With a global burden of 844 million,
chronic kidney disease (CKD) is now considered a public health priority. Cardiovascular risk is pervasive in this population, and low-grade systemic
inflammation is an established driver of adverse cardiovascular outcomes in these patients. Accelerated cellular senescence, gut microbiota-dependent immune activation, posttranslational
lipoprotein modifications, neuroimmune interactions, osmotic and nonosmotic
sodium accumulation,
acute kidney injury, and precipitation of crystals in the kidney and the vascular system all concur in determining the unique severity of
inflammation in CKD. Cohort studies documented a strong link between various
biomarkers of
inflammation and the risk of progression to
kidney failure and cardiovascular events in patients with CKD. Interventions targeting diverse steps of the innate immune response may reduce the risk of cardiovascular and
kidney disease. Among these, inhibition of IL-1β (interleukin-1 beta) signaling by
canakinumab reduced the risk for cardiovascular events in patients with
coronary heart disease, and this protection was equally strong in patients with and without CKD. Several old (
colchicine) and new drugs targeting the innate immune system, like the
IL-6 (
interleukin 6) antagonist
ziltivekimab, are being tested in large randomized clinical trials to thoroughly test the hypothesis that mitigating
inflammation may translate into better cardiovascular and kidney outcomes in patients with CKD.