CKD, arterial calcification, atherosclerosis and bone health: Inter-relationships and controversies.

Mineral bone disease (MBD) is a common complication of chronic kidney disease (CKD) characterized by disruption of normal mineral homeostasis within the body. One or more of the following may occur: hypocalcemia, hyperphosphatemia, secondary hyperparathyroidism (SHPT), decreased vitamin D and vascular calcification (VC). The greater the decrease in renal function, the worse the progression of CKD-MBD. These abnormalities may lead to bone loss, osteoporosis and fractures. CKD-MBD is a major contributor to the high morbidity and mortality among patients with CKD. Another well-known complication of CKD is cardiovascular disease (CVD) caused by increased atherosclerosis and VC. CVD is the leading cause of morbidity and mortality in CKD patients. VC is linked to reduced arterial compliance that may lead to widened pulse pressure and impaired cardiovascular function. VC is a strong predicator of cardiovascular mortality among patients with CKD. Elevated phosphorus levels and increased calcium-phosphorus product promote VC. Controlling mineral disturbances such as hyperphosphatemia and SHPT is still considered among the current strategies for treatment of VC in CKD through restriction of calcium based phosphate binders in hyperphosphatemic patients across all severities of CKD along with dietary phosphate restriction and use of calciminetics. Additionally, Vitamin D insufficiency is common in CKD and dialysis patients. The causes are multifactorial and a serious consequence is SHPT. Vitamin D compounds remain the first-line therapy for prevention and treatment of SHPT in CKD. Vitamin D may also have atheroprotective effects on the arterial wall, but clinical studies do not show clear evidence of reduced cardiovascular mortality with vitamin D administration. This review discusses the issues surrounding CKD-MBD, cardiovascular disease and approaches to treatment.

The interplay of physician awareness and reporting of incidentally found coronary artery calcium on the clinical management of patients who underwent noncontrast chest computed tomography.

Studies have shown that coronary artery calcium (CAC) incidentally identified on a noncontrast chest computed tomography (NCCT) performed for noncardiac indications has diagnostic and prognostic value. The frequency by which radiologists report incidental CAC and its impact on patient management are unknown. This study included 204 consecutive patients (63 ± 17 years, 59% men) without a history of coronary artery disease referred for an NCCT for noncardiac indications. The presence of CAC was determined by an expert cardiologist and compared with the radiology report. For each patient, the medical record was reviewed for changes in medications. Physicians caring for these patients were surveyed regarding their awareness and the clinical importance of incidental CAC after their patients had been discharged from the hospital. There were 108 of 201 patients (53%) with a CAC score >0 as determined by an expert reader. The interpreting radiologist reported the presence of CAC in 74 of 108 patients (69%). Of the 74 patients, there was an increase in stain and aspirin prescription of 4% and 5%, respectively. Of the 132 physicians surveyed, 54% of physicians surveyed believed that CAC on an NCCT scan was analogous to the presence of coronary artery disease, 23% were aware that incidental CAC was reported, and only 4% said they would make medical management decisions based on the finding of incidental CAC. In conclusion, incidental CAC is under-reported by the interpreting radiologists and suggests an integral role for a cardiovascular imaging specialist. When incidental CAC is reported, physicians are not cognizant of the meaning and importance of this finding. This lack of knowledge is reflected in the negligible impact reported incidental CAC has on clinical management decisions.