LAUSR

Purpose Partial clear cell renal cell carcinoma (CCRCC) may be sensitive to immune checkpoint inhibitor treatment targeting the programmed cell death 1 (PD-1)/programmed cell death 1 ligand 1 (PD-L1) pathway. Assessing the levels of PD-L1 using non-invasive imaging is useful to select immunotherapy-sensitive patients. Currently, whether PD-L1 levels in CCRCC correlate with 18F fluorodeoxyglucose (18F-FDG) uptake is unknown. This study aimed to assess whether 18F-FDG-positron emission tomography (PET) imaging could be used to infer PD-L1 levels in CCRCC. Methods Immunohistochemistry (IHC) was used to assess PD-L1 levels in samples of tumors obtained retrospectively from a cohort of 58 patients with CCRCC who also received 18F-FDG PET/CT imaging. The IHC scores for PD-L1 were compared with the 18F-FDG maximum standardized uptake value (SUVmax), and the mean standardized uptake value (SUVmean) value, with the clinical characteristics of CCRCC, and with the IHC scores of enzymes related to glucose metabolism (glucose transporter type 1 (GLUT1), hexokinase 2 (HK2), lactate dehydrogenase A (LDHA)), and Von Hippel-Lindau tumor suppressor (VHL). Results Increased renal venous invasion, lymph node metastasis, tumor size, SUVmean, and SUVmax correlated significantly with higher PD-L1 levels (P < 0.05). The IHC scores of VHL and LDHA correlated positively with those of PD-L1 (P = 0.035, P = 0.011, respectively). Significant correlations between PD-L1 levels and SUVmean and lymph node metastasis were observed upon multivariate analysis. SUVmean combined with lymph node metastasis predicted that 20.59% of the low probability group would express PD-L1, 29.41% of the medium probability group would express PD-L1, and 71.43% of the high probability group would express PD-L1. Conclusion The status of lymph node metastasis, SUVmax, and SUVmean of the primary lesion correlated with PD-L1 levels in CCRCC. A combination of lymph node metastasis status and SUVmean could be utilized to predict PD-L1 levels, thus allowing monitoring of a tumor’s immunotherapy response.