Peripheral chemosensor function is blunted in moderate to severe chronic kidney disease

BackgroundCardiovascular mortality is 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 tone. The aim of the present study was to examine whether chemosensor function is altered in patients with CKD.Methods and resultsWe assessed CHRS in 20 patients with stage 3 CKD [glomerular filtration rate (GFR) 30–59 ml/min/1.73 m2], in 15 patients with stage 4 CKD [GFR 15–29 ml/min/1.73 m2], as well as in 35 age and gender matched patients without any evidence of CKD. The difference in the R–R intervals divided by the difference in the oxygen pressures before and after deactivation of the chemoreceptors by inhalation of pure oxygen was calculated as the CHRS. A CHRS below 3.0 ms/mmHg was defined as pathological. CHRS was significantly depressed in patients with stage 3 CKD (2.9 ± 0.9 ms/mmHg, P = 0.005) and in patients with stage 4 CKD (2.1 ± 0.6 ms/mmHg, P < 0.001), as compared with patients without CKD (6.7 ± 0.9 ms/mmHg). There was a negative correlation between serum creatinine and CHRS (r = − 0.51; P < 0.001). In patients with CKD, chemosensor deactivation decreased mean arterial pressure from 91 ± 4 mmHg to 87 ± 3 mmHg (P = 0.03). Multivariate analysis showed that GFR (P = 0.001) was the only independent predictor of a pathological CHRS.ConclusionUsing a relatively non-invasive bedside test we provide evidence for a blunted peripheral chemosensor function in chronic kidney disease. We thereby lay the basis for interventional studies assessing chemosensor function in chronic kidney disease.