Secondary hypertension: Differential diagnosis and basic principles of treatment

© 2016, University of Kragujevac, Faculty of Science. All rights reserved. Secondary hypertension occurs in 5-10% of cases in the patient population with primary hypertension. e most common forms of secondary hypertension are as follows: parenchymal renal disease (renoparenchymal hypertension), renal artery stenosis (renovascular hypertension), adrenal gland adenoma (primary hyperaldosteronism), a tumour of the adrenal gland marrow (pheochromocytoma) and adenoma of adrenal and pituitary glands (Cushing’s syndrome). In patients with a typical clinical picture of secondary hypertension, the appropriate diagnostic tests should be conducted based on the suspected form of secondary hypertension. Determining a diagnosis of secondary hypertension is gradual. First, the appropriate screening tests are performed. If the screening test is positive, then additional tests to confirm the forms of secondary hypertension are conducted. Once a diagnosis of the appropriate form of secondary hypertension is confirmed, tests to distinguish causes and laterality tests to determine the precise localisation of the pathological process are applied to evaluate the response to therapy. Analysing the results of endocrine diagnostic tests provides an accurate diagnosis and selection of optimal therapeutic procedures

Secondary Hypertension: Differential Diagnosis and Basic Principles of Treatment

Secondary hypertension occurs in 5-10% of cases in the patient population with primary hypertension. The most common forms of secondary hypertension are as follows: parenchymal renal disease (renoparenchymal hypertension), renal artery stenosis (renovascular hypertension), adrenal gland adenoma (primary hyperaldosteronism), a tumour of the adrenal gland marrow (pheochromocytoma) and adenoma of adrenal and pituitary glands (Cushing’s syndrome). In patients with a typical clinical picture of secondary hypertension, the appropriate diagnostic tests should be conducted based on the suspected form of secondary hypertension. Determining a diagnosis of secondary hypertension is gradual. First, the appropriate screening tests are performed. If the screening test is positive, then additional tests to confirm the forms of secondary hypertension are conducted. Once a diagnosis of the appropriate form of secondary hypertension is confirmed, tests to distinguish causes and laterality tests to determine the precise localisation of the pathological process are applied to evaluate the response to therapy. Analysing the results of endocrine diagnostic tests provides an accurate diagnosis and selection of optimal therapeutic procedures

Acute Kidney Damage in Pregnancy: Etiopathogenesis, Diagnostics and Basic Principles of Treatment

Acute kidney damage associated with pregnancy occurs in 1/20.000 pregnancies. In developing countries, the main cause of the development of acute kidney damage is septic abortion, and preeclampsia in the developed countries of the world. Preeclampsia is defined as newly developed hypertension, proteinuria and swelling in pregnant women after the 20th week of gestation. It occurs due to disorders in the development of placenta and systemic disorders of the function of the endothelium of the mother. It is treated with methyldopa, magnesium sulfate and timely delivery. Urgent delivery is indicated if the age of gestation is ≥ 34 weeks. HELLP syndrome is a difficult form of preeclampsia. Its main characteristics are decreased platelet count, microangiopathic hemolysis anemia, increased concentration of aminotransferase in the serum and acute kidney damage. Severe HELLP syndrome is treated with emergency delivery, antihypertensives, magnesium sulfate, and in some cases plasmapheresis and hemodialysis. Acute fatty liver in pregnancy occurs because of decreased activity of the LCHAD enzyme of the fetus. Due to the reduced beta oxidation of fatty acids in the hepatocytes of the fetus, long chain fatty acids that cause damage to the mother’s hepatocytes are released. Swansea criteria are used for diagnosis, and the difficult form of the disease is treated with plasmapheresis and extracorporeal liver support. Atypical HUS is due to a reduced protein activity that regulates the activity of the alternative pathway of the complement system. Its main features are thrombocytopenia, microangiopathic hemolytic anemia and acute kidney damage. It is treated with plasmapheresis, and in case of resistance with eculizumab. Thrombotic thrombocytopenic purpura is due to decreased activity of the ADAMTS13 enzyme. It is characterized by thrombocytopenia, microangiopathic hemolytic anemia, high temperature, nervous system disorders and acute kidney damage. It is treated with plasmapheresis, and severe form of disease with corticosteroids and azathioprine. Early detection and timely treatment of acute kidney damage provides a good outcome for the mother and fetus

Mitigating RF jamming attacks at the physical layer with machine learning

Abstract Wireless communication devices must be protected from malicious threats, including active jamming attacks, due to the widespread use of wireless systems throughout our every‐day lives. Jamming mitigation techniques are predominately evaluated through simulation or with hardware for very specific jamming conditions. In this paper, an experimental software defined radio‐based RF jamming mitigation platform which performs online jammer classification and leverages reconfigurable beam‐steering antennas at the physical layer is introduced. A ray‐tracing emulation system is presented and validated to enable hardware‐in‐the‐loop jamming experiments of complex outdoor and mobile site‐specific scenarios. Random forests classifiers are trained based on over‐the‐air collected data and integrated into the platform. The mitigation system is evaluated for both over‐the‐air and ray‐tracing emulated environments. The experimental results highlight the benefit of using the jamming mitigation system in the presence of active jamming attacks

The Preparation and Properties of Zinc Coordination Complexes of Poly(4-Vinylpyridine-co-n-Butyl Methacrylate) Copolymers

Two poly(4-vinylpyridine-co-n-butyl methacrylate) copolymers containing 14.2 and 30.0 mo!% of 4-vinylpyridine residues were prepared by free radical copolymerization reactions. Insoluble complexes were obtained for each copolymer by reaction with zinc chloride. The coordination complexes obtained had a molar ratio of 4-vinylpyridine residues to zinc atoms close to 2 in both cases. The rheological behavior of each of these complexes has been compared to that of the corresponding metal-free copolymers, which were recovered by decomplexation. The metal com­plexed polymers exhibited much higher glass transition temperatures and much longer high temperature relaxation times than the corresponding uncomplexed copolymers

Hemolytic-uremic syndrome: Etiopathogenesis, diagnostics and basic principles of treatment

© 2015, Serbian Medical Society. All Rights Reserved. Hemolytic uremic syndrome (HUS) is a clinical syndrome that is manifested by thrombocytopenia, hemolytic anemia and acute renal failure. A typical HUS is caused by the action of verotoxin on endothelial cells of small blood vessels of the kidneys and the brain. The disorder of regulation of the alternative pathway of the complement system (mutations of genes for proteins that regulate the activity of the alternative complement system, antibodies to the complement factor H) plays the main role in the pathogenesis of atypical HUS. The disease is clinically manifested by symptoms and signs of damage to the kidneys and brain. The diagnosis of HUS is set on the basis of the reduced number of platelets, microangiopathic hemolytic anemia (negative Coombs test, decreased haptoglobin concentration, increased serum total bilirubin and lactate dehydrogenase, the number of schizonts in peripheral blood smear) and increased creatinine concentration in serum. To distinguish the typical from the atypical HUS it is necessary to perform microbiological examination chairs, measured titer anti-verotoxin antibodies and anti-lipopolysaccharide-antibodies and determine the activity of the enzyme ADAMTS13 (mutations in ADAMTS13, anti-ADAMTS13 antibody) and examine the activity of the alternative pathway of the complement system (C3 component of complement, the complement factor H. I, B, expression of MCP on mononuclear cells from peripheral blood. anti-CFH-antibodies). Patients with typical HUS infection are treated with solutions for infusion, antibiotics that do not increase the release of verotoxin dialysis and supportive therapy. In patients with atypical HUS, a therapeutic plasmapheresis is a first-line process, while in patients where there is resistance or dependence of applied plasmapheresis the blocker of the C5 component of complement (eculizumab) is used

Erythropoietin Resistance in Hemodialysis Patients

© 2019 Saša Jacović et al., published by Sciendo. Anemia is defined as blood hemoglobin concentration of less than 120 g/l in women and less than 130 g/l in men. The main cause of the development of anemia in patients treated with regular hemodialysis is the lack of endogenous erythropoietin, and its main clinical consequences are: progressive decline in residual renal function, development of cardiovascular disorders, disorders of cognitive functions and a decrease in the quality of life of these patients. Despite the administration of an appropriate dose of erythropoietin, in 5-10% of patients treated with regular hemodialysis, there is resistance to erythropoietin activity. The main risk factors for the development of resistance to the effects of erythropoietin are: iron deficiency, microinflammation, deficiency of vitamin D, secondary hyperparathyroidism, deficiency of vitamin C, and inadequate hemodialysis. The main side effects of erythropoietin are: hypertension, thrombosis of the vascular approach to hemodialysis, and the red blood cell precursor aplasia in the bone marrow. Early detection and elimination of risk factors, optimization and indi-vidualization of hemodialysis prescription prevent the development of resistance to erythropoietin activity, enable the achievement of target blood hemoglobin, reduce the development of cardiovascular morbidity, and improve the quality of life of these patients

Acute kidney damage: Definition, classification and optimal time of hemodialysis

© 2019, University of Kragujevac, Faculty of Science. All rights reserved. Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated