[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.]

[Hantaviruses are widespread infectious agents carried by different rodent species. The majority of them belongs to viral zoonotic pathogens, sometimes causing severe human infections. Hantaviruses inflict hemorrhagic fever with renal syndrome in Eurasia and supposedly in Africa, and hantavirus cardio-pulmonary syndrome in the Americas. The relationship between the virus and its host species is a result of a several million year co-evolution. Although virus replication is most intense in the infected rodents' lungs, these animals do not develop disease, instead they carry and spread the pathogens throughout their lifetime by body fluids. In the majority of infections, the virus gets into the human body by vaporization of rodent body fluids or by direct contact. In Europe, Puumala (PUUV) and Dobrava-Belgrade (DOBV) hantaviruses are the most abundant hantaviral infectious agents. There are numerous studies described the presence of different genotipes of hantaviruses circulating in Hungary. Although the number of clinical and epidemiolgical studies are limited, the medical importance - especially in a high risk population - of these viruses are unqustionable. There are a variety of methods to identify hantaviral infections. Molecular biological methods (RT-PCR) - also enabling genotyping - and virus neutralization tests proved to be the most reliable tools. The latter technique requires virus culturing, which can only be carried out in high-containment laboratories.]

[The author summarizes knowledge about Reynolds risk assessment system based on data of references and own experiences. The first part of article is about how the results of study of pathogenesis of atherosclerosis were converted into new risk assessment systems. One result of this process is the Reynolds system wich is consisted of traditional riks factors, high sensitive C-reactive protein and the patients’ family medical history. He demonstrates essence of Reynolds system and process of it’s validity. The author deals with comparison of Reynolds system with other traditional risk assessment systems. The practical issues of application of Reynolds system are detailed in the conclusion of the article.]

[Objectives: To evaluate a possible link between serum uric acid (SUA) levels, arterial stiffness and atherogenic index of plasma on one hand and renal function on the other and to test the role of SUA in the assessment of total cardiovascular risk. Materials and methods: We studied serum uric acid levels (SUA) in 1975 subjects included in SEPHAR II survey. We measured arterial stiffness parameters, calculated atherogenic index of plasma and estimated glomerular filtration rate (eGFR) by MDRD and CKD-EPI formulae and assessed total cardiovascular risk according to current ESH-ESC risk stratification chart. Results: The highest SUA values were recorded in subjects with grade III HT and were correlated with increased arterial stiffness and with increased atherogenic index of plasma. The lowest eGRF values, assessed by both MDRD and CKD-EPI, were observed among subjects with hyperuricemia and a significant indirect correlation between SUA and eGFR was evidenced. A proportional correlation between SUA values and total CV risk was also obtained. Conclusions: The study supports SUA implication in the pathogenesis of elevated blood pressure and the role of uric acid as a cardiovascular risk factor, particularly for the development of hypertension and renal disease.]