https://cyberleninka.org/article/n/1458900.pdf

Uric acid in the pathogenesis of metabolic, renal, and cardiovascular diseases: A review

Hyperuricemia has been reported to be associated with chronic kidney disease (CKD). However whether an elevated serum uric acid level is an independent risk factor for new-onset CKD remained controversial. A systematic review and meta-analysis using a literature search of online databases including PubMed, Embase, Ovid and ISI Web/Web of Science was conducted. Summary adjusted odds ratios with corresponding 95% confidence intervals (95% CI) were calculated to evaluate the risk estimates of hyperuricemia for new-onset CKD. Thirteen studies containing 190,718 participants were included. A significant positive association was found between elevated serum uric acid levels and new-onset CKD at follow-up (summary OR, 1.15; 95% CI, 1.05–1.25). Hyperuricemia was found be an independent predictor for the development of newly diagnosed CKD in non-CKD patients (summary OR, 2.35; 95% CI, 1.59–3.46). This association increased with increasing length of follow-up. No significant differences were found for risk estimates of the associations between elevated serum uric acid levels and developing CKD between males and females. With long-term follow-up of non-CKD individuals, elevated serum uric acid levels showed an increased risk for the development of chronic renal dysfunction.

/pdf/is-hyperuricemia-an-independent-risk-factor-for-new-onset-4ccy75xwok.pdf

Is hyperuricemia an independent risk factor for new-onset chronic kidney disease?: A systematic review and meta-analysis based on observational cohort studies.

Uric acid, the end product of purine metabolism, is excreted predominantly by the proximal tubules. Abnormal serum levels of uric acid are due to alterations in production or excretion. Fractional excretion of uric acid is helpful in determining the underlying etiology of hypouricemia or hyperuricemia in children. Abnormalities in the molecular mechanisms that control renal uric acid tubular transport are implicated in various disorders associated with abnormal uric acid levels. Gout is rare in children; yet its presence necessitates evaluation for enzymatic defects in purine metabolism. Well-known effects of uric acid on the kidney include nephrolithiasis and acute kidney injury (AKI) in the setting of tumor lysis. However, recent data suggest that uric acid may be an important factor in the pathogenesis of AKI in general, as well as of chronic kidney disease (CKD) and hypertension. Hence, uric acid may not only be a marker but also a potential therapeutic target in kidney disease. Nonetheless, because of confounders, more studies are needed to clarify the association between uric acid and multifactorial disorders of the kidney.

Uric acid and the kidney.

Hyperuricemia (HUA) is a metabolic disorder caused by abnormal uric acid (UA) metabolism, which is a complex physiological process involving multiple organs (liver, kidney, and intestine) Although UA metabolism in the liver and kidneys has been elucidated, only a few studies have focused on the process in the intestine With our growing knowledge of the effects of gut microorganisms on health, the gut microbiota has been identified as a new target for HUA treatment In this review, the relationship between HUA and the gut microbiota is elucidated, and anti-hyperuricemia mechanisms targeting the intestine are discussed, such as the promotion of purine and UA catabolism by the gut microbiota, increases in UA excretion by the gut microbiota and its metabolites, regulation of UA absorption or secretion in the intestinal tract by certain transporters, and the intestinal inflammatory response to the gut microbiota Additionally, probiotics (Bifidobacteria and Lactobacilli) and prebiotics (polyphenols, peptides, and phytochemicals) with UA-lowering effects targeting the intestinal tract are summarized, providing reference and guidance for further research

The gut microbiota as a target to control hyperuricemia pathogenesis: Potential mechanisms and therapeutic strategies.

It has been reported that oxidative stress has a pivotal role in many disorders such as chronic kidney diseases. Free radicals can directly attack cellular elements, trigger intracellular signaling pathways, or induce systemic responses leading to renal damages. In the current review, we evaluated the literature focusing on the main recognized effects of oxidative stress on the pathophysiology of chronic renal disorders. We searched the PubMed-Medline and Scopus databases by using the following key words: oxidative stress, kidney, chronic kidney diseases, and free radicals and found about 200 related articles. Then, we focused on the molecular mechanisms underlying chronic kidney diseases which can be induced by oxidative stress and explored how free radicals stimulate these mechanisms. By reviewing the literature, we found that there are almost nine important molecular pathways through which free radicals influence the renal function. Based on the retrieved data, oxidative stress has an important role in the pathophysiology of chronic kidney diseases. Understanding these pathophysiologic pathways may lead us to find new approaches for the management of these debilitating disorders.

Oxidative stress induces renal failure: A review of possible molecular pathways.

Uric acid and chronic kidney disease: new understanding of an old problem.

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Uric acid and chronic kidney disease: new understanding of an old problem.