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uric acid and progression of kidney disease

Ana Isabel Ilundain-González, José Antonio Gimeno-Orna, Daniel Sáenz-Abad, Jordi Pons-Dolset, Jesús Cebollada-Del Hoyo, María Del Carmen Lahoza-Pérez
BACKGROUND: Hyperuricemia is associated to cardiovascular disease. However, the contribution of uric acid (UA) to cardiovascular mortality in diabetic patients is controversial. OBJECTIVE: To assess the impact of UA levels on the risk of cardiovascular mortality risk in a cohort of patients with type 2 diabetes mellitus (T2DM). PATIENTS AND METHODS: A prospective cohort study on outpatients with T2DM. The clinical endpoint was cardiovascular death...
March 7, 2018: Endocrinología, Diabetes y Nutrición
Orestes Foresto-Neto, Victor Ferreira Ávila, Simone Costa Alarcon Arias, Fernanda Florencia Fregnan Zambom, Lisienny Campoli Tono Rempel, Viviane Dias Faustino, Flavia Gomes Machado, Denise Maria Avancini Costa Malheiros, Hugo Abensur, Niels Olsen Saraiva Camara, Roberto Zatz, Clarice Kazue Fujihara
Recent studies suggest that NLRP3 inflammasome activation is involved in the pathogenesis of chronic kidney disease (CKD). Allopurinol (ALLO) inhibits xanthine oxidase (XOD) activity, and, consequently, reduces the production of uric acid (UA) and reactive oxygen species (ROS), both of which can activate the NLRP3 pathway. Thus, ALLO can contribute to slow the progression of CKD. We investigated whether inhibition of XOD by ALLO reduces NLRP3 activation and renal injury in the 5/6 renal ablation (Nx) model...
March 6, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
Ambreen Gul, Philip Zager
PURPOSE OF REVIEW: Multiple experimental and clinical studies have identified pathways by which uric acid may facilitate the development and progression of chronic kidney disease (CKD) in people with diabetes. However, it remains uncertain if the association of uric acid with CKD represents a pathogenic effect or merely reflects renal impairment. RECENT FINDINGS: In contrast to many published reports, a recent Mendelian randomization study did not identify a causal link between uric acid and CKD in people with type 1 diabetes...
March 1, 2018: Current Diabetes Reports
Antoine Humbert, Fabien Stucker
Uric acid has been known since long ago for its implication in gout and in certain kinds of nephrolithiasis. However, its role in models of acute and chronic nephropathies has been the focus of many new developments. The so called Mesoamerican nephropathy is a devastating disease that has caused more than 20'000 deaths in central America these last few years among sugarcane workers. Acid uric could play a key role in its physiopathology. Moreover, acid uric tends to be recognized as an independent factor of development and progression in chronic kidney disease, opening a way for new therapeutic targets...
February 21, 2018: Revue Médicale Suisse
Keith C Norris, Karen E Smoyer, Catherine Rolland, Jan Van der Vaart, Eliza Beth Grubb
BACKGROUND: Albuminuria, elevated serum creatinine and low estimated glomerular filtration rate (eGFR) are pivotal indicators of kidney decline. Yet, it is uncertain if these and emerging biomarkers such as uric acid represent independent predictors of kidney disease progression or subsequent outcomes among individuals with type 2 diabetes mellitus (T2DM). This study systematically examined the available literature documenting the role of albuminuria, serum creatinine, eGFR, and uric acid in predicting kidney disease progression and cardio-renal outcomes in persons with T2DM...
February 9, 2018: BMC Nephrology
G-X Li, X-H Jiao, X-B Cheng
OBJECTIVE: To investigate the relationships between blood uric acid (BUA) level and the incidence, progression and deterioration of diabetic nephropathy (DN) in patients with type 2 diabetes mellitus (T2DM). PATIENTS AND METHODS: A total of fifty patients with T2DM alone whose glycosylated hemoglobin (HbA1c) were under normal range (4-6.5%) at their admission to our hospital were randomly selected as diabetes mellitus (DM) group. Fifty patients with hyperuricemia alone were randomly selected as hyperuricemia (HUA) group...
January 2018: European Review for Medical and Pharmacological Sciences
Kaoru Toyoda, Yusuke Suzuki, Kyotaka Muta, Taku Masuyama, Kochi Kakimoto, Akio Kobayashi, Toshiyuki Shoda, Shoichiro Sugai
Diabetic nephropathy (DN) is one of the complications of diabetes and is now the most common cause of end-stage renal disease. Fructose is a simple carbohydrate that is present in fruits and honey and is used as a sweetener because of its sweet taste. Fructose has been reported to have the potential to progress diabetes and DN in humans even though fructose itself does not increase postprandial plasma glucose levels. In this study, we investigated the effects of high fructose intake on the kidney of the Spontaneously Diabetic Torii (SDT) rats which have renal lesions similar to those in DN patients and compared these with the effects in normal SD rats...
2018: Journal of Toxicological Sciences
Konstantinos Stavropoulos, Konstantinos Imprialos, Nikiforos Stavropoulos, Sofia Bouloukou, Georgios Kerpiniotis, Kyriakos Dimitriadis, Constantinos Tsioufis, Michael Doumas
BACKGROUND: Diabetic nephropathy is a crucial microvascular complication of diabetes mellitus that is associated with elevated cardiovascular risk. SGLT-2 inhibitors are a new class of hypoglycemic drugs that positively affect several risk factors of cardiorenal damage. OBJECTIVES: To review and critically discuss available data on the association of SGLT-2 inhibitors treatment with kidney function, progress of diabetic kidney disease, and renal related outcomes, as well to unveil potential mechanisms of action that mediate such effects...
February 6, 2018: Cardiovascular & Hematological Disorders Drug Targets
Muhammed Khairujjaman Mazumder, Banashree Chetia Phukan, Aradhana Bhattacharjee, Anupom Borah
Chronic kidney disease (CKD) is an increasing global health burden. Disturbance in purine metabolism pathway and a higher level of serum uric acid, called hyperuricemia, is a risk factor of CKD, and it has been linked to increased prevalence and progression of the disease. In a recent study, it has been demonstrated that purine nucleotides and uric acid alter the activity of acetylcholinesterase (AChE). Thus, we hypothesize that adenine, hypoxanthine, xanthine, 2,8-dihydroxyadenine and uric acid may potentially interfere with the activity of AChE...
February 2018: Medical Hypotheses
Michael Mauer, Alessandro Doria
BACKGROUND: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) in the western world. Current treatment methods, with better control of glycemia and blood pressure, including renin-angiotensin system blockade (RASB), appear to have slowed the DN progression rate but have not substantially decreased the annual incidence of new DN ESRD cases. Thus, new treatment targets are needed. SUMMARY: Higher levels of serum uric acid (UA) are associated with increased risk of the clinical manifestations of DN in persons with types 1 and 2 diabetes...
2018: Contributions to Nephrology
Kunitoshi Iseki
BACKGROUND: Chronic kidney disease (CKD) is a risk factor of cardiovascular disease (CVD) and end-stage renal disease (ESRD). Early detection and management of risk factors of incidence and progression of CKD are necessary. We have been studying these risk factors among community-based screening participants in Okinawa, Japan. Okinawa was one of the longevity areas in the world; however, the incidence and prevalence of ESRD increased. In Japan, the incidence of ESRD is 2 times higher in men compared to that in women...
2018: Contributions to Nephrology
Juan C Ramirez-Sandoval, Magdalena Madero
Hyperuricemia may be a major contributor to the development or progression of chronic kidney disease (CKD). Although there is no clear cutoff uric acid (UA) value associated to the risk for kidney damage, it appears to be an increased risk as UA rises. Lifestyle interventions such as exercise, weight reduction, low consumption of purine-rich meat, or avoiding high fructose intake are recommended for all hyperuricemic patients. Lowering urate drugs such as allopurinol or febuxostat may be an option as a renoprotective agent; yet, randomized clinical trials evaluating the safety and efficacy of these drugs are limited to a small number of single-center studies...
2018: Contributions to Nephrology
Shunya Uchida, Takanori Kumagai, Wen Xiu Chang, Yoshifuru Tamura, Shigeru Shibata
Uric acid (UA) remains a risk factor for the progression of chronic kidney disease (CKD). Most observational studies showed a slight elevation in the serum UA level and this independently predicts the incidence and development of CKD. The recent meta-analysis, however, did not reach the conclusion that urate-lowering therapy with allopurinol retards the progression of CKD. The target level of serum UA if treated is another issue of debate. Our recent analysis by propensity score analysis has shown that the serum UA should be targeted below 6...
2018: Contributions to Nephrology
Duk-Hee Kang
BACKGROUND: Although the clinical implication of hyperuricemia in chronic kidney disease has been an issue of active debate, recent data suggested a causative role of uric acid (UA) in the development of renal disease. Afferent arteriopathy, an induction of oxidative stress and an activation of local inflammation, have been regarded as the mechanisms of UA-induced renal disease, which contribute to glomerular hypertrophy and interstitial fibrosis via endothelial dysfunction. However, there have been rare studies on the direct effect of UA on phenotype transition of renal cells such as epithelial-to-mesenchymal transition (EMT) or endothelial-to-mesenchymal transition (EndoMT)...
2018: Contributions to Nephrology
Carlos Enrique Méndez Landa
BACKGROUND: From a clinical point of view, uric acid has been dismissed as a cause of injury and renal progression, and the mechanisms by which uric acid directly causes renal injury have not been fully understood. Hyperuricemia is associated with metabolic syndrome, diabetes, hypertension, and kidney and cardiovascular diseases. Although it remains controversial whether hyperuricemia is a causal factor for kidney disease, kidneys play a major role in the regulation of serum uric acid levels...
2018: Contributions to Nephrology
Alejandro Treviño-Becerra
This review brings together concepts of uric acid metabolism affecting renal parenchyma and its function and the current therapies to reduce hyperuricemia (HyU) and avoid renal disease progression. High uric acid plays an important role in several chronic diseases including kidney diseases such as lithiasis, gout nephropathy, and preeclampsia. In the last 30 years, it has been shown that reducing HyU with low protein and low purine diets in addition to allopurinol creates physiopathological conditions that produce a slight increase in the glomerular filtration rate (GFR)...
2018: Contributions to Nephrology
Carlo Garofalo, Toni De Stefano, Carlo Vita, Giorgia Vinci, Francesco Balia, Francesca Nettuno, Luisa Scarpati, Azzurra Sguazzo, Alessandra Sagliocchi, Mario Pacilio, Roberto Minutolo, Luca De Nicola, Silvio Borrelli
Hyperuricemia is defined as serum uric acid values greater than 6 mg/dl and could occur either due to hyperproduction or as a result of reduced renal excretion, which exceeds gut compensation. In Italy, prevalence is around 12% of the general population and increases in renal disease up to 60%. Recent experimental studies demonstrated a role of uric acid in the development of arterial hypertension and systemic arteriosclerosis, with an increase in cardiovascular risk. It also appears from observational studies that high uric acid is an independent risk factor associated with de novo onset of chronic kidney disease after adjustment of main confounding variables...
February 2018: Giornale Italiano di Nefrologia: Organo Ufficiale Della Società Italiana di Nefrologia
Yan Liu, David Goldfarb, Tarek M El-Achkar, John C Lieske, Xue-Ru Wu
Expression of Tamm-Horsfall protein (THP or uromodulin) is highly restricted to the kidneys' thick ascending limb (TAL) of loop of Henle. Despite the unique location and recent association of THP gene mutations with hereditary uromodulin-associated kidney disease and THP single nucleotide polymorphisms with chronic kidney disease and hypertension, the physiological function(s) of THP and its pathological involvement remain incompletely understood. By studying age-dependent changes of THP knockout (KO) mice, we show here that young KO mice had significant salt and water wasting but were partially responsive to furosemide, due to decreased luminal translocation of Na-K-Cl cotransporter 2 (NKCC2) in the TAL...
January 10, 2018: American Journal of Physiology. Renal Physiology
Wen Xiu Chang, Ning Xu, Takanori Kumagai, Ryutaro Iijima, Kaito Waki, Masaki Yamanaka, Michito Nagura, Shigeyuki Arai, Yoshifuru Tamura, Shigeru Shibata, Yoshihide Fujigaki, Shunya Uchida
BACKGROUND/AIMS: Higher level of serum uric acid (SUA) predicts early entry to dialysis in chronic kidney disease (CKD) patients. However, a short-term effect of SUA remains to be elucidated using a novel surrogate endpoint. METHODS: Japanese CKD stage 3 to 4 patients were retrospectively examined (n= 701). The follow-up level of SUA was estimated as time-averaged uric acid (TA-UA). A propensity score for 6.0, 6.5 or 7.0 mg/dL of TA-UA was respectively calculated using baseline 23 covariates...
2017: Kidney & Blood Pressure Research
Makiko Nakamura, Kyoko Fujita, Yu Toyoda, Tappei Takada, Hiroshi Hasegawa, Kimiyoshi Ichida
Hyperuricemia induces gout and kidney stones and accelerates the progression of renal and cardiovascular diseases. Adenosine 5'-triphosphate-binding cassette subfamily G member 2 (ABCG2) is a urate transporter, and common dysfunctional variants of ABCG2, non-functional Q126X (rs72552713) and semi-functional Q141K (rs2231142), are risk factors for hyperuricemia and gout. A recent genome wide association study suggested that allopurinol, a serum uric acid-lowering drug that inhibits xanthine dehydrogenase, is a potent substrate of ABCG2...
November 22, 2017: Drug Metabolism and Pharmacokinetics
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