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Meta-analysis of 24 animal studies shows emodin reduces kidney injury markers in preclinical modelsAnimal studies suggest emodin may lower kidney injury markers, but human data is missing

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Key Takeaway
Note that emodin reduces kidney injury markers in animal models but requires precise dosing control.

This systematic review and meta-analysis synthesized evidence from 24 studies conducted exclusively in in vivo animal models, involving a total population of 408 animals comprising 396 rodents and 12 canines. The primary outcomes assessed were serum blood urea nitrogen (BUN) and creatinine (Cr), with the kidney index serving as a secondary outcome. The authors note that follow-up duration was not reported for these studies.

Key findings from the pooled analysis indicate that emodin exposure was associated with significantly reduced BUN (SMD = -2.39; 95% CI -3.54 to -1.25; P < 0.0001; I2 = 78.5%) and significantly reduced Cr (SMD = -3.44; 95% CI -4.83 to -2.05; P < 0.0001; I2 = 86.3%). In a subset analysis of emodin-alone exposure, no overall significant elevation was observed for BUN (SMD = 2.11; 95% CI -1.51–5.72) or Cr (SMD = 0.65; 95% CI -3.15–4.45). However, the kidney index decreased significantly under emodin-alone exposure (SMD = -0.68; 95% CI -1.27 to -0.10; P = 0.022).

Regarding safety, toxicity signals were associated with high-dose exposure (>1,000 mg/kg), intraperitoneal administration, and treatment duration exceeding 1 month. The authors explicitly state that serious adverse events, discontinuations, and tolerability were not reported. A major limitation is that the evidence is restricted to in vivo animal models, excluding in vitro and clinical data. Consequently, the review underscores the need for precise dosing and exposure control in the further development of emodin as a renal therapeutic agent.

Researchers analyzed data from 24 studies involving 408 animals, including 396 rodents and 12 canines, to see how emodin affects kidney health. The main goal was to measure changes in serum blood urea nitrogen and creatinine, which are common signs of kidney stress. The review also looked at kidney size as a secondary measure of health.

The analysis showed that emodin significantly reduced levels of blood urea nitrogen and creatinine across the studies. These markers are often used to track kidney function, and lower levels generally suggest less injury. However, the studies varied in how they gave the substance and how long they treated the animals.

Safety concerns emerged when animals received very high doses, over 1,000 mg per kilogram, or were treated for more than one month. Under these specific conditions, signs of toxicity were observed. The researchers noted that precise dosing and exposure control are essential for future development of emodin as a potential kidney treatment.

Readers should understand that these findings are limited to animals and cannot be directly applied to humans. More research is needed to determine if emodin is safe and effective for people with kidney problems. Until clinical trials are done, this information should not be used to change medical treatment plans.

What this means for you:
Animal studies show emodin may lower kidney injury markers, but human safety and effectiveness are unknown.

Study Details

Study typeMeta analysis
EvidenceLevel 1
PublishedApr 2026
View Original Abstract ↓
BackgroundKidney injury is a growing global health problem with limited treatments. Emodin, an anthraquinone found in traditional Chinese medicinal herbs, shows both renoprotective and nephrotoxic effects in animal studies. This study aimed to systematically assess the effects of emodin on kidney injury in vivo and determine how dose, administration route, and treatment duration influence whether the overall outcome is beneficial or harmful.MethodsA pre-registered systematic review and random-effects meta-analysis was conducted, focusing exclusively on in vivo animal models and excluding in vitro and clinical data. Eight electronic databases were searched from inception to 1 October 2025. Two reviewers independently performed study selection, data extraction, and risk-of-bias assessment using the SYRCLE tool. The primary efficacy outcomes were serum blood urea nitrogen (BUN) and creatinine (Cr). Pre-specified subgroup analyses were undertaken according to disease model, dose, administration route, and intervention duration. Publication bias was evaluated using funnel plots and Egger’s regression test.ResultsFrom 2,915 records, 24 studies (408 animals: 396 rodents, 12 canines) met inclusion criteria (17 therapeutic, 7 toxicity). In kidney injury models, emodin significantly reduced BUN (n = 182; SMD = −2.39; 95% CI −3.54 to −1.25; P < 0.0001; I2 = 78.5%) and Cr (n = 284; SMD = −3.44; 95% CI −4.83 to −2.05; P < 0.0001; I2 = 86.3%). Subgroup results indicated robust effects at low–moderate doses (60 mg/kg) and with certain routes. For emodin-alone exposure studies, pooled BUN (n = 92; SMD = 2.11; 95% CI −1.51–5.72) and Cr (n = 112; SMD = 0.65; 95% CI −3.15–4.45) showed no overall significant elevation, but the kidney index decreased significantly (n = 100; SMD = −0.68; 95% CI −1.27 to −0.10; P = 0.022). High-dose exposure (>1,000 mg/kg), intraperitoneal administration and treatment >1 month were associated with toxicity signals.ConclusionEmodin exhibits dual effects on the kidney, with its net outcome determined primarily by dosage, administration route, and treatment duration. These findings underscore the need for precise dosing and exposure control in the further development of emodin as a renal therapeutic agent.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261326554, identifier CRD420261326554.
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