Chronic kidney failure is a pathology affecting several million people worldwide. Vascular calcification is one of the dreaded complications of the disease. A recent study, based on proteomic analysis, has highlighted a key element of this mechanism: the inflammatory protein calprotectin. These new data on the pathology open up promising therapeutic perspectives, offering a glimmer of hope to patients.
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Chronic kidney failure is a common disease. It results from the progressive and irreversible destruction of kidneyskidneys. It is a fatal disease. In Europe, almost 30% of people over 70 are affected. The two main causes are diabetes and hypertension. Vascular calcification is a severe complication of the disease. It is characterized by an accumulation of mineralsminerals in blood vessels, leading to serious cardiovascular pathologies. It is one of the leading causes of death among patients with chronic kidney disease. Current therapeutic solutions are insufficient. Researchers from Toulouse University Hospital, Inserm and Toulouse III-Paul Sabatier University decided to look into the question. Their work was published in the journal Science Translational Medicine.
Calprotectin, a crucial inflammatory protein
The authors employed proteomic analysis, supplemented by Elisa tests on plasma samples from chronic kidney disease patients undergoing dialysis. A proteomic analysis is an exploration method used to identify the presence of proteins in a biological sample.
A first study involving 112 Spanish patients and 171 French patients highlighted the presence of a proteinprotein inflammatory, calprotectin, in the serumserum patients. A high level of this protein was correlated with an increased risk of cardiovascular complications and greater mortality. These results could be confirmed in a group of 170 Swedish patients.
Additional research, on human and mouse cells, has proven the role of calprotectin in vascular calcification.
New therapeutic hopes
This opens the way to new therapeutic avenues. In particular, paquinimod – a calprotectin inhibitor – has been shown to be potentially effective in limiting vascular calcification in human and mouse cell models. Indeed, paquinimod helped prevent vascular calcification in mice suffering from chronic renal failure. These data confirm the role of calprotectin in vascular calcification.
Even if much work is still necessary, these new data on the understanding of vascular calcification offer promising prospects for improving patient care and reducing mortality linked to cardiovascular events.
