Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation (original) (raw)
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Seminars in Nephrology, 2020
Kidney disease, especially when it is associated with a reduction in eGFR, can be associated with an increase in serum urate (uric acid), suggesting that hyperuricemia in subjects with kidney disease may be strictly a secondary phenomenon. Mendelian randomization studies that evaluate genetic scores regulating serum urate also have generally not found evidence that serum urate is a causal risk factor in chronic kidney disease. Nevertheless, this is countered by a large number of epidemiological, experimental, and clinical studies that suggest a potentially important role for Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
High Blood Pressure & Cardiovascular Prevention
The relationship between Serum Uric Acid (UA) and Cardiovascular (CV) diseases has already been extensively evaluated, and it was found to be an independent predictor of all-cause and cardiovascular mortality but also acute coronary syndrome, stroke and heart failure. Similarly, also many papers have been published on the association between UA and kidney function, while less is known on the role of UA in metabolic derangement and, particularly, in metabolic syndrome. Despite the substantial number of publications on the topic, there are still some elements of doubt: (1) the better cutoff to be used to refine CV risk (also called CV cutoff); (2) the needing for a correction of UA values for kidney function; and (3) the better definition of its role in metabolic syndrome: is UA simply a marker, a bystander or a key pathological element of metabolic dysregulation?. The Uric acid Right for heArt Health (URRAH) project was designed by the Working Group on uric acid and CV risk of the Italian Society of Hypertension to answer the first question. After the first papers that individuates specific cutoff for different CV disease, subsequent articles have been published responding to the other relevant questions. This review will summarise most of the results obtained so far from the URRAH research project.
Hyperuricemia and Hypertension, Coronary Artery Disease, Kidney Disease: From Concept to Practice
International Journal of Molecular Sciences, 2020
Since the publication of the Framingham Heart Study, which suggested that uric acid should no longer be associated with coronary heart disease after additional adjustment for cardiovascular disease risk factors, the number of publications challenging this statement has dramatically increased. The aim of this paper was to review and discuss the most recent studies addressing the possible relation between sustained elevated serum uric acid levels and the onset or worsening of cardiovascular and renal diseases. Original studies involving American teenagers clearly showed that serum uric acid levels were directly correlated with systolic and diastolic pressures, which has been confirmed in adult cohorts revealing a 2.21-fold increased risk of hypertension. Several studies involving patients with coronary artery disease support a role for serum uric acid level as a marker and/or predictor for future cardiovascular mortality and long-term adverse events in patients with coronary artery di...
Current medical research and opinion, 2017
Hyperuricemia has long been known to cause gout, and has recently been correlated with cardiovascular disease, hypertension, and renal disease. In the last few years, several large clinical studies have confirmed that hyperuricemia is a significant and independent risk factor for hypertension, ischemic heart disease, and heart failure, after an extensive adjustment for almost all the possible confounding conditions. This article reviews published literature on the subject, and describes ongoing studies on the use of urate-lowering therapy for cardiovascular and renal diseases.
American Journal of Kidney Diseases, 1999
An elevated uric acid level is associated with cardiovascular disease. Hyperuricemia is predictive for the development of both hypertension and coronary artery disease; it is increased in patients with hypertension, and, when present in hypertension, an elevated uric acid level is associated with increased cardiovascular morbidity and mortality. Serum uric acid level should be measured in patients at risk for coronary artery disease because it carries prognostic information. Hyperuricemia is caused by decreased renal excretion. In this article, we suggest that this may be mediated by intrarenal ischemia with lactate generation and the inhibition of the secretion of urate by the anion-exchange transport system. The possibility that hyperuricemia directly contributes to cardiovascular or renal disease needs to be reconsidered. Although hyperuricemia is associated with a number of cardiovascular or renal risk factors, several studies have found uric acid level to be independently associated with increased mortality by multivariate analysis. If hyperuricemia is directly toxic, the most likely site is the kidney. Chronic hyperuricemia is strongly associated with chronic tubulointerstitial disease, and many of these patients have decreased renal function. Although it is possible that the hyperuricemia could simply be the consequence of the renal disease, further studies are necessary to rule out a pathogenic role for uric acid in the development of renal disease and salt-dependent hypertension. 1999 by the National Kidney Foundation, Inc.
Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?
Hypertension, 2003
Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal disease. Thus, 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.
Journal of Evidence-Based Medicine, 2019
Introduction: Current data on the role of hyperuricemia as a risk factor for renal progression in patients with hypertension is inconclusive. This study aimed to assess the association of uric acid and chronic kidney disease (CKD) in hypertensive patients using a nationwide patient sample. Methods: We conducted a nationwide cross-sectional study based on the DM/HT study of the Medical Research Network of the Consortium of Thai Medical Schools. This study evaluated adult patients with hypertension from 831 Thailand public hospitals in the year 2014. Serum uric acid (SUA) was categorized into quintiles (≤4.5, 4.6 to 5.4, 5.5 to 6.2, 6.3 to 7.4, ≥7.5 mg/dL). CKD was defined as estimated glomerular filtration rate of ≤ 60 mL/min/1.73 m 2. Multivariate logistic regression was performed to assess the association between SUA and CKD using uric acid of ≤4.5 mg/dL as the reference group. Results: A total of 9776 hypertensive patients with available SUA were included in the analysis. The mean SUA was 6.1±1.8 mg/dL. The prevalence of CKD in hypertensive patients was 31.8%. SUA of 4.6 to 5.4, 5.5 to 6.2, 6.3 to 7.4, and ≥7.5 mg/dL were associated with an increased CKD with ORs of 1.57 (95% CI 1.28 to 1.92), 2.15 (95% CI 1.74 to 2.66), 3.31 (95% CI 2.72 to 4.04), and 7.11 (95% CI 5.76 to 8.78), respectively. The restricted cubic spline showed significant increased CKD prevalence when uric acid ≥4.6 mg/dL. Conclusion: Higher SUA was associated with increased CKD prevalence in patients with hypertension. SUA should be monitored in hypertensive patients for CKD prevention.
Associations between Hyperuricemia and Chronic Kidney Disease: A Review
Nephro-Urology Monthly, 2015
In human beings, uric acid is the poorly soluble circulating end product of the purine nucleotide metabolism. A reduction in the glomerular filtration rate (GFR) contributes to hyperuricemia, which is frequently observed in patients with chronic kidney disease (CKD). Evidence Acquisition: Hyperuricemia is defined as a serum uric acid level > 7.0 mg/dL in males and > 6.0 mg/dL in females, while CKD is defined as kidney damage or a GFR < 60 mL/min/1.73 m 2 for 3 months or more, irrespective of the cause. Hyperuricemia is common in CKD and may occur because of decreased excretion, increased production, or a combination of both mechanisms. Results: The causes for hyperuricemia in overproducers may be either exogenous or endogenous. CKD has become a global public health problem because of its high prevalence and the accompanying increase in the risk of end-stage renal disease, cardiovascular disease, and premature death. The most common risk factors for CKD are obesity and the metabolic syndrome, which is strongly associated with hyperuricemia probably as a consequence of insulin resistance and the effects of insulin to reduce the urinary urate excretion. For recurring bouts of hyperuricemia or gout, patients should have a blood test and joint fluid test to determine whether the medication taken is effective. Interventional studies are a useful clinical research tool in clarifying the role of hyperuricemia in CKD. Conclusions: Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy. Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.