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Contrast-induced acute kidney injury (AKI) (also known as contrast-induced nephropathy) is an abrupt deterioration in renal function that can be associated with use of iodinated contrast medium. Although the increase in serum creatinine concentration is transient in most cases, contrast-induced AKI may lead to increased morbidity and mortality rates in selected at-risk populations. This review summarizes the findings of a multidisciplinary panel composed of computed tomography radiologists, interventional radiologists, cardiologists, and nephrologists convened to address the specialty-specific issues associated with minimizing the incidence of contrast-induced AKI. As part of this initiative, the panel developed specialty-specific protocols for preventing contrast-induced AKI, taking into account, for example, the variations in patient risk profile, inpatient or outpatient status, and staffing resources that characterize various clinical settings. The 3 protocols, each reflecting a consensus of expert opinion, address the prevention of contrast-induced AKI in interventional radiology, diagnostic computed tomography radiology, and interventional cardiology settings. The protocols are presented in the context of a review of recent guidelines and published reports of trials that discuss contrast-induced AKI and its prevention. © 2009 Mayo Foundation for Medical Education and ResearchA cute kidney injury (AKI) is a heterogeneous disorder with multiple etiologies, risk factors, and clinical presentations. Although patients with AKI are ultimately cared for by nephrologists, AKI occurs in various clinical settings and is associated with a specific etiology in each. The term contrast-induced AKI refers to the disorder as it occurs after exposure to iodinated contrast media, a disorder that has been more commonly known as contrastinduced nephropathy (CIN). The Acute Kidney Injury Network, recognizing the need for improving outcomes associated with the various forms of AKI, recently proposed using the following standardized diagnostic definition in all cases: an abrupt (within 48 hours) reduction in kidney function, evidenced by an increase in the serum creatinine concentration of at least 0.3 mg/dL (to convert to µmol/L, multiply by 88.4) or at least 50% from baseline or a reduction in urine output (documented oliguria of <0.5 mL/kg/h for >6 hours).1,2 The criterion of oliguria does not apply for many cases of contrast-induced AKI because patients are treated with intravenous fluids before and after the procedure with the goal of increasing periprocedural urine output. The most commonly used definition of CIN is an increase from the baseline serum creatinine concentration of at least 0.5 mg/dL or at least 25% within 48 to 72 hours after exposure to contrast media. [3][4][5] Because the medical community is moving to adopt the concept and terminology of the American College of Radiology (ACR) in reference to studies of contrast-induced renal dysfunction and its prevention, 6 this report will do the same. However, we rec...

Hypogonadism, usually hypogonadotropic in origin, is the most common nondiabetic endocrinopathy in hereditary hemochromatosis (HH). Early studies, usually evaluating small numbers of patients with advanced HH, report prevalence rates of 10-100%. The clinical presentation of HH has changed in recent years as a result of increased awareness and screening. We assessed the prevalence of hypogonadism in a large group of patients with HH diagnosed in a single center over the past 20 yr, the period of follow-up spanning the time before and after widespread screening was introduced and the HFE gene was recognized. Abnormally low plasma testosterone levels, with low LH and FSH levels, were found in nine of 141 (6.4%) male patients tested. Eight of nine (89%) had associated hepatic cirrhosis; three of nine (33%) had diabetes. Inappropriately low LH and FSH levels were found in two of 38 females (5.2%) in whom the pituitary-gonadal axis could be assessed. This is the largest detailed study of hypogonadism reported in HH. The lower prevalence of hypogonadism compared with other reported series reflects the earlier diagnosis of HH in an unselected group of patients attending a single center. Patients with lesser degrees of hepatic siderosis at diagnosis are unlikely to develop hypogonadism.

This study highlights the challenges facing clinicians in improving exercise levels in patients, and the need to identify the specific barriers to exercise in the individual to improve health outcomes.

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Aim. To investigate the association between sleep quality and duration with lipid and glycaemic control in Caucasian subjects with type 2 diabetes. Methods. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) in 114 type 2 diabetes (T2DM) subjects. Comparisons were made between subjects with different sleep quality and sleep duration. Hierarchical multiple regression analyses were used to determine contributors to metabolic parameters. Results. Subjects with poor sleep quality (PQ; PSQI ≥ 6) had higher systolic blood pressure, glycated haemoglobin, urine albumin : creatinine ratio (UAC), total cholesterol (TC), and triglycerides (TG) (P < 0.05 for all) compared to those with good sleep quality (GQ; PSQI ≤ 5). Long sleep duration (LSD) subjects had higher TC and short sleep duration (SSD) subjects had higher TG compared to those with medium sleep duration. Sleep duration and PSQI score were independent predictors of TC and low-density lipoprotein cholesterol (LDL), contributing to 14.0% and 6.1% of the total variance, respectively. Conclusions. In this Caucasian T2DM population, PQ is associated with adverse cardiovascular risk markers, and long and short sleep disruptions have an independent negative impact on lipids. Sleep assessment should be included as part of a diabetes clinic review.

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