Acute Kidney Injury Induces Remote Cardiac Damage and Dysfunction Through the Galectin-3 Pathway

Prudhomme, Mathilde; Coutrot, Maxime; Michel, Thilo; Boutin, Louis; Genest, Magali; Poirier, Françoise; Launay, Jean‐Marie; Kane, Bocar; Kinugasa, Satoshi; Prakoura, Niki; Vandermeersch, Sophie; Cohen‐Solal, Alain; Delcayre, Claude; Samuel, Jane-Lise; Mehta, Ravindra L.; Gayat, Étienne; Mebazaa, Alexandre; Chadjichristos, Christos; Legrand, Matthieu

doi:10.1016/j.jacbts.2019.06.005

Cited by 55 publications

(55 citation statements)

References 40 publications

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“…Similarly, as advanced by Prud’homme et al. (1), AKI, through circulating hormones or mediators, induces cardiac injury and dysfunction. The current Gal-3 inhibition studies, however, did not demonstrate noticeable improvement on renal function (creatinine and blood urea nitrogen levels) or renal hypertrophy, although significant improvements were observed in cardiac parameters.…”

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confidence: 83%

“…Here in this elegantly designed study, Prud’homme et al. (1) demonstrated that Gal-3 can serve as both a drug target for AKI-induced cardiac dysfunction and a biomarker for AKI.…”

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confidence: 95%

“…In this issue of JACC: Basic to Translational Science , Prud’homme et al. (1) report that experimental acute kidney injury (AKI) in mice induces remote cardiac injury through the upregulation of a novel mediator galectin-3 (Gal-3). The major findings are that acute (up to 72 h) ischemia/reperfusion-induced AKI in mice stimulated an increase in Gal-3 expression in tubular inflammatory cells in the kidney and in cardiac tissues, with an increase in circulating levels of Gal-3.…”

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confidence: 99%

“…This second model was a rigorous test of the hypothesis of Prudhomme et al. (1) that the kidney communicates with the heart via Gal-3.…”

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confidence: 99%

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The Kidney, Bone Marrow, and Heart Connection in Acute Kidney Injury

Chen

Burnett

2019

JACC: Basic to Translational Science

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mentioning

confidence: 83%

“…Here in this elegantly designed study, Prud’homme et al. (1) demonstrated that Gal-3 can serve as both a drug target for AKI-induced cardiac dysfunction and a biomarker for AKI.…”

mentioning

confidence: 95%

mentioning

confidence: 99%

“…This second model was a rigorous test of the hypothesis of Prudhomme et al. (1) that the kidney communicates with the heart via Gal-3.…”

mentioning

confidence: 99%

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The Kidney, Bone Marrow, and Heart Connection in Acute Kidney Injury

Chen

Burnett

2019

JACC: Basic to Translational Science

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“…Epidemiologic studies have found an association between serum Gal-3 level and risk of sepsis [20][21][22] as well as development of chronic kidney disease (CKD) [23][24][25]. Pertinent ndings show that serum Gal-3 predicts 30-day all-cause mortality in sepsis [26], preoperative serum Gal-3 predicts AKI after cardiac surgery [27], and serum Gal-3 at ICU discharge is associated with severity of AKI [28]. However, no previous study has examined the relationship between serum Gal-3 at the time of admission and the subsequent development of AKI in patients with sepsis.…”

Section: Introductionmentioning

confidence: 99%

Galectin-3 In Septic Acute Kidney Injury: A Translational Study

Sun

Jiang

Eliaz

et al. 2021

Preprint

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Background Galectin-3 (Gal-3) is a pleiotropic glycan-binding protein shown to be involved in sepsis and acute kidney injury (AKI). However, its role has never been elucidated in sepsis-associated AKI (S-AKI). We aimed to explore Gal-3’s role and its potential utility as a therapeutic target in S-AKI. MethodsIn 57 patients admitted to the intensive care unit (ICU) with sepsis, serum Gal-3 was examined as a predictor of ICU mortality and AKI. In a rat model of S-AKI induced by cecal ligation and puncture (CLP), 7-day mortality and serum Gal-3, IL-6, and creatinine were examined at baseline, 2, 8, and 24 hours (h) post-CLP. Two experimental groups received the Gal-3 inhibitor modified citrus pectin (P-MCP) at 400 mg/kg/day and 1200 mg/kg/day, while the control group received water only (n = 18 in each group). ResultsAmong 57 patients, 27 developed AKI and 8 died in the ICU. Serum Gal-3 was an independent predictor of AKI (OR = 1.2 [95% CI 1.1-1.4], p = 0.01) and ICU mortality (OR = 1.4 [95% CI 1.1-2.2], p = 0.04) before and after controlling for age, AKI, and acute physiology and chronic health evaluation (APACHE II) score. In the CLP rat experiment, serum Gal-3 peaked earlier than Interleukin-6 (IL-6). Serum Gal-3 was significantly lower in both P-MCP-treated groups compared to control at 2 h post-CLP (400 mg: p = 0.003; 1200 mg: p = 0.002), and IL-6 was significantly lower in both P-MCP-treated groups at all time points with a maximum difference at 24 h post-CLP (400 mg: p = 0.015; 1200 mg: p = 0.02). In the Gal-3 inhibitor groups, 7-day mortality was significantly reduced from 61% in the control group to 28% (400 mg P-MCP: p = 0.03) and 22% (1200 mg P-MCP: p = 0.001). Rates of AKI per RIFLE criteria were significantly reduced from 89% in the control group to 44% in both P-MCP-treated groups (400mg: p = 0.007; 1200mg: p = 0.007). ConclusionsThis translational study demonstrates the importance of Gal-3 in the pathogenesis of S-AKI, and its potential utility as a therapeutic target.

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