The aim of the present study was to establish a rat model of acute ischemic kidney injury by continually occluding the bilateral renal artery and renal veins, as well as to examine the role of asymmetric dimethylarginine (ADMA) in acute lung injury (ALI) induced by acute kidney injury (AKI). In total, 45 male Wistar rats were randomly divided into the control, AKI and AKI + SB203580 groups. The enzyme-linked immuno-sorbent assay method was used to assess the plasma levels of ADMA in each group. The activation of p38 mitogen-activated protein kinase (MAPK) and heat shock protein 27 (HSP27) was detected using western blot analysis. Immunofluorescence analyses of filamentous actin (F-actin) and globular actin (G-actin) were performed. The levels of plasma ADMA and the permeability index in the AKI group were significantly higher than those in the control and AKI + SB203580 groups. The expression of phosphorylated p38 (p-p38) and p-HSP27 was significantly higher in the AKI and AKI + SB203580 groups compared with the control group. The AKI group also demonstrated a higher expression of p-p38 and p‑HSP27 than the AKI + SB203580 group. The expression of F-actin was more marked in the AKI group than in the control and AKI + SB203580 groups. The F-/G-actin ratio in the AKI group was also higher compared with that in the control and AKI + SB203580 groups. The results from the present study indicated that plasma ADMA levels may be a good biomarker for AKI‑induced ALI. In addition, the p38 MAPK/HSP27 pathway is important in modulating the levels of ADMA.