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  • 1
    In: Nephron, S. Karger AG, Vol. 147, No. 9 ( 2023), p. 521-530
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The association between potassium (sK) level trajectory and mortality or the need for kidney replacement therapy (KRT) during acute kidney injury (AKI) has not been adequately explored. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 In this prospective cohort, AKI patients admitted to the Hospital Civil de Guadalajara were enrolled. Eight groups based on the sK (mEq/L) level trajectories during 10 days of hospitalization were created (1) normokalemia (normoK), defined as sK between 3.5–5.5; (2) hyperkalemia to normoK; (3) hypokalemia to normoK; (4) fluctuating potassium; (5) persistent hypoK; (6) normoK to hypoK; (7) normoK to hyperK; (8) persistent hyperK. We assessed the association of sK trajectories with mortality and the need for KRT. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A total of 311 AKI patients were included. The mean age was 52.6 years, and 58.6% were male. AKI stage 3 was present in 63.9%. KRT started in 36% patients, and 21.2% died. After adjusting for confounders, 10-day hospital mortality was significantly higher in groups 7 and 8 (OR, 1.35 and 1.61, 〈 i 〉 p 〈 /i 〉 & #x3c; 0.05, for both, respectively), and KRT initiation was higher only in group 8 (OR 1.38, 〈 i 〉 p 〈 /i 〉 & #x3c; 0.05) compared with group 1. Mortality in different subgroups of patients in group 8 did not change the primary results. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 In our prospective cohort, most patients with AKI had alterations in sK 〈 sup 〉 + 〈 /sup 〉 . NormoK to hyperK and persistent hyperK were associated with death, while only persistent hyperK was correlated with the need for KRT.
    Type of Medium: Online Resource
    ISSN: 1660-8151 , 2235-3186
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2023
    detail.hit.zdb_id: 2810853-X
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  • 2
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 20, No. 1 ( 2022-12)
    Abstract: Post-cardiac surgery acute kidney injury (AKI) is associated with increased mortality. A high-protein meal enhances the renal blood flow and glomerular filtration rate (GFR) and might protect the kidneys from acute ischemic insults. Hence, we assessed the effect of a preoperative high-oral protein load on post-cardiac surgery renal function and used experimental models to elucidate mechanisms by which protein might stimulate kidney-protective effects. Methods The prospective “Preoperative Renal Functional Reserve Predicts Risk of AKI after Cardiac Operation” study follow-up was extended to postoperative 12 months for 109 patients. A 1:2 ratio propensity score matching method was used to identify a control group (n = 214) to comparatively evaluate the effects of a preoperative protein load and standard care. The primary endpoints were AKI development and postoperative estimated GFR (eGFR) loss at 3 and 12 months. We also assessed the secretion of tissue inhibitor of metalloproteases-2 (TIMP-2) and insulin-like growth factor–binding protein 7 (IGFBP7), biomarkers implicated in mediating kidney-protective mechanisms in human kidney tubular cells that we exposed to varying protein concentrations. Results The AKI rate did not differ between the protein loading and control groups (13.6 vs. 12.3%; p = 0.5). However, the mean eGFR loss was lower in the former after 3 months (0.1 [95% CI − 1.4, − 1.7] vs. − 3.3 [95% CI − 4.4, − 2.2] ml/min/1.73 m 2 ) and 12 months (− 2.7 [95% CI − 4.2, − 1.2] vs − 10.2 [95% CI − 11.3, − 9.1] ml/min/1.73 m 2 ; p  〈  0.001 for both). On stratification based on AKI development, the eGFR loss after 12 months was also found to be lower in the former (− 8.0 [95% CI − 14.1, − 1.9] vs. − 18.6 [95% CI − 23.3, − 14.0] ml/min/1.73 m 2 ; p = 0.008). A dose–response analysis of the protein treatment of the primary human proximal and distal tubule epithelial cells in culture showed significantly increased IGFBP7 and TIMP-2 expression. Conclusions A preoperative high-oral protein load did not reduce AKI development but was associated with greater renal function preservation in patients with and without AKI at 12 months post-cardiac surgery. The potential mechanisms of action by which protein loading may induce a kidney-protective response might include cell cycle inhibition of renal tubular epithelial cells. Clinical trial registration ClinicalTrials.gov: NCT03102541 (retrospectively registered on April 5, 2017) and ClinicalTrials.gov: NCT03092947 (retrospectively registered on March 28, 2017).
    Type of Medium: Online Resource
    ISSN: 1479-5876
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2118570-0
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