Renal Injury is Worsened when Consuming a Caffeinated Soft‐Drink during and after Exercise in the Heat
Authors: Chapman Christopher L. , Johnson Blair D. , Sackett James R. , Parker Mark D. , Schlader Zachary J. 
Published: June 2021

An epidemic of chronic kidney disease is occurring in people regularly working in hot environments. Hyperthermia and dehydration due to physical work in the heat induces acute kidney injury (AKI). It is believed that recurrent AKI can cause chronic kidney disease. In rats, AKI caused by hyperthermia and dehydration is worsened when consuming a soft drink‐like beverage, but if this is also true in humans is not known.PurposeTest the hypothesis that consuming a caffeinated soft drink during exercise in the heat worsens renal dysfunction and AKI in humans.MethodsTwelve healthy adults (24 ± 5 y, 3 F) completed randomized soft drink (Mtn Dew, Soda) and water control (Water) trials. Subjects completed four 1 h work‐rest cycles (45 min exercise, 15 min seated rest) in a 35°C, 65% RH environment. During rest, subjects drank 0.5 L of the assigned beverage (~11°C). After leaving the laboratory, subjects drank 1 L of the beverage or a volume equal to 115% of body mass lost, whichever was greater. Thermal data, and venous blood and urine samples were taken pre‐ (PRE) and post‐ (POST) exercise, and 24 h after PRE (24h). Urine flow rate was calculated from the overnight period, providing an index of renal function. Stage 1 AKI was defined as an increase in serum creatinine ≥0.3 mg/dL from PRE. Plasma and urine neutrophil gelatinase‐associated lipocalin (NGAL), a novel biomarker of AKI, were also measured. Percent changes in plasma volume were estimated from changes in hemoglobin and hematocrit. Data are reported as a change from PRE (mean ± SD) unless otherwise indicated.ResultsIncreases in intestinal temperature (Soda: 0.8 ± 0.3, Water: 0.8 ± 0.3°C, p=0.46) and changes in body weight (Soda: −0.3 ± 0.8, Water: 0.0 ± 0.7%, p=0.20) were not different between trials at POST. At POST, plasma osmolality was elevated in Soda (2±3 mOsm/kg) and reduced in Water (−6±3 mOsm/kg, p<0.01), but was restored in both trials at 24h (p=0.96). Plasma volume was reduced in Soda at POST (p=0.02), but did not differ between trials (Soda: −5 ± 6%, Water: −2 ± 7%, p=0.15). The increase in serum creatinine was greater in Soda at POST (0.3 ± 0.1 vs. 0.2 ± 0.1 mg/dL, p<0.01) and 24h (0.1 ± 0.1 vs. 0.0 ± 0.1 mg/dL, p=0.01). Serum uric acid was elevated in Soda at POST (1.1 ± 0.5 vs 0.4 ± 0.3 mg/dL, p<0.01), and 24h (0.3 ± 0.5 vs 0.0 ± 0.6 mg/dL, p=0.05). Overnight urine flow rate (1.5 ± 0.5 vs. 1.8 ± 0.6 mL/min, p=0.01) was lower in Soda. The incidence of Stage 1 AKI at POST was higher in Soda (75 vs. 8%, p<0.01) and was fully recovered at 24h in both trials. Plasma NGAL increased at POST (P<0.01) in both trials, but did not differ between trials (Soda: 13 ± 10, Water: 16 ± 10 ng/mL, p=0.43) and was restored at 24h in both trials (p≥0.90). Urine NGAL was not different between trials at POST (11 ± 33 vs. 8 ± 17 ng/mL, p=0.99) and was elevated at 24h in only Soda (35 ± 50 ng/mL, p=0.02), but this was not different from Water (34 ± 51 ng/mL, p=0.15). Urine NGAL in the overnight sample was higher in Soda (9 ± 11 vs. 7 ± 7 ng/mL, p=0.04).ConclusionConsuming a caffeinated soft‐drink during and following physical work in the heat acutely exacerbates renal dysfunction and AKI in humans.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.