Serum Uric Acid Independently Predicts Mortality in Patients with Significant, Angiographically Defined Coronary Disease

Madsen, Troy; Muhlestein, Joseph B.; Carlquist, John F.; Horne, Benjamin D.; Bair, Tami L; Jackson, Jean; Lappé, Jason M.; Pearson, Robert R.; Anderson, Jeffrey L.

doi:10.1159/000084085

Cited by 62 publications

(51 citation statements)

References 38 publications

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“…Glycosuria, which is a pertinent diagnostic feature of diabetes, imposes dehydration via glucose osmotic dieresis [68,69,70]. In the present study, our findings showed that there was a significant decrease in the serum sodium ion concentration when compared with the normal control animals.…”

Section: Discussionsupporting

confidence: 62%

Effect of Lycopene on Altered Kidney Antioxidant Enzymes Activity and Functions in Streptozotocin-Induced Diabetic Wistar Rats

Daniel¹

2015

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Abstract:The present study assessed the effects of lycopene on kidney antioxidant enzymes activities and functions in streptozotocin-induced diabetic Wistar rats.Diabetes was induced in animals by single intra-peritoneal injection of streptozotocin. Thereafter the animals were randomly assigned into the following groups: Group I and II (Normal control + olive oil and Diabetic control + olive oil)while Group III to VI were treated with (10, 20 and 40 mg/kg of lycopene and 2 mg/kg glibenclamide) respectively. Alltreatments were givenonce daily orally for four weeks. Results obtained showed that blood glucose was significantly (P < 0.05) reduced. MDAconcentration was reduced in kidney tissue, with increased activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) in diabetic animals administered with lycopene when compared with diabetic control group.There was significant (P < 0.05) increase in the level of serum sodium ion and reduction in serum urea level in diabetic rats treated with lycopene when compared with the diabetic control group. Histological findings showed improved renal architecture as reflected by reduced glomerular and tubular necrosisin all treated groups when compared with control group. It can be concluded that lycopene protects against diabetes-induced kidney damage through elevation of endogenous antioxidant enzymes and improved renal dysfunction in diabetic animals.

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Section: Discussionsupporting

confidence: 62%

Effect of Lycopene on Altered Kidney Antioxidant Enzymes Activity and Functions in Streptozotocin-Induced Diabetic Wistar Rats

Daniel¹

2015

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“…While many have found an independent association of higher serum uric acid (SUA) concentrations with increased risk of adverse cardiovascular outcomes [1][2][3][4][5][6][7] , others have not [8][9][10] . Biological mechanisms linking hyperuricemia to CVD risk exist, but direct effects of uric acid on the vasculature remain controversial 11,12 .…”

mentioning

confidence: 99%

Serum Uric Acid Is Associated with Carotid Plaques: The National Heart, Lung, and Blood Institute Family Heart Study

Neogi

Ellison

Hunt³

et al. 2009

J Rheumatol

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Objective-To examine the association of serum uric acid (SUA) with a marker of preclinical cardiovascular disease (CVD), carotid atherosclerotic plaques (PLQ), where early evidence of risk may be evident, focusing on individuals without CV risk factors.Methods-The National Heart, Lung, and Blood Institute Family Heart Study is a multicenter study designed to assess risk factors for heart disease. PLQ were assessed with carotid ultrasound. We conducted sex-specific logistic regression to assess the association of SUA with presence of PLQ, including analyses among persons without risk factors related to both CVD and hyperuricemia.Results-In total, 4866 participants had both SUA and carotid ultrasound assessed (54% women, mean age 52 yrs, mean body mass index 27.6). The association of SUA with PLQ increased with increasing SUA levels, demonstrating a dose-response relation for men [OR 1.0, 1.29, 1.61, 1.75, for SUA categories < 5 (reference), 5 to < 6, 6 to < 6.8, ≥ 6.8 mg/dl, respectively; p = 0.002]. Similar associations were found in men without CV risk factors. We found no relation of SUA with PLQ in women. Studies examining the relation of hyperuricemia with cardiovascular disease (CVD) have had conflicting results. While many have found an independent association of higher serum uric acid (SUA) concentrations with increased risk of adverse cardiovascular outcomes 1-7 , others have not [8][9][10] . Biological mechanisms linking hyperuricemia to CVD risk exist, but direct effects of uric acid on the vasculature remain controversial 11,12 . Moreover, some have argued that the positive association between SUA and CVD may be due to the concurrent cardiovascular comorbidities seen in many persons with hyperuricemia, including diabetes, dyslipidemia, hypertension, and obesity [13][14][15] . Conclusion-In NIH Public AccessClarifying the relation of SUA to CVD risk has clinical implications and public health importance. First, there has been a secular increase in the incidence and prevalence of gout and hyperuricemia 16,17 . Second, asymptomatic hyperuricemia is presently not an indication for urate-lowering therapy. If hyperuricemia is indeed an independent risk factor for CVD, it might motivate a change in traditional treatment recommendations. [20][21][22][23][24][25][26] . Such conflicting results may in part be related to differences in analytic approaches and/or effectiveness of controlling for potential confounding.Further, prior studies have not examined SUA's effects in individuals who are free from comorbidities, which themselves can both increase SUA and increase risk for preclinical CVD. If SUA were associated with preclinical CVD in persons without any such comorbidities, it would constitute stronger evidence for SUA's association with CVD than has been presented in previous studies.We evaluated the association of SUA with carotid plaques in a large multicenter study, the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study, and further assessed these associations for the modifyi...

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“…35,36 Some evidence suggests that CIN may be dose dependent. Several studies [37][38][39] have indicated that lower volumes of contrast material, less than 70 mL, are associated with lower rates of CIN than are higher volumes, although conflicting reports 37 have also been published. One study 37 revealed that volumes as low as 20 mL can be associated with CIN in patients with diabetic nephropathy.…”

Section: Risk Factorsmentioning

confidence: 99%

“…Whether or not the volume of contrast material used is a risk factor for CIN remains unclear. 37,38 Higher osmolality is also associated with an increased risk for CIN, especially in patients whose fluid volume is already decreased or who have a low-flow state such as heart failure or shock. Even the newer, low-osmolality agents are associated with CIN, although the number of annual cases appears to be lower than the number when high-osmolality agents were the predominant imaging agent.…”

Section: Risk Factorsmentioning

confidence: 99%

“…The administration of sodium bicarbonate alkalinizes the urine, a change that may reduce the production and increase the neutralization of oxygen free radicals. 4,28,48 The results of several randomized controlled trials 34,38,48 have indicated that sodium bicarbonate is modestly better than 0.9% saline for hydration. Similar to the studies of hydration with isotonic saline, other trials with sodium bicarbonate hydration have had inconclusive results or have indicated no effect.…”

Section: Clinical and Laboratory Findingsmentioning

confidence: 99%

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Contrast-Induced Nephropathy in Critical Care

Wood

2012

Critical Care Nurse

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minutes before the imaging study to protect against contrast-induced nephropathy (CIN). Because of the frequency of nausea and vomiting associated with use of N-acetylcysteine, a nurse practitioner in the department suggests that the patient be given an infusion of sodium bicarbonate 150 mEq/L at a rate of 3.5 mL/kg per hour for 1 hour before the CT scan. A hospitalist who is with another patient overhears the discussion and adds that some evidence suggests that hydration with physiological saline at 1 mL/kg per hour may suffice.What is CIN and what is the best course of action for this patient? In this article, I describe CIN; the patients at risk for this abnormality; and the etiology, pathophysiology, preventive interventions, and treatments for this iatrogenic complication of imaging with contrast material. BackgroundCIN is a disorder characterized by the onset of acute renal failure within 24 to 72 hours after the administration of iodinated contrast medium. Contrast-induced nephropathy is an iatrogenic disease caused by the administration of iodinated contrast material to certain at-risk patients. The clinical features include renal failure, with oliguria, anuria, and electrolyte derangements. Contrastinduced nephropathy can prolong hospitalization, result in greater morbidity and mortality, and increase patients' costs. A variety of preventive and treatment strategies exist, including use of alternative imaging. Critical care nurses need to understand the nephropathy and the patients at risk and to develop a familiarity with prevention, treatment, and outcome. (Critical Care Nurse. 2012;32[6]:15-24) This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:1. State the pathophysiology of contrast-induced nephropathy 2. Identify patients at risk for developing contrast-induced nephropathy 3. State preventive therapies useful in high-risk patients CNEContinuing Nursing EducationA 62-year-old woman with a history of congestive heart failure and type 2 diabetes mellitus comes to the emergency department because she has had pain in the left lower quadrant of her abdomen and fever for 3 days.by AACN on May 9, 2018 http://ccn.aacnjournals.org/ Downloaded from typically asymptomatic, although a few patients experience renal dysfunction and may require dialysis. Despite its typically mild manifestations, CIN is associated with increases in hospital stays, [4][5][6] in-hospital mortality, 7,8 and 1-year mortality. 4,5,7 Lengths of stay can be twice as long as the stays of patients without CIN, 4,6 and both inpatient and 30-day mortality can be as much as 10-fold greater. 4,6,8 Several populations of patients are at risk, including patients with preexisting renal disease, congestive heart failure, and diabetes mellitus. Several treatment regimens are available to protect the kidneys during administration of contrast material. Contrast MediaContrast media are used in a wide array of medical imaging, inclu...

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Serum Uric Acid Independently Predicts Mortality in Patients with Significant, Angiographically Defined Coronary Disease

Cited by 62 publications

References 38 publications

Effect of Lycopene on Altered Kidney Antioxidant Enzymes Activity and Functions in Streptozotocin-Induced Diabetic Wistar Rats

Effect of Lycopene on Altered Kidney Antioxidant Enzymes Activity and Functions in Streptozotocin-Induced Diabetic Wistar Rats

Serum Uric Acid Is Associated with Carotid Plaques: The National Heart, Lung, and Blood Institute Family Heart Study

Contrast-Induced Nephropathy in Critical Care

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