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Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease?
TLDR
It is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension and to design human studies to address this controversy.
Uric Acid Induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress
TLDR
It is shown that fructose also stimulates triglyceride synthesis via a purine-degrading pathway that is triggered from the rapid phosphorylation of fructose by fructokinase, which provides new insights into the pathogenesis of hepatic fat accumulation under normal and diseased states.
The current state of poststreptococcal glomerulonephritis.
TLDR
Poststreptococcal glomerulonephritis is one of the oldest recognized renal diseases and prognosis is excellent in children but significantly worse when it occurs in elderly individuals and in populations that present other risk factors of chronic kidney disease.
Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats.
TLDR
These studies provide a potential mechanism by which hyperuricemia can mediate hypertension and renal disease and partially prevented arteriolopathy and glomerular hypertension associated with significantly less infiltration of CD5+ cells.
Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice
TLDR
By reducing the amount of fructose for metabolism in the liver, fructokinase A protects against fructkinase C-mediated metabolic syndrome, providing insights into the mechanisms by which fructose causes obesity and metabolic syndrome.
The role of uric acid in the pathogenesis of human cardiovascular disease
TLDR
Uric acid may also have emerging roles in the pathogenesis of kidney disease, metabolic syndrome and diabetes and more studies need to be performed on the pathophysiology and clinical consequences of hyperuricaemia in cardiovascular disease.
Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all.
TLDR
The mechanisms involved in the hypertensive effects of oxidant stress and tubulointerstitial inflammation, in particular intrarenal ANG II activity, are discussed, focusing on their potential for sodium retention.
Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.
TLDR
This review provides an explanation of how initially subtle renal injury promotes a tendency toward hypertension, and how decreasing salt intake ameliorates the hypertension.
Mechanisms of Disease: oxidative stress and inflammation in the pathogenesis of hypertension
TLDR
Observations indicate that oxidative stress, inflammation and arterial hypertension participate in a self-perpetuating cycle which, if not interrupted, can lead to progressive cardiovascular disease and renal complications.
Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Development of Fatty Liver
TLDR
It is shown in human hepatocytes that uric acid up-regulates KHK expression thus leading to the amplification of the lipogenic effects of fructose, which markedly blocked fructose-induced triglyceride accumulation in hepatocytes in vitro and in vivo.
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