defined as pathological. It should be shown that using a simple clinical bedside test we provide the first evidence for impaired hyperoxic chemoreflex sensitivity in stage 3 and 4 chronic kidney disease. We thereby may lay the basis for future intervention studies assessing chemosensor function in these patients.

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