Cardiovascular is the major cause of death in chronic kidney disease and end-stage renal disease. The cardiovascular mortality rate of patients with renal impairment is evaluated to be higher than general population. Coronary artery disease seems to be an important type of cardiovascular complication among patients with chronic kidney disease and end-stage renal disease before the renal replacement therapy. Due to the strong association between chronic kidney disease and the incidence of coronary artery disease, accurate screening, diagnosis, and management of cardiovascular complications would be essential in patients at different stages of renal dysfunction. Despite the need for the comprehensive knowledge about different aspects of coronary artery disease in patients with renal failure, there is not sufficient evidence regarding the pathophysiology, ideal diagnosis, and treatment strategies for coronary heart disease in population with chronic kidney disease. In this study, we briefly reviewed the existing literatures about the possible screening, diagnosis, and the treatment approaches of risk of coronary heart disease in patients with kidney dysfunction.

Background Considering the significant geographical and ethnical differences in pattern of incidence, etiology and outcome of chronic kidney disease (CKD), the present study aimed to assess the etiology and outcome of CKD in Iranian children. Materials and Methods In a cross-sectional study etiology and outcome of 372 children aged 3 months to 18 years with CKD was studied during the period 1991 – 2014. Children (186 boys, 186 girls) with Stage 3 to 5 CKDs, defined as a glomerular filtration rate below 60 ml/min per 1. 73 m2body surface area, were identified. Results Etiology was congenital anomalies of the kidney and urinary tract in 125 (33. 60%), cystic/ hereditary/ congenital diseases in 91 (24. 46%), glomerulopathy in 73(19. 62%), and cause unknown in 71 (19. 09%) patients. Forty-eight (13. 22%) were on conservative treatment, 174(47. 93%) had end-stage renal disease (ESRD) with chronic hemodialysis, 24 (6. 61%) were on continuous ambulatory peritoneal dialysis. Sixty-eight (18. 74%) underwent on renal transplant which was successful in 52 (14. 33%) patients but was associated with abnormal renal function in 16(4. 41%) children. Finally, 49 (13. 50%) patients died. Conclusion A large number of children developed CKD secondary to congenital anomalies of the kidney and urinary tract. Planning for screening, early detection and instituting timely treatment of preventable causes could lead to a lower incidence of CKD in this group of children.

Vascular calcification is a well-known complication of chronic kidney disease and one of the main predictors for increased cardiovascular morbidity and mortality in these patients. It may happen in 2 main types of intimal calcification, as a part of diffuse atherosclerosis, and medial calcification, which is generally focal in distribution, unrelated to atherosclerotic risk factors, and seen in younger hemodialysis patients. Pathogenesis may be genetic, mineral metabolism related, or nonmineral metabolism related. Increased calcium, phosphorus, and calcium-phosphorus product, decreased parathyroid hormone level, and overzealous use of active vitamin D supplements are the main mineral metabolism-related mechanisms of vascular calcification. Other mechanisms are formation of matrix vesicles and cellular apoptosis, with generation of hydroxyapatite crystals within vesicles and apoptotic bodies. The interplay of various activator proteins of vascular calcification such as bone morphogenetic proteins and receptor activator of nuclear factor-kappa B ligand, or inhibitor proteins like matrix Gla protein, bone morphogenetic protein-7, osteopontin, osteoprotegerin, fetuin-A, Smad6, and pyrophosphate are important in establishment of vascular calcification. Vascular calcification is related to all-cause and cardiovascular mortality both in general population and dialysis patients. Minimizing traditional risk factors of vascular calcification, prevention of hypercalcemia, and avoidance of high doses of calcium-based phosphate binders and vitamin D analogues are important measures for prevention or attenuation of progression of vascular calcification. Sevelamer and cinacalcet may prevent progression of vascular calcification. With the evolving knowledge of the pathogenesis of vascular calcification, we can look forward to emergence of novel therapies for this complication in the future.