3.6 Alterations of urine and serum metabolites over time in
patients without clinical acute kidney injury
Urine and serum samples from the no AKI group were analyzed via one-way
ANOVA to investigate the effects of cisplatin treatment independent of
AKI. Following cisplatin infusion, metabolites primarily followed one of
two trends: 1) an initial increase or decrease 24-48 hours after
cisplatin, and a subsequent return to baseline at the post timepoint; 2)
an initial increase or decrease at the 24-48h timepoint that was
sustained at the post timepoint. In urine, L-acetylcarnitine
(↑3.64-fold), L-carnitine (↑8.91-fold), 3-hydroxydecanedioc acid
(↑2.42-fold), malate (↑3.56-fold), pyruvate (↑4.87-fold), and
valerylcarnitine (↑4.76-fold), followed the first trend, where
metabolite levels were significantly increased 24-48h following
cisplatin treatment and returned to baseline levels by the post
timepoint (Figure 6A, 6B, 6E, 6F, 6H ). Serum levels of
L-arginine (↑1.96-fold), L-carnitine (↑1.40-fold), proline (↑1.63-fold),
TMAP (↑4.14-fold), and valerylcarnitine (↑1.79-fold) followed the same
pattern, with a significant increase at 24-48h, and a return to baseline
at the post timepoint (Figure 6I, 6K, 6N, 6O, 6P ). Conversely,
levels of urine indole-3-acetate (↓1.82-fold) and serum cortisol
(↓5.18-fold) were significantly lower 24-48h following cisplatin
treatment, with a subsequent return to baseline by the post timepoint
(Figure 6D, 6J ). Urinary succinate and serum 4-hydroxycinammic
acid and phenylalanine followed the second trend, where metabolite
levels were significantly altered 24-48h following cisplatin infusion
(↓1.88-fold for succinate; ↑1.56-fold and ↑1.43-fold for
4-hydroxycinammic acid and phenylalanine, respectively), with the
alterations being sustained at the post timepoint (Figure 6G,
6L, 6M ). Similar metabolite alterations were observed over time for
patients in the AKI group (Figure S1 ).