KIM-1: A Non-Invasive Marker for Kidney Injury and Treatment Efficacy in FMF

Familial Mediterranean Fever (FMF) arises from mutations in the MEFV gene, which encodes the immune-regulatory protein pyrin. Early detection of FMF-associated kidney injury and identification of noninvasive biomarkers to monitor disease progression and treatment response are critical. This study aimed to measure serum Kidney Injury Molecule-1 (sKIM-1) levels in FMF patients, assess its potential as an early indicator of renal damage, and evaluate its utility in monitoring treatment efficacy.

Fifty FMF patients and 36 healthy controls were enrolled. Serum KIM-1 levels were determined by ELISA. Clinical and laboratory data were extracted from patient records. The relationships between sKIM-1, urine protein/creatinine ratio (UPCR), and estimated glomerular filtration rate (eGFR) were analyzed. Subgroup analyses compared sKIM-1 levels in patients treated with anakinra or canakinumab.

Median sKIM-1 was significantly higher in FMF patients than controls [571.30 pg/mL (562.50-586.90) vs. 562.40 pg/mL (558.10-580.40), p=0.040]. No correlation was observed between sKIM-1 and UPCR (p=0.547) or eGFR (p=0.232) in the FMF group. Canakinumab-treated patients exhibited significantly lower sKIM-1 levels [561.10 pg/mL (556.10-567.00) vs. 575.4 pg/mL (564.00-591.20), p=0.036], whereas anakinra treatment showed no significant difference [561.20 (558.40-595.70), 572 (564.60-588), (p=0.430)].

Elevated sKIM-1 in FMF patients and its reduction with canakinumab support KIM-1 as a noninvasive biomarker of renal involvement in FMF. These findings suggest KIM-1 may serve as a tool for monitoring disease activity and treatment response.