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 ).