Recent studies have suggested that some blood physicochemical and urinary biochemical parameters have a standardized behavior during acute kidney injury (AKI) development. The changes in these parameters frequently begin to occur before significant rises in serum creatinine (sCr) and may help in identifying patients with more subtle decreases in glomerular filtration rate (GFR). Surgical patients have an increased risk of AKI but renal impairment is usually not evident at ICU admission. We hypothesized that the surgical patients who have AKI diagnosed in the early postoperative period have an impaired GFR since ICU admission, indirectly inferred by alterations in these blood physicochemical and urinary biochemical parameters even in the presence of a still normal sCr. We retrospectively evaluated 112 surgical patients who were categorized according to AKI development during the first 3 ICU days. Twenty-eight patients developed AKI, most of them in the first day (D1) after ICU admission (D0). AKI patients had, at D0, lower serum pH and albumin, higher C -reactive protein (CRP), lower urine sodium (NaU) and fractional excretion of urea (FEUr). Fractional excretion of potassium (FEK) was high in both groups at D0 but remained high in the subsequent days only in AKI patients. Very low CRP and high serum albumin, high NaU and FEUr values at ICU admission had a significant negative predictive value for AKI. We concluded that some easily assessed parameters in blood and urine may help to identify patients with indirect signs of increased inflammatory response and decreased GFR at ICU admission, which could help to predict the risk of postoperative AKI development. ARTICLE HISTORY

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In the past, urine biochemistry was a major tool in acute kidney injury (AKI) management. Classic papers published some decades ago established the values of the urine indices which were thought to distinguish "pre-renal" (functional) AKI attributed to low renal perfusion and "renal" (structural) AKI attributed to acute tubular necrosis (ATN). However, there were a lot of drawbacks and limitations in these studies and some recent articles have questioned the utility of measuring urine electrolytes especially because they do not seem to adequately inform about renal perfusion nor AKI duration (transient vs. persistent). At the same time, the "pre-renal" paradigm has been consistently criticized because hypoperfusion followed by ischemia and ATN does not seem to explain most of the AKI developing in critically ill patients and distinct AKI durations do not seem to be clearly related to different pathophysiological mechanisms or histopathological findings. In this new context, other possible roles for urine biochemistry have emerged. Some studies have suggested standardized changes in the urine electrolyte composition preceding increases in serum creatinine independently of AKI subsequent duration, which might actually be due to intra-renal microcirculatory changes and activation of sodium-retaining mechanisms even in the absence of impaired global renal blood flow. In the present review, the points of controversy regarding urine biochemistry assessment were evaluated as well as future perspectives for its role in AKI monitoring. An alternative approach for the interpretation of measured urine electrolytes is proposed which needs further larger studies to be validated and incorporated in daily ICU practice.

We have recently suggested that sequential urine electrolyte measurement in critically ill patients may be useful in monitoring kidney function. Cardiac surgery is one of the leading causes of acute kidney injury (AKI) in the intensive care unit (ICU). In this paper, we describe the sequential behavior of urine electrolytes in three patients in the early (first 60 hours) postoperative period after cardiac surgery according to AKI status: no AKI, transient AKI, and persistent AKI. We have found that the patient with no AKI had stable and high concentrations of sodium (NaU) and chloride (ClU) in sequential spot samples of urine. AKI development was characterized in the other two patients by decreases in NaU and ClU, which have started early after ICU admission. Transient AKI was marked by also transient and less severe decreases in NaU and ClU. Persistent AKI was marked by the less favorable clinical course with abrupt and prolonged declines in NaU and ClU values. These electrolytes in urine had a behavior like a “mirror image” in comparison with that of serum creatinine. We suggest that sequential urine electrolytes are useful in monitoring acute kidney injury development in the early postoperative period after cardiac surgery.