Association between low-molecular weight apolipoprotein(a) isoforms and obesity in Italian women

Low-molecular weight (MW) apolipoprotein(a) [apo(a)] isoforms are closely associated with an increased incidence of atherothrombotic disease, prevalence of which is higher in obese individuals, particularly in women. The hypothesis of this study was to assess whether there are differences in the distribution of apo(a) phenotypes between obese patients and healthy controls.One hundred three obese Italian women (BMI > or = 30.0 kg/m2) were enrolled in the study, and apo(a) phenotyping was performed in all subjects. The prevalence of low-MW apo(a) isoforms, detected in plasma samples of our obese women, was compared with that found in a control group of 84 normal-weight, never-obese (BMI < 25.0 kg/m(2)), age-matched women.The distribution of apo(a) isoforms in the population of obese women was significantly different from that found in normal-weight female subjects. In particular, the percentage of subjects in the obese group with at least one apo(a) isoform of low MW was significantly higher than that in the control group (51.4\% vs. 32.1\%, p = 0.0079).Our results seem to suggest the possibility that small-sized apo(a) isoforms may be used together with other traditional risk factors to better assess the overall predisposition to atherothrombotic disease in obese women

Cardiorenal syndrome: pathophysiology and potential targets for clinical management

Combined dysfunction of the heart and the kidneys, which can be associated with haemodynamic impairment, is classically referred to as cardiorenal syndrome (CRS). Cardiac pump failure with resulting volume retention by the kidneys, once thought to be the major pathophysiologic mechanism of CRS, is now considered to be only a part of a much more complicated phenomenon. Multiple body systems may contribute to the development of this pathologic constellation in an interconnected network of events. These events include heart failure (systolic or diastolic), atherosclerosis and endothelial cell dysfunction, uraemia and kidney failure, neurohormonal dysregulation, anaemia and iron disorders, mineral metabolic derangements including fibroblast growth factor 23, phosphorus and vitamin D disorders, and inflammatory pathways that may lead to malnutrition-inflammation-cachexia complex and protein-energy wasting. Hence, a pathophysiologically and clinically relevant classification of CRS based on the above components would be prudent. With the existing medical knowledge, it is almost impossible to identify where the process has started in any given patient. Rather, the events involved are closely interrelated, so that once the process starts at a particular point, other pathways of the network are potentially activated. Current therapies for CRS as well as ongoing studies are mostly focused on haemodynamic adjustments. The timely targeting of different components of this complex network, which may eventually lead to haemodynamic and vascular compromise and cause refractoriness to conventional treatments, seems necessary. Future studies should focus on interventions targeting these components