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Marilda Mazzali - One of the best experts on this subject based on the ideXlab platform.
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Uric Acid and transplantation.
Seminars in nephrology, 2011Co-Authors: Fernanda Cristina Mazali, Marilda MazzaliAbstract:HyperUricemia is a common complication in organ transplant recipients, with a higher incidence in kidney and heart recipients. Risk factors for post-transplant hyperUricemia include reduced glomerular filtration rate, diuretic use, cyclosporine therapy, increasing age at transplant, obesity, and metabolic syndrome, as well as the presence of pretransplant hyperUricemia. The impact of hyperUricemia in patient and graft survival is unclear because Uric Acid only recently has been considered a risk factor for cardiovascular disease and graft survival. The effect of Uric Acid on graft function remains controversial, with studies suggesting that Uric Acid is an independent risk factor for chronic allograft dysfunction, contrasting with other studies suggesting that hyperUricemia is only a marker of reduced glomerular filtration rate. Strategies to reduce Uric Acid levels include reduction or avoidance of cyclosporine treatment, adequacy of antihypertension treatment, avoidance of diuretics, nutritional management, and use of Uric Acid-lowering agents. In this article, we review the incidence and risk factors for the development of post-transplant hyperUricemia, the effect of different immunosuppressive regimens in Uric Acid handling, and recent results from studies comparing Uric Acid levels and renal function in organ transplant recipients that try to identify which comes first: hyperUricemia or chronic allograft dysfunction?
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Uric Acid and Hypertension: Cause or Effect?
Current Rheumatology Reports, 2010Co-Authors: Marilda Mazzali, Daniel I. Feig, Diana Jalal, Mehmet Kanbay, Mark S. Segal, Mohamed Shafiu, Richard J. JohnsonAbstract:Uric Acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, Uric Acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that Uric Acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which Uric Acid could initiate this response. It remains possible that Uric Acid is a marker for xanthine oxidase–associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that Uric Acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperUricemia might delay the development of essential hypertension.
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Uric Acid and hypertension.
Current hypertension reports, 2006Co-Authors: Daniel I. Feig, Duk-hee Kang, Takahiko Nakagawa, Marilda Mazzali, Richard J. JohnsonAbstract:Epidemiologic studies published during the past 3 years support the possible role of Uric Acid in the onset of essential hypertension. Data from several large, longitudinal cardiovascular disease studies indicate that elevated serum Uric Acid is a predictor of incident hypertension and blood pressure progression. In a pediatric study, more than 90% of children with essential hypertension have serum Uric Acid levels above 5.5 mg/dL. During the same period, laboratory studies have provided compelling mechanistic evidence to explain the clinical observations. Uric Acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. Ongoing clinical trials will elucidate the role of Uric Acid in human hypertension and will determine whether control of Uric Acid may be a new way to prevent or treat essential hypertension.
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Uric Acid--a uremic toxin?
Blood purification, 2005Co-Authors: Takahiko Nakagawa, Duk-hee Kang, Marilda Mazzali, L. Gabriela Sanchez-lozada, Jaime Herrera-acosta, Richard J. JohnsonAbstract:Uric Acid might often be regarded as a simple marker of renal disease. Although it is well known that hyperUricemia causes gout which is associated with renal insufficiency and cardiovascular disease, one might think that it could attribute to the intrarenal urate crystal, but not to Uric Acid per se. In order to clarify the role of Uric Acid in the kidney, we hypothesized that Uric Acid causes renal disease. To generate mild hyperUricemia without intrarenal crystal in rats, we used low doses of an Uricase inhibitor (2% oxonic Acid). HyperUricemia induced systemic hypertension, glomerular hypertrophy/hypertension, afferent arteriolar sclerosis, and macrophage infiltration in normal rat kidney. In progressive renal disease, such as cyclosporine nephropathy and remnant kidney in rat, Uric Acid accelerated the progression of renal disease. Thus, we concluded that Uric Acid is not a simple marker, but a cause of renal disease.
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Uric Acid And Transplantation
Seminars in nephrology, 2005Co-Authors: Marilda MazzaliAbstract:HyperUricemia is a common complication in organ transplant recipients, and frequently is associated with chronic cyclosporine immunosuppressive therapy. Kidney and heart transplant recipients are prone to develop posttransplant hyperUricemia. Risk factors for hyperUricemia include decreased glomerular filtration rate (GFR), diuretic use, and preexistent history of hyperUricemia. The influence of hyperUricemia in patient and graft survival is unclear because Uric Acid is not usually considered a common risk factor for cardiovascular disease that affects graft and patient survival. However, there have been small studies that have suggested that control of Uric Acid levels contributes to recovery of renal function (in heart and liver transplant recipients) and in an improvement in GFR in renal transplant recipients. Despite controversies in the need for hyperUricemia treatment in transplant patients, strategies to decrease Uric Acid levels includes a decrease or avoidance of cyclosporine treatment, adequacy of antihypertension treatment, avoidance of diuretics, nutritional management, and use of Uric Acid-decreasing agents. In this article we review the incidence and risk factors for the development of posttransplant hyperUricemia, discuss the influence of different immunosuppressive agents on Uric Acid metabolism, and suggest some alternative treatments for posttransplant hyperUricemia. We also consider that Uric Acid should be considered as a potential risk factor for renal allograft nephropathy or for renal dysfunction in nonrenal transplant recipients, as well as a comorbid factor for a decrease in patient and graft survival.
Richard J. Johnson - One of the best experts on this subject based on the ideXlab platform.
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Fructose and Uric Acid in diabetic nephropathy
Diabetologia, 2015Co-Authors: Petter Bjornstad, Richard J. Johnson, Miguel A. Lanaspa, Takuji Ishimoto, Tomoki Kosugi, Shinji Kume, Diana Jalal, David M. Maahs, Janet K. Snell-bergeon, Takahiko NakagawaAbstract:Clinical studies have reported associations between serum Uric Acid levels and the development of diabetic nephropathy, but the underlying mechanisms remain elusive. There is evidence from animal studies that blocking Uric Acid production protects the kidney from tubulointerstitial injury, which may suggest a causal role for Uric Acid in the development of diabetic tubular injury. In turn, when fructose, which is endogenously produced in diabetes via the polyol pathway, is metabolised, Uric Acid is generated from a side-chain reaction driven by ATP depletion and purine nucleotide turnover. For this reason, Uric Acid derived from endogenous fructose could cause tubulointerstitial injury in diabetes. Accordingly, our research group recently demonstrated that blocking fructose metabolism in a diabetic mouse model mitigated the development of tubulointerstitial injury by lowering tubular Uric Acid production. In this review we discuss the relationship between Uric Acid and fructose as a novel mechanism for the development of diabetic tubular injury.
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Uric Acid Metabolism and the Kidney
Chronic Renal Disease, 2015Co-Authors: Duk-hee Kang, Richard J. JohnsonAbstract:HyperUricemia and gout are common in CKD patients. This relationship has been noted since the 1800s. Over the years there has been great controversy over the biologic significance of hyperUricemia, with some individuals arguing it is a major cause of CKD, and others viewing the rise in S[UA] as strictly an epiphenomenon. During the last 10 to 15 years, interest in Uric Acid has reawakened with the realization that an elevated S[UA] can predict the development of CKD and by experimental studies that document a causal role for Uric Acid in both the development and progression of CKD. Today there is great interest in the potential that Uric Acid may represent a remediable risk factor for CKD. We provide an update on Uric Acid and the kidney, focusing both on Uric Acid metabolism and a critical evaluation of the current evidence base for Uric Acid as a risk factor for CKD.
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Uric Acid and Hypertension: Cause or Effect?
Current Rheumatology Reports, 2010Co-Authors: Marilda Mazzali, Daniel I. Feig, Diana Jalal, Mehmet Kanbay, Mark S. Segal, Mohamed Shafiu, Richard J. JohnsonAbstract:Uric Acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, Uric Acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that Uric Acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which Uric Acid could initiate this response. It remains possible that Uric Acid is a marker for xanthine oxidase–associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that Uric Acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperUricemia might delay the development of essential hypertension.
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Uric Acid and cardiovascular risk
The New England Journal of Medicine, 2008Co-Authors: Daniel I. Feig, Duk-hee Kang, Richard J. JohnsonAbstract:This review summarizes relevant studies concerning Uric Acid and possible links to hypertension, renal disease, and cardiovascular disease. Whether Uric Acid is an independent risk factor for such diseases is still a point of debate. Current evidence is presented.
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Uric Acid the oxidant antioxidant paradox
Nucleosides Nucleotides & Nucleic Acids, 2008Co-Authors: Yuri Y Sautin, Richard J. JohnsonAbstract:Uric Acid, despite being a major antioxidant in the human plasma, both correlates and predicts development of obesity, hypertension, and cardiovascular disease, conditions associated with oxidative stress. While one explanation for this paradox could be that a rise in Uric Acid represents an attempted protective response by the host, we review the evidence that Uric Acid may function either as an antioxidant (primarily in plasma) or pro-oxidant (primarily within the cell). We suggest that it is the pro-oxidative effects of Uric Acid that occur in cardiovascular disease and may have a contributory role in the pathogenesis of these conditions.
Toshikazu Hada - One of the best experts on this subject based on the ideXlab platform.
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Spot urine Uric Acid to creatinine ratio used in the estimation of Uric Acid excretion in primary gout.
The Journal of rheumatology, 2001Co-Authors: Yuji Moriwaki, Zenta Tsutsumi, Jun-ichi Yamakita, Tetsuya Yamamoto, Sumio Takahashi, Toshikazu HadaAbstract:OBJECTIVE: Uric Acid overexcretion in patients with gout is frequently assessed by the measurement of 24 hour urinary Uric Acid excretion, which is cumbersome with ambulatory patients, and requires accurate timing and complete collection of the specimen. We assessed whether Uric Acid to creatinine ratio (Uua/Ucr) in spot urine is useful for the estimation of Uric Acid overexcretion in patients with gout. METHODS: One hundred thirty male patients with gout and 33 non-gout male control subjects were studied. Early morning urine and/or a portion of 24 h collected urine (24 h urine) were used as spot urine samples. Uric Acid overexcreters were defined as those with a 24 h urinary Uric Acid excretion > or = 1000 mg/day, while Uric Acid underexcreters were defined as those with Uric Acid clearance
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Effect of urine storage on urinary Uric Acid concentrations
Annals of Clinical Biochemistry, 2000Co-Authors: Jun-ichi Yamakita, Zenta Tsutsumi, Tetsuya Yamamoto, Yuji Moriwaki, Sumio Takahashi, Toshikazu HadaAbstract:Accurate determination of serum and urinary Uric Acid concentrations is essential for the diagnosis and classification of gout according to Uric Acid metabolism derangement. Urine and/or serum samples are often kept at either 4°C or -20°C until assayed, when a large number of samples are handled simultaneously. Our preliminary study indicated a significant decrease in urinary Uric Acid concentration after preservation, regardless of the storage temperature. Uric Acid crystals were often observed in these cases which showed a marked decrease in urinary Uric Acid concentration after storage. In the present study, we sought the factor(s) that might cause this decrease in urinary Uric Acid concentration, as well as measures to overcome the problem. High urinary Uric Acid concentration and low pH proved to play major roles in the decrease in urinary Uric Acid concentration after storage. In contrast, dilution of the urine samples before storage resulted in no significant change in urinary Uric Acid concentration. Based on these results, we recommend diluting urine before storage for determination of Uric Acid concentration and avoiding underestimation.
Michael A. Linshaw - One of the best experts on this subject based on the ideXlab platform.
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Uric Acid Crystals
The New England journal of medicine, 1994Co-Authors: F. Bruder Stapleton, Michael A. LinshawAbstract:Figure 1. Uric Acid Crystals. Typical Uric Acid crystals from fresh, centrifuged urinary sediment are shown through polarized light (x400).
S. Mantalenakis - One of the best experts on this subject based on the ideXlab platform.
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Acute Uric Acid nephropathy in pregnancy.
Obstetrics & Gynecology, 1992Co-Authors: E. Alexopoulos, P. Tampakoudis, Bili H, S. MantalenakisAbstract:BACKGROUND Although Uric Acid clearance increases during gestation, Uric Acid nephropathy is a rare cause of acute renal failure in the pregnant woman. CASE A 38-year-old woman experienced acute renal failure due to acute Uric Acid nephropathy at 30 weeks' gestation. The diagnosis was based on extreme hyperUricemia and an elevated Uric Acid-creatinine ratio. Treatment with forced diuresis, urine alkalinization, and mannitol infusion resulted in a prompt and complete recovery of renal function. The woman ultimately gave birth to a healthy child. CONCLUSION Acute Uric Acid nephropathy during pregnancy responds to conventional medical therapy.
