Introduction and Aims: Acute kidney injury (AKI) complicates over 50% of ICU admissions. Episodes of AKI are a major risk factor for development or progression of chronic kidney disease (CKD). However, critical illness is associated with reduction in muscle mass, potentially reducing creatinine production and its serum concentration. Conversely active muscle breakdown and protein catabolism may increase urea production and its serum concentration. Thus neither marker may accurately assess true recovery of renal function after AKI. Methods: We performed a single‐centre, retrospective analysis of AKI diagnosis in patients with ICU admissions of 5 days or more who survived to hospital discharge between 2009 and 2011. We have previously analysis serum creatinine changes and the assessment of renal function in this population [1]. In an additional analysis we have now compared serum creatinine with urea at hospital admission, ICU discharge and hospital discharge. We stratified our analysis by maximal AKI category in hospital. Results: We studied 700 ICU admissions, with a 66% incidence of AKI. In all patients median creatinine decreased significantly from hospital admission to ICU discharge (84 vs. 56mumol/L p<0.001). Conversely, Urea rose significantly from hospital admission to discharge (5.8 vs 7.5mmol/L p<0.001). These changes occurred irrespective of the presence and severity of AKI. Decrease in Creatinine persisted to hospital discharge whereas Urea increases were more transient (Figs 1,2). Median Urea:Creatinine ratio almost doubled (67 to 126, p<0.001) from admission to ICU discharge was significantly elevated in all AKI categories at hospital discharge. Conclusions: We observed a divergence between creatinine and urea changes from admission to ICU discharge across all AKI categories. This calls into question the validity of passing validity of renal recovery on the basis of serum creatinine. Reduction in serum creatinine at ICU and hospital discharge may reflect reduced creatine production [2] and loss of muscle mass that accompanies critical illness [3]. Increases in urea may accompany reduced urea clearance or increased urea production accompanying protein breakdown. While urea levels can be acutely effected by severe dehydration or gastrointestinal haemorrhage, such conditions are very unlikely to apply in patients considered fit for ICU or Hospital discharge. Interpretation of renal function and nutritional status in survivors of critical illness is complicated by competing influences on the production of traditional biochemical markers of renal function, creatinine and urea and neither is likely to be reliable. (Figure Presented).
CITATION STYLE
Prowle, J. R., Kolic, I., & Kirwan, C. (2015). SP243DIVERGENT CHANGES IN SERUM CREATININE AND UREA IN SURVIVORS OF PROLONGED CRITICAL ILLNESS. Nephrology Dialysis Transplantation, 30(suppl_3), iii458–iii459. https://doi.org/10.1093/ndt/gfv190.55
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