Animal models of chronic kidney disease (CKD) [1] and CKD patients [2] have reduced plasma hydrogen sulfide (H2S) concentrations. H2S inhibits phosphate-induced calcification and osteoblastic differentiation of vascular smooth muscle cells [2] , which may suggest it has a role in arterial calcification. The aim of the present study was to measure plasma H2S concentrations in CKD patients and investigate whether these measurement correlate with markers of vascular calcification or arterial stiffness. 54 Hypertensive non-diabetic patients (⩾70 years) with CKD stages 3 and 4 (n = 29), and hypertensive non-CKD matched controls (n = 25) were used in this study. Pulse wave velocity (PWV) and analysis were assessed by applanation tonometry, central hemodynamics by continuous digital pulse wave analysis, and vascular calcification (VC) by superficial femoral artery CT. Plasma hydrogen sulfide was determined following conversion to methylene blue using the zinc–dimethyl phenylenediamine trapping method described by Stipanuk and Beck [3] . Data was analysed by Spearman correlation. Plasma concentrations of H2S were not different between CKD (range 0.34 to 9.99 μM, mean 3.27 ± 0.40 (SEM)) and non-CKD patients (range 0.45 to 10.93 μM, mean 2.99 ± 0.58 (SEM)). Plasma H2S measurements did not correlate with vascular calcification scores, total peripheral resistance or pulse wave velocity. However, within the CKD patients only (n = 28), a negative correlation was observed between plasma H2S and pulse wave velocity (r=-0.36, P = 0.0545). A negative correlation was also found between plasma H2S and plasma parathyroid hormone levels (r=-0.3, P = 0.0379), but not between plasma H2S and plasma vitamin D levels. There was a trend for a positive correlation between plasma corrected calcium levels and plasma H2S (r = 0.26, P = 0.0620) but not with plasma phosphate levels. This reached significance in the CKD patient only group for corrected calcium levels (r = 0.47, P = 0.0101). This pilot data did not find a correlation between vascular calcification in a population of elderly CKD and non-CKD patients, but did observe a relationship between arterial stiffness and H2S in the CKD patients. Correlations between plasma H2S levels and plasma calcium and parathyroid hormone do suggest a role for H2S in the regulation of calcium levels within the body, which warrants further research.