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In septic shock, bacterial LPS is able to activate the CaSR of cardiomyocytes inducing their apoptosis in vitro. CaSR activation in monocytes is responsible for activation of the NLRP3 inflammasome and macropinocytosis. In front of this immune axis, a variation in the monocyte expression of the CaSR is expected in the state of shock. This is already observed in other pathologies such as renal failure or in animal models of severe burns. If this is considered as an overall reflection of CaSR expression in the body, it would be consistent with the phosphocalcic disturbances associated with septic shock. The phosphocalcic balance is often modified, and not treated during the acute episode, with in particular hypocalcaemia which could be consecutive to a hyperactivation or overexpression of the CaSR. This study proposes to explore for the first time the expression of monocytic CaSR in patien
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