Among all patients admitted to intensive care, it is estimated that more than half of them are exposed during their stay to acute renal failure (ARF). Impacting the vital prognosis to short term, the occurrence of renal failure is not without consequences in intensive care survivors, presenting an increased risk of death mainly mediated by an excess risk with regard to chronic kidney disease and/or certain cardiovascular pathologies.
Malnutrition, particularly vitamin deficiency, has already been reported as a risk factor for AKI. Studies on two models (animal and human) have recently highlighted the importance of NAD+ production failure in the onset of renal failure.
NAD+ synthesis can be done from tryptophan or via a salvage pathway from vitamin PP.
In a phase 2 study in patients undergoing cardiac surgery, vitamin B3 supplementation was accompanied by a reduction in the occurrence of AKI and a limitation of the duration / intensity of renal dysfunction.
This innovative research aims to identify an alteration in the metabolic pathway of NAD+ production as a risk factor for AKI in intensive care patients. This would be the first study to address this issue in this specific population.
The main objective of this research is to describe the association between the urinary Quinolinate/Tryptophan ratio on admission and the occurrence of acute renal failure in patients admitted to intensive care unit.
Patient, male or female aged over 18,
Patient admitted to intensive care for a reason with a high risk of ARI: shock, sepsis, cardio-circulatory arrest, post-operative unscheduled surgery, post-operative cardiac surgery,
Patient with normal renal function on admission,
Patient affiliated to or beneficiary of a social security scheme,
Minor patient,
History of chronic kidney disease,
History of kidney transplant,
Admission for a reason with a low risk of ARI (neuroresuscitation, voluntary drug intoxication with anxiolytics - antidepressants - psychotropic drugs),