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Hypertension and nephrology

FEBRUARY 20, 2020

Clinical Oncology

SEPTEMBER 10, 2017

[Challenges in Molecular Targeted Therapy for Gastric Cancer: Considerations for Effi cacy and Safety]

KEI Muro

[The Cancer Genome Atlas Research Network recently proposed a molecular classifi cation for gastric cancer (GC) into four subtypes based on comprehensive evaluation. While the mechanisms of molecular targeted therapies in GC were confi rmed by multiple clinical studies, only a limited number of therapeutics for GC have been approved to date. In this systematic review of the available literature, we discuss the completed and ongoing clinical trials of molecular targeted therapies in patients with GC, with a focus on their effi cacy and safety. Results of recent studies clearly demonstrated that trastuzumab and ramucirumab, monoclonal antibodies (mAbs) against human epidermal growth factor receptor 2 (HER2) and vascular endothelial growth factor (VEGF), respectively, improved overall survival (OS) in GC with manageable safety profi les. Careful surveillance of ongoing clinical trials and timely profi ling and monitoring of genetic signatures are imperative to establish a strong foundation for precision medicine in GC.]

Hypertension and nephrology

DECEMBER 20, 2016

[Deeper analysis of nebivolol effects]


[Author presents the formation of nitric oxide as a largest vasodilator of human endothelium as well as the endothelial dysfunction a result of formation at adrenergic stimulus. He demonstrates in detail the benefits of selective β-1 blocker and β-3 adrenergic agonist nebivolol in the vascular system. This drug has also receptor independent effects. Complex effects of nebivolol causes vasodilation, inhibits oxidative stress and it is capable to neutralize the effects of free oxygen radicals and as a result the endothelial function will be better. Its clinical effects and the less wellknown beneficial properties are listed. The use of drug is discussed especially in hypertensives with smoking, COPD or PAD. The β-3 agonist effect provides positive reactions not only in the adipocytes and the myocardial tissue. but in the skeletal muscle as well: Increase in energy expenditure - as a compensatory mechanism - is increased in obesity and the glucose uptake + storage on skeletal muscle cells are increased in hyperglycemia. The insulin sensitivity will be better, leptin level is decreased, adiponectin level is increased by nebivolol. It is assumed this drug has antidiabetic and anti-obesity effects.]

Hypertension and nephrology

SEPTEMBER 10, 2016

[A new, effective tool in the treatment of hypertension in light of the available evidence]

MASSZI Gabrilella

[Hypertension is important even in the group of common diseases. Cardiovascular mortality could be significantly reduced if high blood pressure could not only be treated, but controlled as well. The newly introduced fixed combination perindopril-amlodipin-indapamide medication could be a good tool for genereal practitioners, specialists in internal medicine and cardiologists. Combined treatment with the ACE inhibitor perindopril, the new vasorelaxant type diuretic indapamide and the third generation type Ca-chanel blocker amlodipin is effective in reducing blood pressure. Besides effectivity the organ protective pleiotrop qualities (cardioprotective, plakk stabilising, antiatherosclerotic, antithrombotic, stroke preventive, endothel dysfunction reducing, renal protetcion granting) provide a long lasting beneficial impact on life expectancy and a better quality of life to the patients. If we choose the right dosage, we could raise the compliance level of patients resulting in excellent degrees of compliance. In our article we wanted to draw attention to the major evidencies which are the best acknowledgements of this triple combination although we didn’t explore all avenues.]

Hypertension and nephrology

SEPTEMBER 20, 2014

[Visualization of glomerular filtration in animals in vivo - significant filtration in afferent arteriola. Regulation of endothelial permeability]


[Recently we have in vivo visualized glomerular filtration and fluid flow from the JGA portion of afferent arteriole into JGA using intravital multiphoton microscopy. Fluorescence of the extracellular fluid marker lucifer yellow appeared in the interstitium around the distal portion of afferent arteriole before the filtration into Bowman's capsule. In isolated microperfused JGA we demonstrated fluid movement from the glomerulus into the MD tubule. All these prove that there is a significant and dynamic fluid flow exists in the JGA. Angiotensin II similar to VEGF plays a role in regulation of permeability/fenestration formation. Angiotensin II acts through AT1 receptor and PV-1 protein synthesis.]

Hypertension and nephrology

DECEMBER 30, 2012

[Molecular mechanisms leading to renal fibrosis: the origin of myofibroblasts]

HIMER Leonóra, SZIKSZ Erna, KOVÁCS S. Krisztián, ÓNODY Anna, Reusz Anna, REUSZ György, FEKETE Andrea, TULASSAY Tivadar, VANNAY Ádám

[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]

Hypertension and nephrology

DECEMBER 22, 2011

[The importance of white-coat hypertension in adolescents]

LENGYEL Szabolcs, SZÁNTÓ Ildikó, KATONA Éva, PARAGH György, FÜLESDI Béla, PÁLL Dénes

[The importance of adolescent hypertension is that there is tight correlation between blood pressure data in adolescents and in adulthood. In case of sustained adolescent hypertension increase of the left ventricular mass and the intima-media thickness of the carotid artery is also detected. The prevalence of adolescent hypertension is about 1-4%. Among them 1-41% is the frequency of white-coat hypertension. Diagnosis can be set up with repeated measurements at home, or with ambulatory blood pressure monitoring. In the background of adolescent white-coat hypertension the increased sympathetic activity has outstanding importance, which causes endothel dysfunction and increased arterial stiffness. There are growing evidence, that adolescent white coat hypertension is not a harmless condition, because sustained hypertension can develop in the future. In its case risk survey, start of non-pharmacological treatment, and follow-up has major importance.]

Lege Artis Medicinae

OCTOBER 20, 2011

[Pulmonary arterial hypertension in systemic autoimmune diseases]

VÉGH Judit, ZEHER Margit

[Pulmonary arterial hypertension is a rare disease, but it occurs more often in systemic autoimmune diseases, where it represents one of the most severe, life-threatening complications. Its development is due to an immunoregulatory disorder characteristic to systemic diseases, persistent inflammation and the subsequent endothelial dysfunction, the presence of pathogenic autoantibodies, smooth muscle cell dysfunction and complex angiogenetic disorder. As a consequence of endothelial cell dysfunction, the balance between regulatory factors of vasoconstriction and vasodilation is disrupted. Intimal hyperplasia, endothelial cell proliferation, media hypertrophy and local thrombus formation can be observed and one of the main pathomorphological characteristic features, plexiform lesion develops, leading to obliterative vasculopathy. A more severe form of the disease develops in systemic sclerosis, which is explained by the main pathophysiological elements of scleroderma, namely immunoregulatory disorder, vasculopathy and fibroblast dysfunction. It is not easy to monitor the disease in these cases, because the deterioration can be caused by many other factors as well. Therefore, beseides the usual examinations, biomarkers and screening methods have a significant role. Treatment is not simple either, since no wellapplicable algorithms are available. In many disorders (systemic lupus erythematosus, mixed connective tissue disease, rheumatoid arthritis), effective immunosuppressive therapy started in time is crucial, whereas in case of systemic sclerosis, the principles of therapy applied for the idiopathic form should be followed.]

Lege Artis Medicinae

JULY 20, 2004



[The author presents a review about the fundamental principles of normal endothelial function and the main causes for the development of endothelial dysfunction. First of all, endothelial dysfunction results in structural alterations in the wall of the vessel - the „vascular remodelling” in hypertension - and that is the base of hypertensive microangiopathy and target organ damage. In patients with high blood pressure the reactivity of vessels is impaired by the endothelial dysfunction. The members of the main drug groups can influence the vasoactive factors produced in endothelium differently. This different effects of drugs create different clinical benefits. Especially, the ACE inhibitors, the calcium antagonists (mostly the new generation of dihydropyridines) have endothelial protective effects, but some β-blockers, α-1 adrenergic blockers and - in a totally different way of action - the statins are capable of influencing the endothelial dysfunction.]

Lege Artis Medicinae

JUNE 21, 2006


FARKAS Katalin

[Dyslipidaemia is one of the known main risk factors of atherosclerosis by causing endothelial dysfunction that initiates and promotes vascular remodelling. Recent data from experimental and clinical studies suggest the existence of lipoprotein- neurohormonal interactions that may adversely affect vascular structure and function. Elevated lipid levels enhance the activation of the renin-angiotensin system, and, on the other hand, activation of the renin-angiotensin system leads to increased LDL cholesterol biosynthesis and oxidized-LDL uptake. These findings may explain the synergistic effect on cardiovascular risk observed in patients with coexisting hypertension and dyslipidaemia. The combined use of cholesterol-lowering drugs and inhibition of the tissue renin-angiotensin system may be more efficient in reducing cardiovascular risk.]