Clinical and Biological Relevance of Kidney Injury Molecule-1 and Beta-2 Microglobulin in Monitoring Patients with Systemic Lupus Erythematosus

Introduction: Variations in kidney injury molecule-1 (KIM-1) and beta2-microglobulin (β2MG) levels, both involved in the pathogenesis of systemic autoimmunity, have been linked to tubulointerstitial lesions in patients with systemic lupus erythematosus (SLE). However, the significance of KIM-1 and β2MG in the pathogenesis and development of extrarenal manifestations in SLE remains unclear. This study aims to investigate the relationship between KIM-1 and β2MG levels, measured in both serum and urine, and their association with the clinical and biological features of SLE. Materials and Methods: KIM-1 and β2MG levels were measured in 80 adult patients with SLE (who exhibited mucocutaneous, hematological, and renal manifestations) and 30 control subjects. All patients with renal abnormalities related to SLE underwent a renal biopsy. The serum and urinary levels of KIM-1 (measured in pg/mL for serum and ng/mL for urine) and β2MG (measured in ng/dl for serum and mg/l for urine) were determined for each subject using the ELISA method and immunoturbidimetry, respectively. Results: There were significant differences in the serum and urinary levels of KIM-1 and β2MG between the SLE group and the control group, as well as among subgroups with different manifestations (renal, cutaneous, and hematological). Elevated levels of KIM-1 and β2MG, in both serum and urine, were associated with the clinical activity of the disease, the inflammatory process, and the development of tissue damage in various organs, leading to declines in renal function, hematological disorders, and mucocutaneous manifestations. Conclusions: KIM-1 may play a pathogenic role in kidney injury and disease, while β2MG could have a pathogenic role in both kidney and non-kidney diseases. In summary, KIM-1 characterizes renal involvement, while serum β2MG correlates with the progression of cumulative lesions in SLE patients. Our findings could enhance early diagnosis, predict disease progression, and elucidate the pathogenic mechanisms underlying SLE.