Clinical studies suggest a strong link between tissue calcification and pressure hyperpulsatility in end stage renal disease patients. Using a Wistar rat model of arterial elastocalcinosis and hyperpulsatility (vitamin D and nicotine (VDN) treatment), we evaluated the relative importance of tissue calcification and hyperpulsatility in the etiology of renal failure. VDN rats showed significant increases in aortic wall calcium content (992±171 µmol.g^-1 dry weight, x50 control 19±1) and pulse pressure (61±4 mmHg, x1.5 control 40±2). Significant renal calcification (124±27 µmol.g^-1 dry weight, x16 control 8.1±0.7) occurred mainly within the media of the preglomerular vasculature and in the areas of interstitial fibrosis in VDN. Extensive renal damages (26±5% of collapsed-atrophic or sclerotic glomeruli, or glomerular cycts, x5 control 5.2±0.3; 61±12 areas of focal, cortical areas exhibiting interstitial fibrosis per section, x28 control 2.2±0.6) were observed histologically. Glomerular filtration rate significantly decreased (880±40 µL.min^-1.g^-1 kidney weight vs control 1058±44). Albuminuria increased 6x (1.6±0.4 mg.24h^-1, control 0.27±0.04). There were significant linear relationships between albuminuria and pulse pressure (r² 0.408, n = 24) or renal calcium content (r² 0.328, n = 24, p < 0.05), and between glomerular filtration rate and pulse pressure (r² 0.168, n = 27). To our knowledge, this study provides the first evidence of links between both (i) hyperpulsatility and renal dysfunction, and (ii) renal calcification and renal dysfunction. Given the increasing frequency of end-stage renal disease, this model could prove useful for preclinical evaluation of drugs that prevent or attenuate hyperpulsatility and/or tissue calcification.