Secondary hyperparathyroidism and cardiorenal syndrome type iv: Etiopathogenesis, clinical significance and treatment

© 2014, Serbian Medical Society. All rights reserved. Cardiorenal syndrome is a psychophysical disorder of the functions of the heart and kidneys, where the acute or chronic disorder of the functioning of one organ causes the acute or chronic disorder of the functioning of the other organ. In the type 4 of the cardiorenal syndrome (chronic renocardial syndrome), the deficiency of the vitamin D and the secondary hyperparathyroidism cause a disorder of the functioning of the heart and kidneys. The goal of this work is to analyze the risk factors, pathogenetic mechanisms of the development of the secondary hyperparathyroidism and to point out the clinical importance of its early detection and timely treatment. Works written by experts have been examined, as well as the clinical studies researching etiopathogenesis, diagnostics and treatment of secondary hyperparathyroidism. In the chronic kidney disease (stadiums 2 and 3), adaptation mechanisms are activated, while the concentration of FGF-23 and the concentration of parathyroid in the serum both increase. These hormones increase the fractional excretion of the phosphates within the kidney, while parathyroid releases the calcium from the bone tissue, therefore maintaining the concentration of calcium and phosphates in the serum within the normal range. The kidneys' loss of ability to create active vitamin D metabolites and excrete phosphate out of the organism significantly contributes to the development and progress of type 4 cardiorenal syndrome. The main clinical consequences of the secondary hyperparathyroidism are the high turnover bone disease, vascular and valvular calcification and the development of heart diseases. Modern treatment includes the use of phosphate binders that not contain calcium, new vitamin D metabolites and the use of calcimimetics. The early diagnosis and optimal control of secondary hyperparathyroidism prevent the progress of the chronic kidney disease and the development of cardiovascular diseases, reduce the rate of cardiovascular morbidity and mortality and improve the patients' quality of life

Glucagon effects on ischemic vasodilatation in the isolated rat heart

The myocardial reperfusion following ischemia leads to the ischemic vasodilation by affecting the release of various vasoactive substances, such as free radicals, NO, and histamine. In addition, some evidences suggest that glucagon itself may alter the release of those substances. In this study, we investigated the ischemic vasodilation of the isolated rat heart, as well as the concentrations of NO, TBARS, and histamine in the coronary venous effluent either in the presence or in the absence of glucagon. Our results showed that in the presence of glucagon, there was a faster restoration of coronary perfusion pressure during ischemic vasodilation compared to the absence of glucagon (124 ± 5.6 versus 81 ± 5.2 s) with no apparent changes in TBARS concentration. The glucagon's administration leads to the decreased release of histamine by approximately 35%. Biphasic release of NO in the presence of glucagon initially showed augmentation by 60, followed by the significant attenuation of 45%. © 2010 Mirko Rosic et al

Effects of different dietary regimes alone or in combination with standardized Aronia melanocarpa extract supplementation on lipid and fatty acids profiles in rats

© 2019, Springer Science+Business Media, LLC, part of Springer Nature. This study investigated different dietary strategies, high-fat (HFd), or standard diet (Sd) alone or in combination with standardized Aronia melanocarpa extract (SAE), as a polyphenol-rich diet, and their effects on lipids and fatty acids (FA) in rats with metabolic syndrome (MetS). Wistar albino rats were randomly divided into two groups: healthy and rats with MetS, and then depending on dietary patterns on six groups: healthy rats fed with Sd, healthy rats fed with Sd and SAE, rats with MetS fed with HFd, rats with MetS fed with HFd and SAE, rats with MetS fed with Sd, and rats with MetS fed with Sd and SAE. 4 weeks later, after an overnight fast (12–14 h), blood for determination of total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), index of lipid peroxidation (measured as TBARS), and FA was collected. Increased FA and lipid concentration found in MetS rats were reduced when changing dietary habits from HFd to Sd with or without SAE consumption. Consumption of SAE slightly affects the FA profiles, mostly palmitoleic acid in healthy rats and PUFA in MetS + HFd rats. Nevertheless, in a high-fat diet, SAE supplementation significantly decreases n-6/n-3 ratio, thereby decreasing systemic inflammation. Further researches are warranted to confirm these effects in humans