scholarly journals Soft drink consumption during and following exercise in the heat elevates biomarkers of acute kidney injury

2019 ◽  
Vol 316 (3) ◽  
pp. R189-R198 ◽  
Author(s):  
Christopher L. Chapman ◽  
Blair D. Johnson ◽  
James R. Sackett ◽  
Mark D. Parker ◽  
Zachary J. Schlader

The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine ≥0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial ( P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise ( P < 0.01) and 24 h ( P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial ( P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0004802021
Author(s):  
Kelly R. McMahon ◽  
Hayton Chui ◽  
Shahrad Rod Rassekh ◽  
Kirk R. Schultz ◽  
Tom D. Blydt-Hansen ◽  
...  

Background: Few studies have described associations between acute kidney injury (AKI) biomarkers, urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), and AKI in cisplatin-treated children. We aimed to describe excretion patterns of urine NGAL and KIM-1 and associations with AKI in children receiving cisplatin. Methods: Participants (n=159) were enrolled between 2013 and 2017 in a prospective cohort study conducted in 12 Canadian pediatric hospitals. Participants were evaluated at early cisplatin infusions (at first or second cisplatin cycle) and late cisplatin infusions (last or second-to-last cycle). Urine NGAL and KIM-1 were measured (1) pre-cisplatin infusion, (2) post-infusion (morning after), and (3) at hospital discharge at early and late cisplatin infusions. Primary outcome: AKI defined by serum creatinine rise within 10 days post-cisplatin based on Kidney Disease: Improving Global Outcomes guidelines criteria (≥stage 1). Results: Of 159 children, 156 (median [interquartile (IQR)] age: 5.8 [2.4-12.0] years; 78 [50%] female) had biomarker data available at early cisplatin infusions and 127 had data at late infusions. Forty-six of 156 (29%) and 22/127 (17%) developed AKI within 10 days of cisplatin administration following early and late infusions, respectively. Urine NGAL and KIM-1 concentrations were significantly higher in patients with vs. without AKI (near hospital discharge of late cisplatin infusion, median [IQR]: NGAL: 76.1 [10.0-232.7] vs. 14.9 [5.4-29.7] ng/mg creatinine; KIM-1: 4415 [2083-9077] vs. 1049 [358-3326] pg/mg creatinine; P<.01). These markers modestly discriminated for AKI (area under receiver-operating characteristic curve (AUC-ROC) range: NGAL: 0.56-0.72; KIM-1: 0.48-0.75). Biomarker concentrations were higher and better discriminated for AKI at late cisplatin infusions (AUC-ROCs range: 0.54-0.75) vs. early infusions (AUC-ROCs range: 0.48-0.65). Conclusions: Urine NGAL and KIM-1 were modest at discriminating for cisplatin-associated AKI. Further research is needed to determine clinical utility and applicability of these markers and late kidney outcomes associations.


Author(s):  
Ahmad El Samra ◽  
Ayesa Mian ◽  
Marc Lande ◽  
Hongyue Wang ◽  
Ronnie Guillet

Objective The aim of this study was to determine the effects of a 2-day prenatal course of indomethacin on the premature kidney as reflected by serum creatinine and urinary biomarkers. Study Design Urine of infants ≤ 32 weeks was collected for the first 14 days and analyzed for cystatin C, neutrophil gelatinase-associated lipocalin, osteopontin, β2 microglobulin, epidermal growth factor, uromodulin, and microalbumin. Bivariate analysis compared serum creatinine and biomarkers of exposed (INDO) and unexposed (CONT) subjects. Results Fifty-seven infants (35 CONT and 22 INDO) were studied. The cohorts were similar in gestational age, birthweight, race, gender, nephrotoxic medication exposure, and Apgar scores. CONT had more dopamine exposure and included more pre-eclamptic mothers (p = 0.005). No difference in creatinine-based acute kidney injury or the log transformed mean, maximum, and minimum values of urinary biomarkers was detected. Conclusion Our findings suggest that a short course of tocolytic indomethacin does not result in neonatal acute kidney injury. Key Points


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