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Labudovic T.,Center for Urology and Nephrology | Labudovic T.,University of Kragujevac | Nedeljkovic B.,Center for Urology and Nephrology | Petrovic D.,Center for Urology and Nephrology | And 3 more authors.
Medicinski Casopis | Year: 2014

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. © 2014, Serbian Medical Society. All rights reserved.

Miloradovic V.,Clinical Center Kragujevac | Jagic N.,Center for Cardiology | Petrovic D.,Center for Urology and Nephrology | Popovic M.,Clinical Center Kragujevac
Serbian Journal of Experimental and Clinical Research | Year: 2010

Introduction: The prediction of improvements in left ventricular ejection fraction (EF) after revascularisation in patients with ischemic cardiomyopathy relies only on the extent of viable myocardium. The amounts of viable tissue and scar tissue are important but their relationship is different in diabetic and non-diabetic patients. Design and Methods: This study included 50 patients with a low EF (EF<40% by the Simsons method) divided into two groups. The first group consisted of 30 patients with registered coronary artery disease and normal glycoregulation, and the second group consisted of 20 patients with diabetes mellitus and registered coronary artery disease. All patients underwent Dobutamine stress echocardiography before surgical revascularisation and 8 weeks after surgery (2-5 months). Dobutamine infusion was terminated at 15 μg/kg/min. Results: The mean number of hypokinetic segments was 4.32±2.9 before testing, 1.9±2.07 at a 15 μg/kg/min dose of Dobutamine, 2.5±2.12 after revascularisation in the group with diabetes mellitus type II and 4.77±2.11, 1.87±2.18, and 2.97±2.28, respectively, in the group without diabetes mellitus type II. The mean number of akinetic segments was 5.95±2.63, 5.45±2.65 and 5.35±2.62 in the group with diabetes mellitus type II and 4.57±1.68, 3.5±2.26, 3.2±2.16 in the group without diabetes mellitus type II. The wall motion score index (WMSI) was 1.99±0.32 before and 1.86±,031 after revascularisation in the first group and 1.85±0.27 and 1.58±0.24, respectively, in the second group. The sensitivity for the detection of viable myocardium was 100% CI (93%-100%) in both groups, and the specificity was 96% CI (93%-98%) in the group with diabetes mellitus type II and 91% (89%-95%) in the group without diabetes mellitus type II. Conclusions: Our study shows that recovery of function occurs in a sizeable number of revascularised dysfunctional segments. This method was very helpful for the assessment of truly "viable" segments in patients with a poor prognosis.

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