Hyperphosphatemia is a known predictor of cardiovascular death and specifically of cardiac death in hemodialysis patients. The pathomechanisms involved have not been completely clarified. In this study we tried to assess for the presence of hyperphosphatemia in our patients on chronic hemodialysis and if it has an association with extraskeletal manifestations as increased cardiac wall thickness and also increased intimal medial thickness of carotid arteries.Subjects of the study included patients with hyperphosphatemia whom were subsequently divided into two groups; group I (secondary hyperparathyroidism) & group II (tertiary hyperparathyroidism) according to the presence of hyperparathyroidism in order to examine its added effect on vascular complications. Another group of Predialysis patients (group III) was added to the study and finally a control group (group IV) which consists of normal subjects.Serum phosphate level was highly significant in both group I and II (p value < 0.002& <0.001) and also Ca X P product (p value <0.002 &<0.001) respectively. Left ventricular posterior wall thickness (LVPW) is considered as the most suggestive of cardiac thickness but there was no significant difference between both groups I and II and the control group (P value 0.248 & 0.951 respectively). Ejection fraction (EF) was significantly lower in both groups I & II than control group (p value 0.028 and 0.029 respectively). The correlation coefficient of phosphorus to LVPW was found insignificant in group I and significant in group II (in secondary PTH -0.22, p value 0.539) and (in tertiary PTH; -0.5, p value 0.049). Concerning common carotid artery intimal medial thickness, it was measured by Doppler study and was correlated to different parameters of the study. There no significant increase in intimal thickness in all groups in comparison to control group. The more leading causes of vascular complications would be dependent on the duration of dialysis and long term exposure to hyperphosphatemia and consequently hyperparathyroidism. Although the pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis.