Intermediate monocytes in blood correlate with subclinical vascular changes in lupus nephritis

Atherosclerosis cardiovascular disease (ASCVD)-related mortality is higher in patients with lupus nephritis (LN) compared with those without nephritis (11.7 vs 3.6 per 100 patient-years).1 Accelerated atherosclerosis risk in LN cannot be fully explained by traditional risk factors. Many hypothesise that dysregulated cytokine profiles and altered cellular subsets may trigger endothelial dysfunction and plaque destabilisation, accelerating atherosclerosis risk in LN.2 We recently established that moderate-severe renal arteriosclerosis (ASCL) in kidney biopsies is a marker of premature endothelial dysfunction in LN and is associated with three times higher 10-year clinical ASCVD occurrence, underscoring its role as potential proxy for clinical ASCVD.3 Yet, long-term monitoring of renal ASCL is difficult, as it requires baseline and repeat invasive kidney biopsies. Therefore, a cellular surrogate biomarker of renal vascular changes that may predict clinical ASCVD risk is needed in LN.