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At least 19 recordsLinked to original sources
PubMed2026

Black Rice Anthocyanin-Hyaluronic Acid Complex Alleviates Hyperuricemia-Associated Renal Injury Through Synergistic Inhibition of the TLR4/NF-κB Pathway and Modulation of Uric Acid Transport.

Hyperuricemia-associated renal injury is closely linked to oxidative stress and inflammation, highlighting the need for safe dietary intervention. This study evaluated the protective effects of a black rice anthocyanin (ATC)-hyaluronic acid complex (HAA) against uric acid (UA)-induced injury. In UA-induced human renal proximal tubular epithelial (HK-2) cells, black rice ATCs, HA, and HAA improved cell viability and antioxidant defenses, as shown by increased glutathione (GSH) levels and catalase (CAT) and superoxide dismutase (SOD) activities. They also reduced malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). HAA produced a greater reduction in TLR4/NF-κB-related inflammatory gene expression, suggesting that its cytoprotective and anti-inflammatory effects may be associated with modulation of this inflammatory axis. In hyperuricemic mice, HAA lowered serum UA, creatinine, and blood urea nitrogen levels, inhibited hepatic xanthine oxidase and adenosine deaminase activities, and attenuated renal histopathological injury. HAA also reduced the mRNA expression of urate reabsorption-related genes, including GLUT9, OAT4, and OAT10, while increasing that of urate excretion-related genes, including OAT1 and ABCG2, which may contribute to improved urate homeostasis. These findings support the potential of HAA as a functional dietary ingredient for the management of hyperuricemia-associated metabolic disturbances and renal injury.

Hyperuricemia↗
PubMedDate not supplied

Etiology of hyperuricemia.

Hyperuricemia is a common laboratory finding with significant clinical implications. It is easily detected, but its mechanisms may not be clearly elucidated. A scheme of pathogenesis has been outlined and diagrammed but much is conjectural; therefore, the classification is merely tentative. About 45 diseases or categories of conditions, 20 drugs, and nine states of intoxication have been surveyed. Hyperuricemia can be a multifactorial genetic disorder or a discrete response to a specific stimulus. It may be governed by a complex interplay of biochemical disorders for a lifetime duration, or it may be determined by environmental forces for a very transient course. Some conditions have both increased production of uric acid as well as decreased renal outflow. For many patients, the underlying mechanisms have not yet been elucidated.

Anemia↗
PubMed1976

[Plasma fibrinogen activity in diabetes mellitus, hyperlipoproteinemia and hyperuricemia (author's transl)].

Plasma fibrinogen content was measured in 20 normal subjects, 20 patients with diabetes mellitus, 20 patients with hyperlipoproteinemia type II or IV (Fredrickson) and 10 patients with hyperuricemia. These vascular risks were accompanied by significant increase of plasma fibrinogen in comparison with the normal collective. The highest fibrinogen concentrations were found in diabetics, followed by hyperuricemias and hyperlipoproteinemias. The importance of coagulation disturbances is discussed in regard of angiopathogenesis.

Adult↗
PubMed2026

Associations between multiple essential trace metal concentrations and risk of hyperuricemia: insights from a central Chinese population.

Previous studies have indicated that levels of individual essential trace metals are related to hyperuricemia (HUA), but evidence on their combined effects is limited. To address this gap, the associations of individual and joint levels of 12 essential trace metals (manganese, selenium, nickel, chromium, cobalt, tin, iron, molybdenum, zinc, strontium, vanadium, and copper) with the risk of HUA were investigated in 2,021 adults recruited from Hunan Province, China. Inductively coupled plasma mass spectrometry (ICP-MS) was employed to determine urinary metal concentrations. Logistic regression, Bayesian kernel machine regression (BKMR), and quantile g calculation (Qgcomp) were applied to evaluate the associations of single and mixture metal concentrations with HUA. Of the participants, 516 (25.53%) were diagnosed with HUA. Inverse associations were found between vanadium, chromium, manganese, iron, cobalt, selenium, strontium, and molybdenum levels and HUA, with ORs ranging from 0.63 to 0.91. Conversely, a positive association was observed between zinc concentration and HUA [OR (95% CI): 1.17 (1.01, 1.37)]. Both BKMR and Qgcomp models showed a negative overall effect of essential trace metals on HUA risk, with strontium (- 43.6%) and vanadium (- 27.8%) being the main contributors. In addition, formal interaction tests revealed significant effect modification by age for tin and by BMI for zinc. In conclusion, the levels of essential trace metals were linked to a decreased risk of HUA, and these associations were modified by age and BMI only for specific metals.

Humans↗
PubMed2026

Integrative multi-omics analysis unravels the metabolic landscape and reveals serum biomarkers for early diagnosis of hyperuricemia.

BACKGROUND: Hyperuricemia (HUA) is a major risk factor for gout and multiple metabolic disorders. Although serum uric acid (UA) is the gold standard for HUA diagnosis, it fails to reflect early metabolic disturbances and shows limited predictive value for asymptomatic HUA. This study sought to elucidate the pathological mechanisms underlying HUA and identify novel diagnostic biomarkers beyond UA. METHODS: This study enrolled 195 patients with HUA and 98 healthy controls. Global metabolomics and proteomics profiling were performed to characterize molecular alterations underlying HUA. Based on the biological relevance of the shared dysregulated pathways, a pathway correlation network was constructed to elucidate the pathological mechanisms driving HUA initiation and progression. Furthermore, diagnostic biomarkers for HUA were identified using machine learning algorithms, and were validated with an external cohort. RESULTS: HUA patients exhibited distinct metabolic and proteomic profiles compared with healthy controls. Integrated multi-omics pathway analysis revealed that peroxisome proliferators-activated receptor signaling pathway, arachidonic acid metabolism, purine metabolism, pyrimidine metabolism and sphingolipid signaling pathway were significantly dysregulated in HUA. Among them, arachidonic acid metabolism was identified as a hub pathway involved in HUA progression. Furthermore, a metabolite panel consisting of cysteine-S-sulfate, glycerophosphocholine and 4-hydroxyphenylpyruvic acid was screened by machine learning and validated in an independent cohort, which showed slightly higher diagnostic performance for HUA than UA. CONCLUSIONS: This study reveals the core metabolic and protein regulatory networks of HUA, and identifies a novel serum metabolite panel for the diagnosis of HUA. These findings provide new insights for improved clinical diagnosis and management.

Humans↗
PubMed1975

[Diet in hyperuricemia (author's transl)].

The idea that, in view of potent drugs, the dietary treatment of a metabolic disease must be reserved for a small group of particularly susceptible patients or even for a minority of neurotically structured patients who would alone be capable of bearing the hardship of a consequent change of accustomed feeding habits needs correction. Considerably greater importance must be attached to dietetics in disorders of uric acid metabolism than formerly, particularly with a view to the status already gained by the dietary treatment of diabetes mellitus a long time ago. Dietetic therapy of familial hyperuricemia and its later clinical manifestation, gout, is a basic therapy of a preventive character. Because today, superiority is increasingly conceded to prophylaxis rather than to the treatment of late sequelae.

Adenosine Monophosphate↗
PubMed1975

[Physical and mental fatigue of probable hyperuricemia origin].

A blood uric acid analysis has been effected on 193 Iranians of the intellectual group aged from 25 to 60, of which the normal average rate for 99 women and 94 men of a normal state are (47.5 +/- 2.73) and (53.62 +/- 2.73) respectively. After having controlled the uricemia of these subjects during a period of three years in the three states of healthiness, fatigue or physical strains and sickness, we have been able to note that during physical fatigue and intellectual strains the uricemia presents an augmentation notable as in the case of the sicknesses. Taking into consideration the hyperuricemia resulting from fatigue and strains, it may be noteworthy to be taken into consideration by the clinical laboratories and the physicians as well.

Adult↗
PubMed1978

Grand mal-provoked hyperuricemia.

A significant increase in S-urate was found postictally in 17 patients with two or more grand mal seizures within 24 h. In six patients S-urate was above the level at which hyperuricemic renal failure may develop. Impaired renal function was observed in two patients who had extremely high S-urates. It is proposed that prophylactic procedures against hyperuricemic renal failure should be carried out in all patients with repetitive convulsions.

Acute Kidney Injury↗
PubMed1978

[Incidence of hyperuricemia in atrioventricular block. Systematic study of 158 cases which required implantation of an isotopic cardiac pacemaker].

This is a study of 158 patients in whom the placement of an isotopic cardiac pacemaker was indicated; this procedure was carried out Broussais Hospital between 1970 and 1975. These patients, whose mean age was 39 (84 males, 47 females, 12 young men and 15 young women) were examined for uricaemia, and the levels compared with the mean for control population. The results were as follows: 91% had uricaemia at a level higher than the controls. Of these, 61% had uricaemia above 70 mg/l in the men and youths of over 15 years of age, and above 60 mg/l in the women and 50 mg/l in the adolescents. The highest uric acid levels were found in adults with post-operative atrio-ventricular block following surgical correction of a congenital cardiac abnormality, and also in children and adolescence with block which appeared to be congenital.

Adolescent↗