Cardiovascular disease (CVD) is the major cause of morbidity and mortality in people with diabetes and in those with chronic kidney disease (CKD). Diabetes, occurring in epidemic proportions in the United States and worldwide, is also the leading cause of CKD and kidney failure. Identification of modifiable risk factors for CVD in patients with diabetes and CKD is thus of paramount importance. Anemia is increasingly recognized as a potential CVD risk factor in patients with diabetic nephropathy, in whom it is generally more severe and occurs at an earlier stage of CKD. In this review, we discuss the epidemiologic evidence, pathophysiologic mechanisms, and the current research findings, highlighting the role of anemia as a potential modifiable risk factor for CVD in patients with diabetic nephropathy, a particularly vulnerable population for CVD.

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Based upon numerous reported cases and despite widespread beliefs to the contrary, sickle cell trait (SCT) may be deemed a quantifiable risk factor in certain subsets of patients. As a result of common misconceptions regarding SCT, most individuals with the condition are generally not informed regarding the possible consequences of certain activities such as venturing to high altitudes or participating in overly exertional physical activities. Acute exertional rhabdomyolysis is a potentially serious clinical illness and is caused by skeletal muscle injury resulting in the release of myoglobin and other cellular contents, including creatine kinase, into the circulatory system. Mild to moderate cases of acute exertional rhabdomyolysis can cause metabolic disorders including hypernatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, lactic acidosis and hyperuricemia. Severe cases may result in renal failure and even death. Several case reports have been published since the early 1970s describing significant morbidity and mortality of acute exertional rhabdomyolysis in patients with SCT. We present the case of a 27-year-old male with a past medical history significant only for SCT who presented after a 1.5 mile run with severe exertional rhabdomyolysis and subsequent acute renal failure requiring hemodialysis (HD). In presenting this case, we hope to raise awareness of a possible underlying cause to many cases of exertional rhabdomyolysis and encourage physicians to counsel their patients with SCT in order to avoid the significant morbidity and mortality that may be associated with the condition.

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BackgroundCrohn’s disease and ulcerative colitis are both systemic chronic diseases that alter bowel physiology. The central process in inflammatory bowel disease (IBD) and the associated manifestations are the result of B-cell production of IgG autoantibodies directed against self-antigens in various organ systems including coronary endothelium. Previous studies have demonstrated significant micro-vascular endothelial dysfunction in patients with IBD compared to patients not affected by the disease. We sought to analyze the relation, if any, between IBD and the development of premature coronary artery disease (CAD).MethodsWe queried our hospital database to find IBD patients admitted to the hospital from January 1, 2007 to December 31, 2008. Patients with traditional cardiovascular (CV) disease risk factors including hypertension, congestive heart failure (CHF), diabetes, age ≥ 65, hyperlipidemia, family history, end-stage renal disease (ESRD), and greater than five pack-year smoking history were excluded from the study cohort. The charts of the remaining 300 patients with diagnosed IBD were then analyzed for the incidence of CV disease events including acute myocardial infarction (MI), unstable angina, positive stress testing, and any cardiac intervention including coronary angioplasty and/or intracoronary stent implantation.ResultsOf the 300 patients included, only one patient had a CV disease event. This patient had a positive exercise stress thallium test. Otherwise, the remaining 299 patients (99.7%) did not have any reported CV disease events over the 2-year follow-up period.ConclusionMost of the clinical sequelae of CV disease events are the result of inflammatory changes at the vascular level. While IBD is associated with a chronic inflammatory state as reflected by high sedimentation rates, C-reactive protein (CRP), homocysteine levels, etc., our data seem to indicate that chronic inflammation in the absence of traditional risk factors is not associated with an increased risk of premature CV disease events. More wide-scale prospective studies should be performed to elucidate the relationship, if any, between chronic inflammation and CV disease risk.