Patients with Chronic Kidney Disease (CKD) have 2.8 to 3.4-fold higher mortality compared to individuals with normal kidney function, mostly attributed to increased risk for Cardiovascular (CV) events [1,2]; however, this increased risk is not fully explained by the traditional CV risk factors such as diabetes, hypertension, hyperlipidemia, smoking etc [1]. Over last decade, Fibroblast Growth Factor-23 (FGF23) has emerged as a strong predictor of CV disease and all-cause mortality in both general and CKD population [3-5]. In this context; however, it is not clear if the relationship of FGF23 with morbidity and mortality is causative or merely associative. Uncertainties also linger about the regulation of FGF23 in CKD patients. Here is the new insight into the role and regulation of FGF23 in CKD. FGF23 was originally discovered as a phosphaturic hormone. It is produced and secreted by osteoblasts and osteocytes with 1,25(OH)2D as a major direct known stimulus and FGF23 in turn induces phosphaturia by down regulating type IIa and IIc sodium-phosphorus co-transporters on the apical surface of the proximal tubular renal epithelial cells [6]. FGF-23 also down regulates the 1-α-hydroxylase enzyme causing decrease in the active form of vitamin D with resultant decrease in intestinal phosphate absorption. FGF23 exerts these actions by binding to the FGF receptor Klotho complex in kidney and, thus maintains the phosphorus homeostasis. The various FGF23 activating mutations have known to lead to disorders characterized by hyperphosphaturia, hypophosphatemia, fatigue, bone pain and deformities in face of inappropriately low or normal vitamin D levels. Conversely, loss-of-function FGF23 mutations cause hyperphosphatemia, ectopic calcification, premature aging and death [7].

Background: Continuous improvement in the mechanics, preservation and anticalcification treatment made bioprostheses the standard mode of valve replacement in the aging population. A novel Support System with large openings at the Commissural posts has been developed and the performance and durability of bioprostheses constructed went under evaluation.

Methods: This stent was used to create Three trileaflet composite porcine valves of 23mm (titanium), 27mm and 31mm (POM-C) in diameter were constructed. and one 25mm (titanium) bovine pericardial valve. All valves were tested in a heart valve duplicator system. The porcine valves underwent fatigue accelerating testing.

Results: For the porcine valves the peak pressure was measured as 12.5mmHg, 9.1 mmHg and 7.3mmHg for the 23mm, 27mm and for the 31mm valve respectively and the valve area were 2.5 cm², 2.6 cm² and 2.7 cm² respectively. The 25mm pericardial valve showed a peak pressure of 5.5mmHg and a valve area of 3.1 cm². The durability test showed deterioration after 225x106cycles for the 23mm, 265x106 cycles for the 27mm and 240x106 cycles for the 31 mm.

Conclusion: This novel stent for bioprosthetic valves offers excellent hydrodynamic performance for a variety of biological issues tested and above the standards durability.

A 33-year-old woman was referred to cardiology assessment 3 months after the delivery of her f irst child because of fatigue. Her past medical history was insignificant. She had no other history of cardiovascular disease. Her physical examination findings were unremarkable. Her laboratory results, including ECG were within normal limits. An echocardiogram showed a notched, highly mobile, 13.0x4.0 cm huge left atrial myxoma covered with thrombi, which nearly fills the left atrial chamber with prolapsed of the tumor mass across the mitral annulus into the left ventricle in diastole (Figure1A-B). Neither significant mitral regurgitation nor mitral stenosis was seen. There was no evidence for patent foramen ovale or other intra-cardiac shunts by color flow Doppler. She subsequently underwent an uneventful surgical removal of the mass at another cardiac surgery center.