1,720,975 research outputs found
[Hyperuricemia, diabetes and hypertension]
No full textHyperuricemia is frequently found in association with several condition predisposing to cardiovascular events such as arterial hypertension and diabetes mellitus. This has led researchers to investigate possible pathogenetic mechanisms underlying this association. Several experimental studies and some indirect clinical evidence support a causal link between mild hyperuricemia and the developement of hypertension as well as new onset diabetes. At the tissue level, chronic exposure to increased uric acid has been shown to promote vascular changes leading to renal ischemia as well as stimulation of the renin angiotensin system. Furthermore, uric acid has been shown to promote the development of insulin resistance, hypertrglyceridemia and haepatic steatosis through pro-oxidative mechanisms. These experimental pathophysiological changes may be partly preventable by hypouricemic treatments. Whether clinical implications of these findings are confirmed by solid clinical intervention trials, mild hyperuricemia may soon change its status from risk predictor to treatment target for patients at high cardiovascular and renal risk
The uric acid cardio-nephropathy - La cardionefropatia da acido urico
No full textL’acido urico è un prodotto del catabolismo delle purine che si forma grazie all’enzima xantina-ossidasi
ed è eliminato prevalentemente a livello renale. L’urato può avere un effetto sia anti- che
pro-ossidante a seconda delle diverse condizioni biologiche e dei cofattori presenti. Nuove evidenze
suggeriscono che l’iperuricemia lieve asintomatica può avere un ruolo nello sviluppo di ipertensione,
malattia renale e rischio cardiovascolare. I meccanismi patogenetici alla base della relazione
tra acido urico e danno vascolare sono molteplici. L’aumento dei livelli di acido urico può indurre
disfunzione endoteliale, stress ossidativo con riduzione della produzione di ossido nitrico e vasocostrizione,
stimolare i processi infiammatori e l’attività del sistema renina-angiotensina.Questi meccanismi
agiscono a livello delle cellule endoteliali, dei vasi renali, delle cellule tubulari e dei cardiomiociti,
portando allo sviluppo di ipertensione, aterosclerosi e disfunzione miocardica. Attualmente,
l’acido urico non è più considerato uno spettatore “innocente” ma piuttosto un possibile fattore di
rischio per lo sviluppo di patologie renali e cardiovascolari. È stato infatti dimostrato che l’iperuricemia,
anche moderata, è associata allo sviluppo ed alla progressione di malattia renale cronica ed
ipertensione arteriosa. Studi preliminari sembrano suggerire che la riduzione dell’iperuricemia con
farmaci inibitori della xantina-ossidasi possa portare benefici in termini di mortalità cardiovascolare
e renale. I numerosi trial attualmente in corso, soprattutto con allopurinolo e febuxostat potranno
chiarire questo aspetto.Uric acid is a product of purine catabolism formed by the activity of xanthine-oxidase and prevalently excreted by the kidney. In vivo, urate is known to have both an anti- or pro-oxidant role depending on several biological conditions. New evidence suggests that chronic hyperuricemia can contribute to hypertension development, kidney disease and cardiovascular risk. The pathophysiologic mechanisms are various, such as endothelial dysfunction and oxidative stress, vasoconstriction and stimulation of renin angiotensin system. These processes act at the kidney level, within arterioles and tubular cells, as well as at the systemic vasculature and tissue level causing hypertension, atherosclerosis and myocardial dysfunction. In recent years evidence has grown that asymptomatic hyperuricemia is a possible risk factor for the development of hypertension, diabetes as well as renal and cardiovascular events. Preliminary clinical evidence suggests that lowering uric acid levels by the use of xanthine-oxidase inhibitors may improve cardiovascular and renal risk. Several ongoing trials, both with allopurinol and febuxostat, will clarify this issue in the upcoming years
[Hyperuricemia and renal risk]
No full textRecent studies have revealed an association between elevated levels of uric acid and conditions correlated to chronic kidney diseases such as hypertension, cardiovascular and cerebral disease, insulin resistance. Several pathogenetic mechanisms at cellular and tissue levels could justify a direct correlation between serum uric acid levels and renal damage. Growing evidence indicating a correlation between urate lowering therapy and renal morbidity could encourage the use of urate lowering therapy in primary or secondary prevention in chronic kidney disease
Hyperuricemia and renal risk - Iperuricemia e rischio renale
No full textRecent studies have revealed an association between elevated levels of uric acid and conditions correlated to chronic kidney diseases such as hypertension, cardiovascular and cerebral disease, insulin resistance. Several pathogenetic mechanisms at cellular and tissue levels could justify a direct correlation between serum uric acid levels and renal damage. Growing evidence indicating a correlation between urate lowering therapy and renal morbidity could encourage the use of urate lowering therapy in primary or secondary prevention in chronic kidney disease
[Hyperuricemia, diabetes and hypertension]
No full textHyperuricemia is frequently found in association with several condition predisposing to cardiovascular events such as arterial hypertension and diabetes mellitus. This has led researchers to investigate possible pathogenetic mechanisms underlying this association. Several experimental studies and some indirect clinical evidence support a causal link between mild hyperuricemia and the developement of hypertension as well as new onset diabetes. At the tissue level, chronic exposure to increased uric acid has been shown to promote vascular changes leading to renal ischemia as well as stimulation of the renin angiotensin system. Furthermore, uric acid has been shown to promote the development of insulin resistance, hypertrglyceridemia and haepatic steatosis through pro-oxidative mechanisms. These experimental pathophysiological changes may be partly preventable by hypouricemic treatments. Whether clinical implications of these findings are confirmed by solid clinical intervention trials, mild hyperuricemia may soon change its status from risk predictor to treatment target for patients at high cardiovascular and renal risk
[Hyperuricemia and renal risk]
No full textRecent studies have revealed an association between elevated levels of uric acid and conditions correlated to chronic kidney diseases such as hypertension, cardiovascular and cerebral disease, insulin resistance. Several pathogenetic mechanisms at cellular and tissue levels could justify a direct correlation between serum uric acid levels and renal damage. Growing evidence indicating a correlation between urate lowering therapy and renal morbidity could encourage the use of urate lowering therapy in primary or secondary prevention in chronic kidney disease
Renin–angiotensin–aldosterone system blockade in chronic kidney disease: current strategies and a look ahead
No full textThe Renin–Angiotensin–Aldosterone System (RAAS) is profoundly involved in the pathogenesis of renal and cardiovascular organ damage, and has been the preferred therapeutic target for renal protection for over 30 years. Monotherapy with either an Angiotensin Converting Enzime Inhibitor (ACE-I) or an Angiotensin Receptor Blocker (ARB), together with optimal blood pressure control, remains the mainstay treatment for retarding the progression toward end-stage renal disease. Combining ACE-Is and ARBs, or either one with an Aldosterone Receptor Antagonist (ARA), has been shown to provide greater albuminuria reduction, and to possibly improve renal outcome, but at an increased risk of potentially severe side effects. Moreover, combination therapy has failed to provide additional cardiovascular protection, and large prospective trials on hard renal endpoints are lacking. Therefore this treatment should, at present, be limited to selected patients with residual proteinuria and high renal risk. Future studies with novel agents, which directly act on the RAAS at multiple levels or have a more favourable side effect profile, are greatly needed to further explore and define the potential for and the limitations of profound pharmacologic RAAS inhibition
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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