The AKI(+) patients showed a weak interaction between the molecules at T0, with an increase in interactions between chemokines and cytokines after application of antivenom (T1 and T2), highlighting the chemokines CXCL-8 and CCL-2 at T1, in addition to the absence of participation of the regulatory cytokine IL-10 during clinical follow-up. Here, CCL2 is linked to acute kidney injury.