We have located links that may give you full text access.
The Pathophysiology of Uric Acid on Renal Diseases.
BACKGROUND: Asymptomatic hyperuricemia was regarded as a marker and considered secondary to some pathological conditions such as hypertension. During the last 16 years, a vast amount of experimental work has shown that uric acid can cause intracellular alterations that lead to cardiovascular, renal, and metabolic disease. Epidemiological and clinical studies support this notion in specific populations. However, the clinical studies done so far are of such a small number that it is difficult to reach a consensus in regard to the benefit of treating asymptomatic hyperuricemia.
SUMMARY: Mild hyperuricemia in rodents induces hypertension associated to renal microvascular disease, tubulointerstitial inflammation, vasoconstriction, and glomerular hypertension. The cellular mechanisms that lead to those outcomes require an increase in intracellular concentrations of uric acid inducing oxidative stress that then activates the synthesis and secretion of proinflammatory factors and vasoconstrictive substances, and diminishes the bioavailability of nitric oxide produced by eNOS. Uric acid also induces proliferation, senescence, and fat accumulation or inhibits insulin secretion, depending on the cell type. Extracellular uric acid can act as an antioxidant; however, when it crystallizes it also induces the activation of prooxidant and proinflammatory pathways resulting in renal lesion. Key Messages: Experimental evidence shows that uric acid is a true mediator for cardiovascular, renal, and metabolic diseases. However, there is still need for greater and well-controlled intervention studies in humans to define whether treating asymptomatic hyperuricemia is worthwhile or not.
SUMMARY: Mild hyperuricemia in rodents induces hypertension associated to renal microvascular disease, tubulointerstitial inflammation, vasoconstriction, and glomerular hypertension. The cellular mechanisms that lead to those outcomes require an increase in intracellular concentrations of uric acid inducing oxidative stress that then activates the synthesis and secretion of proinflammatory factors and vasoconstrictive substances, and diminishes the bioavailability of nitric oxide produced by eNOS. Uric acid also induces proliferation, senescence, and fat accumulation or inhibits insulin secretion, depending on the cell type. Extracellular uric acid can act as an antioxidant; however, when it crystallizes it also induces the activation of prooxidant and proinflammatory pathways resulting in renal lesion. Key Messages: Experimental evidence shows that uric acid is a true mediator for cardiovascular, renal, and metabolic diseases. However, there is still need for greater and well-controlled intervention studies in humans to define whether treating asymptomatic hyperuricemia is worthwhile or not.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
Perioperative echocardiographic strain analysis: what anesthesiologists should know.Canadian Journal of Anaesthesia 2024 April 11
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app