Fractional Excretion Of Urea Research Articles

Utility of fractional excretion of urea in the differential diagnosis of acute kidney injury in children.

The fractional excretion of sodium (FENa) has been used as an index for the differential diagnosis of acute tubular necrosis (ATN) and prerenal acute kidney injury (AKI). The reliability of this index, however, decreases with the use of the diuretic agent furosemide. The fractional excretion of urea nitrogen (FEUN) has been shown to be useful in such settings in adults. The objective of this study was to examine whether FEUN is also useful in these settings in children. We assessed 102 episodes of AKI in 74 children, classifying these into three groups based on history, physical examination, urine examination and subsequent clinical course: (1) prerenal AKI without furosemide (N = 37), (2) prerenal AKI with furosemide (N = 32) and (3) ATN (N = 33). Of the 37 prerenal AKI episodes without furosemide, 35 showed low FENa of <1%, with an overall average of 0.35 ± 0.11%, whereas prerenal AKI with furosemide (1.63 ± 0.37%) and ATN (8.76 ± 2.11%) were associated with a higher FENa. FEUN in the clinical setting of prerenal AKI was lower than that in ATN (27.9 ± 2.1 vs. 51.6 ± 3.8%, respectively) and, in contrast to FENa, not significantly different between the categories of prerenal AKI with and without furosemide (29.2 ± 3.1 vs. 25.1 ± 2.9, respectively). The sensitivity of FEUN <35% was 75% in prerenal AKI with furosemide, whereas that of FENa was 53%. FEUN is useful in detecting prerenal AKI in children administered furosemide.

Abstract 11007: Biochemical Urinalysis Predicts the Type of Decongestion and Worsening Renal Function due to Tolvaptan Administration in Patients With Acute Decompensated Heart Failure

Introduction: The diuretic response to tolvaptan (TLV) varies among patients with acute decompensated heart failure (ADHF). Although TLV is known to induce the excretion of free water, the accelerated excretion of sodium and urea has also been observed to varying degrees. Purpose: To classify the types of decongestion induced by TLV based on the initial induction of urinary sodium and urea excretion. Methods: We analyzed 90 ADHF patients who had been administered TLV. As markers of the initial TLV-induced excretion of sodium and urea, we measured changes in the fractional excretion of sodium (ΔFENa) and urea (ΔFEUN) prior to the first TLV administration and after eight hours. To evaluate the clinical course until normalization, 3-day and 7-day changes in body weight (ΔBW3, ΔBW7) and the inverse of hematocrit (Δ1/Ht3, Δ1/Ht7) after TLV administration were analyzed as markers of whole body and intravascular dehydration, respectively. Worsening renal function was assessed using 7-day changes in serum urea nitrogen (ΔUN7) and creatinine (ΔCr7) concentration. Results: Our analysis revealed negative correlations between ΔFEUN and ΔBW3 (r=-0.65, p&lt;0.001) and between ΔFENa and Δ1/Ht3 (r=-0.53, p&lt;0.001). Based on these findings, subjects were categorized into three groups. Firstly, subjects with positive and negative ΔFEUN were designated responders (n=60) and non-responders (n=30), respectively. Responders were further categorized based on the median value of ΔFENa (0.7%), where ΔFENa≥0.7 was the Natriuresis Group (n=30) and ΔFENa&lt;0.7 was the Aquaresis Group (n=30). During the 7 days after TLV administration, whole body dehydration was lowest in non-responders, intravascular dehydration was highest in the Natriuresis Group, and worsening renal function was lowest in the Aquaresis Group (Table). Conclusions: The initial induction of urinary sodium and urea excretion by TLV was able to predict the type of decongestion and worsening renal function in ADHF patients.

Fractional excretion of sodium and fractional excretion of urea in differentiating prerenal from renal azotemia complicating circulatory shock

Fractional excretion of sodium and fractional excretion of urea in differentiating prerenal from renal azotemia complicating circulatory shock

Assessment of fractional excretion of urea for early diagnosis of cardiac surgery associated acute kidney injury

Background: Acute kidney injury (AKI) is a common complication after cardiac surgery (CS). Recently, neutrophil gelatinase-associated lipocalin (NGAL) was shown to predict AKI development earlier than serum creatinine, but it is not widely used in clinical practice. Fractional excretion of urea (FeU) has been referred to as a useful tool to discriminate between prerenal and established AKI. The aim of our study is to evaluate the sensitivity and specificity of FeU, in the early diagnosis of AKI in patients undergoing CS. Methods: We performed a prospective study on adults undergoing CS. AKI was defined by AKIN criteria. Individuals suffering from CKD, were excluded. Sensitivity and specificity of FeU, fractional excretion of sodium (FeNa) and urine NGAL, measured at 1, 6 and 24 h following CS, were assessed. Results: We included 66 patients (26% female) aging 68 ± 11 years. AKI prevalence was 24% and mortality was 3.28%. Patients with AKI had a significantly lower FeU compared to those without AKI (23.89 ± 0.67% vs. 34.22 ± 0.58%; p < 0.05) 6 h after CS, but not at the 1- and 24-h time points. NGAL was also statistically significant between both groups. FeU showed a 75% sensitivity and 79.5% specificity; the AUC was 0.786. ROC analysis of FeU and NGAL yielded similar values (p = NS). Conclusion: FeU is useful as an early biomarker to predict AKI after CS and it is comparable to the new biomarker NGAL.

Alkaline phosphatase protects against renal inflammation through dephosphorylation of lipopolysaccharide and adenosine triphosphate.

Recently, two phase-II trials demonstrated improved renal function in critically ill patients with sepsis-associated acute kidney injury treated with the enzyme alkaline phosphatase. Here, we elucidated the dual active effect on renal protection of alkaline phosphatase. The effect of human recombinant alkaline phosphatase (recAP) on LPS-induced renal injury was studied in Sprague-Dawley rats. Renal function was assessed by transcutaneous measurement of FITC-sinistrin elimination in freely moving, awake rats. The mechanism of action of recAP was further investigated in vitro using conditionally immortalized human proximal tubular epithelial cells (ciPTEC). In vivo, LPS administration significantly prolonged FITC-sinistrin half-life and increased fractional urea excretion, which was prevented by recAP co-administration. Moreover, recAP prevented LPS-induced increase in proximal tubule injury marker, kidney injury molecule-1 expression and excretion. In vitro, LPS-induced production of TNF-α, IL-6 and IL-8 was significantly attenuated by recAP. This effect was linked to dephosphorylation, as enzymatically inactive recAP had no effect on LPS-induced cytokine production. RecAP-mediated protection resulted in increased adenosine levels through dephosphorylation of LPS-induced extracellular ADP and ATP. Also, recAP attenuated LPS-induced increased expression of adenosine A2A receptor. However, the A2A receptor antagonist ZM-241385 did not diminish the effects of recAP. These results indicate that the ability of recAP to reduce renal inflammation may account for the beneficial effect observed in septic acute kidney injury patients, and that dephosphorylation of ATP and LPS are responsible for this protective effect.

The Succinate Receptor 1 is a Physiological Regulator of the Renin‐Angiontensin Aldosterone System

It has been shown that oxidative cell stress in diabetes type I (DMI) induces tubular release of mitochondrial succinate and that subsequent activation of the SUCNR1 in the juxta‐glomerular apparatus is needed for renin release and DMI‐induced hypertension. Here, we tested whether the SUCNR1 also has a physiological role in renal water and electrolyte handling.Blood and urine analysis of wild‐type and SUCNR1‐/‐ mice showed that loss of SUCNR1 increased sodium and albumin excretion, and reduced renal renin and plasma angiotensin II (AngII) levels. Immunoblotting revealed decreased proximal tubular and inversely related medullary abundance of sodium‐hydrogen exchanger (NHE)‐3, and decreased abundance of the epithelial sodium channel ENaC. Nitric Oxide (NO) release, and fractional excretion of urea and water were increased, coinciding with reduced AQP2 abundance. With an unchanged overall morphology, wet, but not dry, weights of kidneys of SUCNR1‐/‐ mice were significantly higher than of wild‐type littermates.Our data reveal that the SUCNR1 is essential for the physiological maintenance of renin and AngII levels, and proper proximal tubule and collecting duct sodium reabsorption. Albumin release may be secondary to the decreased cortical NHE3 expression in proximal tubules, due to reduced AngII levels. Increased NO may underlie water loss.The increased wet kidney mass is likely due to tubular dilation due to increased tubular pressure because of life‐long diuresis. Our data thus indicate that the mammalian SUCNR1 is a physiological regulator of water and volume homeostasis.

The Urea-to-Creatinine Ratio Is Predictive of Worsening Kidney Function in Ambulatory Heart Failure Patients

BackgroundChanges in kidney function in heart failure patients convey important prognostic information. We investigated the association of the urea-to-creatinine (BUN/Cr) ratio, the fractional excretion of urea (FeUr), and the fractional excretion of sodium (FeNa) and subsequent declines in kidney function in ambulatory heart failure patients. Methods and ResultsWe prospectively enrolled adult patients with ejection fraction <40% at a multidisciplinary heart failure clinic and measured serial measurements of laboratory values from September 2008 to July 2011. The study outcome was changes in the estimated glomerular filtration rate (eGFR). In 138 patients contributing 10,350 patient-hours of follow-up, we found that participants with a decline of >25% in eGFR had higher mean BUN/Cr ratio (0.110 ± 0.043 vs 0.086 ± 0.026; P = .02) and no difference in the FeNa (1.81 vs 1.43; P = .2) or FeUr (32.3 vs 37.2; P = .9) compared with those with no change. There was an association of BUN/Cr ratio with the rate of change of eGFR (coefficient −25.67, 95% confidence interval [CI] −10.99 to −40.35; P < .0001). The BUN/Cr ratio was an independent predictor of eGFR drop >25% (odds ratio 1.19, 95% CI 1.07–1.32) and improved model discrimination (c-statistic increased from 0.624 to 0.693) and reclassification (net reclassification index 11.38% [P < .0001], integrated discrimination improvement 5.24% [P = .02]). ConclusionsThe BUN/Cr ratio is associated with worsening kidney function and adds incremental risk prediction information relative to traditional predictive measures in outpatients with heart failure at risk for worsening kidney disease.

Abstract 19099: The Fractional Excretion of Urea is Substantially Altered by Diuretics in Heart Failure Patients: Implications for its Use in the Evaluation of Worsening Renal Function

Background: In the setting of acute decompensated heart failure (ADHF), significant renal dysfunction (RD) is a common both at presentation and during treatment. The fractional excretion of urea (FeUrea) is often recommended to differentiate “pre-renal” from intrinsic RD in patients receiving diuretics. However, the intra-renal physiology regulating urea reabsorption theoretically should be affected by high dose loop diuretics which are commonly utilized in ADHF. Methods: Heart failure patients presenting to the Yale Transition Care Clinic who received treatment with loop diuretics were enrolled (n=64). Urine was collected at baseline and 60-90 minutes following administration of loop diuretics. Possible AKI was defined as a presenting serum creatinine ≥0.3 mg/dl above the lowest outpatient level in the prior 12 months. Results: Overall, 75.9% of the cohort had an estimated glomerular filtration rate &lt; 60 ml/min/1.73m^2 and 66.7% met criteria for possible AKI. As would be expected in a sodium avid HF population, the mean pre-diuretic FeUrea was 31.9 ± 10.2%. This was below the “pre-renal” FeUrea cutoff (&lt;35%) in 62.5% of patients. Following administration of 160 mg (50 to 280) of IV furosemide equivalents, FeUrea increased by an average of 7.3 ±8.5% (p&lt;0.0001). After diuretics, the percentage of patients with a “pre-renal” FeUrea decreased to 37.7% which translated into 42.5% of initially “pre-renal” patients no longer being classified as “pre-renal.” The change in FeUrea was unrelated to the diuretic induced urine output (r=0.19 p=0.14) or the dose of diuretic (r=0.17, p=0.20). There was significant individual variability in the change in FeUrea induced by loop diuretics (Figure) such that a loop diuretic “correction factor” would not be appropriate. Conclusion: Contrary to traditional wisdom, FeUrea does not appear to be a reliable tool to workup changes in renal function in ADHF patients receiving treatment with high dose loop diuretics.

Post cardiac surgery acute kidney injury: a woebegone status rejuvenated by the novel biomarkers.

Background:Acute kidney injury (AKI) is common after cardiac surgery, the incidence varying between 7.7% and 28.1%. It significantly increases morbidity and mortality. Creatinine considerably delays the diagnosis with its own attended demerits. Novel urinary biomarkers are emerging which help in rapid diagnosis thus reducing the morbidity and mortality. Biomarkers of our study were neutrophil gelatinase-associated lipocalin (NGAL) and Interleukin-18 (IL-18).Objectives:To find out the incidence of AKI in post-cardiac surgery patients in our hospital, the ability of the two biomarkers in early diagnosis in predicting the severity of AKI based on RIFLE’s criteria and their ability to discriminate pre-renal from intrinsic AKI.Patients and Methods:One-hundred patients who underwent cardiac surgery were selected. Midstream urine samples were collected at 3 time intervals (baseline before surgery, 24 hours and 7 days after surgery). Biomarkers were measured by ELISA using BIORAD processors. Fractional excretion of sodium and urea were used to discriminate pre-renal from intrinsic AKI.Results:Out of 100 patients, 31 had AKI, 11 being pre-renal and 20 intrinsic AKI. Four patients required renal replacement therapy (12.9% among AKI cases and 4% in the overall study cohort). Four among 31 expired in intensive care unit. Identifiable risk factors for AKI included insulin requiring diabetes mellitus, chronic obstructive pulmonary disease, increased cardio-pulmonary bypass time, combined valvular surgery and coronary artery bypass grafting, employment of intra-aortic balloon counter pulsation, left main coronary artery occlusion and an ejection fraction of < 40%. NGAL was extremely sensitive (area under curve-0.96) in detecting intrinsic AKI at 24 hours followed by IL-18 ratio with an area under curve of 0.89. Creatinine at 24 hours was able to detect only 31.6% of intrinsic AKI. None of the pre-renal cases showed rise in the urinary biomarker levels. Patients with higher stages of AKI had higher levels of both biomarkers than those at lower stages.Conclusions:NGAL and IL-18 obviated the disadvantages of creatinine. They were efficient in early detection of AKI, in differentiating pre-renal from intrinsic AKI and in predicting the severity of AKI reliably in post-cardiac surgery patients.

Transient versus Persistent Acute Kidney Injury and the Diagnostic Performance of Fractional Excretion of Urea in Critically Ill Patients

Aims: To evaluate the performance of fractional excretion of urea (FeU) for differentiating transient (T) from persistent (P) acute kidney injury (AKI) and to assess performance of FeU in predicting AKI in patients admitted to the ICU. Methods: We performed secondary analysis of a multicenter prospective observational cohort study on the predictive performance of biological markers for AKI in critically ill patients. AKI was diagnosed according to RIFLE staging. Results: Of 150 patients, 51 and 41 patients were classified as having T-AKI and P-AKI, respectively. The diagnostic performance for FeU to discriminate T-AKI from P-AKI on the day of AKI was poor (AUC-ROC = 0.61; 95% CI: 0.49-0.73). The diagnostic performance of FeU to predict AKI 1 and 2 days prior to AKI was poor as well (AUC-ROC = 0.61; 95% CI: 0.47-0.74, and 0.58; 95% CI: 0.43-0.73, respectively). Conclusions: FeU does not seem to be helpful in differentiating T- from P-AKI in critically ill patients and it is a poor predictor of AKI.

Acute Kidney Injury

1. David T. Selewski, MD* 2. Jordan M. Symons, MD† 1. *Department of Pediatrics and Communicable Diseases, Division of Nephrology, C.S. Mott Children’s Hospital, University of Michigan, Ann Arbor, MI. 2. †Department of Pediatrics, Division of Nephrology, University of Washington School of Medicine, Seattle, WA. * Abbreviations: ACE: : angiotensin-converting enzyme AKI: : acute kidney injury AKIN: : Acute Kidney Injury Network ANCA: : antineutrophil cytoplasmic antibody ATN: : acute tubular necrosis ECG: : electrocardiogram FEurea: : fractional excretion of urea FENa: : fractional excretion of sodium KDIGO: : Kidney Disease: Improving Global Outcomes NSAID: : nonsteroidal anti-inflammatory drug RIFLE: : Risk, Injury, Failure, Loss, and End-stage The term acute kidney injury has replaced acute renal failure and represents a spectrum of clinically meaningful kidney damage. After completing this article, readers should be able to: 1. Recognize and define the spectrum of acute kidney injury (AKI). 2. Understand the diagnostic approach and be able to differentiate the main causes of AKI. 3. Understand the complications of AKI and the treatment of a child with AKI. Acute kidney injury (AKI), formerly called acute renal failure, is characterized by multiple abnormalities, including increases in serum creatinine and blood urea nitrogen, electrolyte abnormalities, acidosis, and difficulties with fluid management. We have come to realize that what was previously thought to be relatively minor damage to the kidney can have significant short-term effects on morbidity and mortality and potential long-term implications for the development of chronic kidney disease. Thus, the term acute kidney injury has replaced acute renal failure , suggesting the spectrum of kidney damage that can occur. ### Definition AKI is classically defined as an acute decrease in glomerular filtration rate, which results in an increase in serum creatinine. It is important to recognize the limitations of creatinine as a marker of AKI because an increase in creatinine can be delayed by as much as 48 hours after damage to the kidney has occurred. Despite this limitation, change in creatinine remains the gold standard for the diagnosis of AKI. An evolution in the definition of AKI to better understand, characterize, and study the disease spectrum, has occurred, which has sought to capture the clinical importance of even small variations in kidney function. In addition, previous definitions used in the literature were widely disparate; this …

Acute Kidney Injury

Acute Kidney Injury

Impacts of active urea secretion into pars recta on urine concentration and urea excretion rate

It has been observed experimentally that early distal tubular urea flow exceeds urea delivery by the proximal convoluted tubule to the pars recta and loop of Henle. Moreover, the fractional excretion of urea in the urine may exceed values compatible with the reabsorption known to occur in the proximal convoluted tubule in the cortex. A likely explanation for these observations is that urea may be actively secreted into the pars recta, as proposed in a few studies. However, this hypothesis has yet to be demonstrated experimentally. In this study, we used a mathematical model of the renal medulla of the rat kidney to investigate the impacts of active urea secretion in the intrarenal handling of urea and in the urine concentrating ability. The model represents only the outer and inner medullary zones, with the actions taking place in the cortex incorporated via boundary conditions. Blood flow in the model vasculature is divided into plasma and red blood cell compartments. We compared urea flow rates and other related model variables without and with the hypothetical active urea secretion in the pars recta. The simulation suggests that active urea secretion induces a “urea-selective” improvement in urine concentrating ability by enhancing the efficiency of urea excretion without requiring a higher urine flow rate, and with only modest changes in the excretion of other solutes. These results should encourage experimental studies in order to assess the existence of an active urea secretion in the rodent kidney.

Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury

Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury

Comparison between fractional excretion of sodium and fractional excretion of urea in differentiating prerenal from renal azotemia in circulatory shock

BackgroundFractional excretion of sodium (FENa) is used to differentiate renal from prerenal azotemia. However, many drugs and medical conditions affect the sodium (Na+) handling in the kidney. But the fractional excretion of urea (FEurea) is dependent on passive forces and is less influenced by the diuretic therapy. ObjectiveComparison between FENa and FEurea in differentiating renal from prerenal azotemia in circulatory shock, and the effect of diuretics on their handling. MethodsBoth FENa and FEurea were measured in 40 patients (pts) with AKI complicating circulatory shock. The pts were divided into 26 pts with prerenal (group-1) and 14 pts with renal azotemia (group-2). Group-1 was subdivided into 12 pts who did not receive diuretics 24 h before the sampling process (group-1a) and 14 pts who received diuretics (group-1b). ResultsCompared to patients with renal azotemia (group-2), those with prerenal azotemia (group-1) showed significantly lower FENa (0.99 ± 0.66 and 2.57 ± 1.73, P < 0.05) respectively, and significantly lower FEurea (29.7 ± 7.6 and 43.7 ± 15.4, P < 0.001) respectively. For differentiating renal from prerenal azotemia, compared to FENa, FEurea showed better sensitivity (78.1% vs. 71.4%) and specificity (88.5% vs. 69.4%) respectively. Moreover, FEurea was not significantly affected by the use of diuretics; sensitivity (78% vs. 78%) and specificity (92% vs. 88%) respectively, compared to pts who did not receive diuretics. On the other hand, compared to pts who did not receive diuretics, the use of diuretics significantly affected FENa; sensitivity (64% vs. 71%) and specificity (58% vs. 70%) respectively. ConclusionsFEurea is more sensitive, specific and less affected by the use of diuretics than FENa in differentiating renal from prerenal azotemia in patients with AKI complicating circulatory shock.

Urinary output and fractional excretion of sodium and urea as indicators of transient versus intrinsic acute kidney injury during early sepsis

IntroductionThe pathophysiology of acute kidney injury (AKI) in sepsis is ill defined. We investigated parameters associated with low glomerular filtration, and their predictive value to discriminate transient from intrinsic septic AKI.MethodsIn 107 sepsis patients, AKI was defined by the Risk, Injury, Failure, Loss of Kidney Function, End-stage renal disease (RIFLE) urinary output or serum creatinine criterion, or both. Transient AKI (TAKI) versus intrinsic AKI was defined as RIFLE R, I, or F on the first day evolving to no AKI or not, respectively, over the following 5 days. Fractional excretion of sodium (FENa), urea (FEUrea), and NGAL (FENGAL) at admission (d0t0), 4 (d0t4), and 24 hours (d1) was determined.ResultsIncluding versus not including the urinary-output criterion of RIFLE increased AKI from 43% to 64.5%. Median uNGAL levels and FENGAL were lower in no AKI versus transient AKI when AKI was defined based on creatinine (P = 0.002 and P = 0.04, respectively), but not when based on urinary output (P = 0.9 and P = 0.49, respectively). FENa < 1% and FEUrea <35% was present in 77.3% and 63.2% of patients. Urinary NGAL was higher (P < 0.001) in those with high versus low fractional sodium excretion, but this was only in patients with transient or intrinsic AKI (P < 0.001 in subgroups), and not in patients without AKI. The negative predictive value for either intrinsic AKI or not restoring diuresis in patients with FENa > 0.36% and FEUrea > 31.5% was 92% and 94.5% respectively.ConclusionsA low FENa and FEUrea is highly prevalent in the first hours of sepsis. In sepsis, oliguria is an earlier sign of impending AKI than increase in serum creatinine. A combination of a high FENa and a low FEUrea is associated with intrinsic AKI, whereas a combined high FENa and FEUrea is strongly predictive of transient AKI.

Diagnostic accuracy of early urinary index changes in differentiating transient frompersistent acute kidney injury in critically ill patients: multicenter cohortstudy

IntroductionUrinary indices have limited effectiveness in separating transient acute kidney injury (AKI) from persistent AKI in ICU patients. Their time-course may vary with the mechanism of AKI. The primary objective of this study was to evaluate the diagnostic value of changes over time of the usual urinary indices in separating transient AKI from persistent AKI.MethodsAn observational prospective multicenter study was performed in six ICUs involving 244 consecutive patients, including 97 without AKI, 54 with transient AKI, and 93 with persistent AKI. Urinary sodium, urea and creatinine were measured at ICU admission (H0) and on 6-hour urine samples during the first 24 ICU hours (H6, H12, H18, and H24). Transient AKI was defined as AKI with a cause for renal hypoperfusion and reversal within 3 days.ResultsSignificant increases from H0 to H24 were noted in fractional excretion of urea (median, 31% (22 to 41%) and 39% (29 to 48%) at H24, P < 0.0001), urinary urea/plasma urea ratio (15 (7 to 28) and 20 (9 to 40), P < 0.0001), and urinary creatinine/plasma creatinine ratio (50 (24 to 101) and 57 (29 to 104), P = 0.01). Fractional excretion of sodium did not change significantly during the first 24 hours in the ICU (P = 0.13). Neither urinary index values at ICU admission nor changes in urinary indices between H0 and H24 performed sufficiently well to recommend their use in clinical setting (area under the receiver-operating characteristic curve ≤0.65).ConclusionAlthough urinary indices at H24 performed slightly better than those at H0 in differentiating transient AKI from persistent AKI, they remain insufficiently reliable to be clinically relevant.

Volume Management in the Critically Ill Patient with Acute Kidney Injury

Acute kidney injury (AKI) frequently occurs in the setting of critical illness and its management poses a challenge for the intensivist. Optimal management of volume status is critical in the setting of AKI in the ICU patient. The use of urine sodium, the fractional excretion of sodium (FeNa), and the fractional excretion of urea (FeUrea) are common clinical tools used to help guide fluid management especially further volume expansion but should be used in the context of the patient's overall clinical scenario as they are not completely sensitive or specific for the finding of volume depletion and can be misleading. In the case of oliguric or anuric AKI, diuretics are often utilized to increase the urine output although current evidence suggests that they are best reserved for the treatment of volume overload and hyperkalemia in patients who are likely to respond to them. Management of volume overload in ICU patients with AKI is especially important as volume overload has several negative effects on organ function and overall morbidity and mortality.

Acute kidney injury in sepsis: transient or intrinsic?

The negative prediction of intrinsic versus transient acute kidney injury (AKI) in septic patients may be facilitated by combined assessment of fractional excretion of sodium and urea. If both excretions are high this would signal the presence of transient AKI and suggest that successful restoration of diuresis by conservative therapy is likely, thus supporting a wait-and-watch approach regarding the initiation of acute renal replacement therapy.

Urine biochemistry in septic and non-septic acute kidney injury: a prospective observational study

PurposeDetermine whether there are unique patterns to the urine biochemistry profile in septic compared with non-septic acute kidney injury (AKI) and whether urinary biochemistry predicts worsening AKI, need for renal replacement therapy and mortality. Materials and MethodsProspective cohort study of critically ill patients with septic and non-septic AKI, defined by the RIFLE (Risk, Injury, Failure, Loss, End-Stage) criteria. Urine biochemistry parameters were compared between septic and non-septic AKI and were correlated with neutrophil gelatinase-associated lipocalin (NGAL), worsening AKI, renal replacement therapy (RRT), and mortality. ResultsEighty-three patients were enrolled, 43 (51.8%) with sepsis. RIFLE class was not different between groups (P = .43). Urine sodium (UNa) <20 mmol/L, fractional excretion of sodium (FeNa) <1%, and fractional excretion of urea (FeU) <35% were observed in 25.3%, 57.8%, and 33.7%, respectively. Septic AKI had lower UNa compared with non-septic AKI (P = .04). There were no differences in FeNa or FeU between groups. Urine NGAL was higher for FeNa≥1% compared to FeNa<1% (177.4 ng/mL [31.9-956.5] vs 48.0 ng/mL [21.1-232.4], P = .04). FeNa showed low correlation with urine NGAL (P = .05) and plasma NGAL (P = .14). There was poor correlation between FeU and urine NGAL (P = .70) or plasma NGAL (P = .41). UNa, FeNa, and FeU showed poor discrimination for worsening AKI, RRT and mortality. ConclusionUrine biochemical profiles do not discriminate septic and non-septic AKI. UNa, FeNa, and FeU do not reliably predict biomarker release, worsening AKI, RRT or mortality. These data imply limited utility for these measures in clinical practice in critically ill patients with AKI.