ReviewBMC nephrology2025
Hyperuricemia-induced kidney injury: a narrative review of mechanisms and therapeutic advances.
Review in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Cinnamaldehyde Attenuates Hyperuricemia-Associated Renal Injury by Modulating Urate Transporters and AIF1- and CMPK2/NLRP3-Related Inflammatory Signaling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Uric Acid and Chronic Kidney Disease.Kidney medicine · 2026Review
- Identification of Risk Factors for Renal Insufficiency in Primary Membranous Nephropathy.Saudi medical journal · 2026Article
- Intestinal Multi-Target Mechanisms of Natural Active Substances in Hyperuricemia Alleviation: Recent Progress.Nutrients · 2026Review
- The Chronic Elevated Consumption ofInternational journal of molecular sciences · 2026Article
- Multidimensional mechanisms of natural products in modulating metabolic dysfunction-associated kidney disease: recent advances and future perspectives.Frontiers in pharmacology · 2026Review
- Programmed cell death in gouty nephropathy: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Uric acid (UA) is the final product of purine metabolism in the human body. Excessive accumulation of UA leads to hyperuricemia (HUA) and the deposition of UA crystals in tissues, including the joints and kidneys. HUA has been identified as an independent risk factor for kidney disease. Although the association between HUA and kidney damage has been long established, the underlying pathological and physiological molecular mechanisms remain incompletely understood. This article reviews the latest advances in the mechanisms of kidney injury caused by HUA, particularly in the context of inflammation, oxidative stress, endothelial dysfunction, renal fibrosis, and imbalanced composition of the intestinal microbiota. Additionally, we discuss the advances in the treatment of HUA, aiming to provide valuable references for the study of HUA-induced kidney diseases and therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.