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Cystatin C and Acute Kidney Injury pp. 165-186 $100.00
Authors:  (M. Guillouet, C. Guennegan, M. Coat, A. Khalifa, F. Lion, R. Deredec, C.C. Arvieux, G. Gueret, Pôle Anesthésie Réanimation, Centre Hospitalier Universitaire, Brest, France, and others)
Abstract:
Acute kidney injury (AKI) is defined as an abrupt and sustained decrease in kidney function. There are a lot of definitions in the literature, which explain the large variations in the reported incidence. It is well recognized for its impact on the outcome of patients, as it increases morbidity and mortality. Diagnosis of AKI is always difficult, particularly in the early stage of the disease. Numerous definitions and parameters have been used but the gold standard in clinical practice remains the creatinine clearance. Recently, in order to develop early biomarkers, cystatin C (CysC) was proposed. CysC is a protease inhibitor produced in a constant manner by nucleated cells. This molecule is passively filtrated by the glomerule and quite completely catabolized in the proximal tubules. It has the advantage of not being influenced by age, sex, race or muscular mass. Its excretion increases after reversible and mild dysfunction and may not necessarily be associated with persistent or irreversible damage. However, it is primilarly a sensitive marker of
reduction in glomerular filtration rate but it cannot differentiate between different types of AKI. Some studies demonstrated the superiority of CysC over plasma creatinine while other studies did not, depending on the population. On the other hand, urinary CysC
seems superior to conventional and new plasma markers, but its main disadvantage is its instability in the urine samples. In conclusion, we can use CysC like an additional argument of renal failure but it does not seem to be superior to plasma creatinine in the early diagnosis of AKI in all situations. 


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Cystatin C and Acute Kidney Injury pp. 165-186