Figure 6

Hypothetical schema integrating experimental findings in this study of KLK1 in AKI. This diagram is presented not as established fact, but rather to generate hypotheses for further investigation. Endogenous factors may influence KLK1 synthesis and renal excretion: lower BP in AKI may activate baroreceptors, thus increasing endogenous secretion of epinephrine, thereby increasing both heart rate and urinary kallikrein excretion. KLK1 promoter genetic variants or CpG methylation can influence renal kallikrein production. Finally, exogenous factors such as adrenergic pressor infusions or diuretic treatment can also increase renal kallikrein production; indeed, since a subset of our AKI cases received such treatments (Table 1), we cannot exclude this possibility.