Fractional Excretion Of Urea Research Articles

Utility of fractional excretion of urea in acute kidney injury with comparison to fractional excretion of sodium: A systematic review and meta-analysis

BackgroundDifferentiating between intrinsic and prerenal acute kidney injury (AKI) presents a challenge. Here, we assessed the performance of the fractional excretion of urea (FEUrea) and compared it to the fractional excretion of sodium (FENa) in distinguishing intrinsic from prerenal AKI. MethodsA thorough search was conducted in several databases until January 16, 2024. We included studies evaluating FEUrea, with or without FENa, for differentiating AKI etiologies in adults. We assessed the methodological quality using the QUADAS-2 and QUADAS-C tools. We performed a meta-analysis using the bivariate random effects model, with subgroup analyses to explore the impact of diuretic therapy on FEUrea, and direct statistical comparisons between FEUrea and FENa involving the subgroups with and without diuretics. ResultsWe included 11 studies with 1108 hospitalized patients. Among eight studies (915 patients) evaluating FEUrea >35% for distinguishing intrinsic from prerenal AKI, the pooled sensitivity and specificity were 66% (95% CI, 49%–79%) and 75% (95% CI, 60%–85%), respectively. In a subset of six studies (302 patients) comparing FEUrea at 35% to FENa at 1% in patients not receiving diuretics, there were no significant differences in sensitivity (77% versus 89%, P = 0.410) or specificity (80% versus 79%, P = 0.956). In four studies, 244 patients on diuretics, FEUrea demonstrated lower sensitivity (52% versus 92%, P < 0.001) but higher specificity (82% versus 44%, P < 0.001) compared to FENa for the diagnosis of intrinsic AKI. ConclusionsFEUrea has limited utility in differentiating intrinsic from prerenal AKI. FEUrea does not provide a superior alternative to FENa, even in patients receiving diuretics.

Urinary biomarkers in different diuretic response groups with heart failure

Abstract Purpose Predicting diuretic response in different hemodynamic profiles is challenging in heart failure patients. Worsening renal function with diuretic therapy leads to decision making more difficult. Spot urinary sodium is an important milestone to determine decongestion therapy intensity. Serum biomarkers are widely used for diagnosis and follow up but more urinary biomarkers can be identified for risk stratification. Methods We enrolled 61 patients with decompansated heart failure on the first day of admission. Baseline characteristics and urinary biomarkers were recorded. Diuretic response was classified as good or poor response groups according to spot urine sodium within second hour after first intravenous diuretic administration. Quantitative variables were specified as mean ± standard deviation, categorical variables were specified as frequency and percentage. Mean differences were assessed with Student-T test and Welch test. Statistically significant parameters were also assessed with logistic regression analysis. Results Only U/P creatinine ratio and urine creatinine were statistically lower in good diuretic response group (p&amp;lt;0.0001). Fractional excretion of urea and potassium were higher in good response group (p&amp;lt;0.0001 and p&amp;lt;0.005). Urinary sodium to potassium ratio, UNa/UCr and UK/UCr are also statistically higher in the good response group (p&amp;lt;0.0001). Sodium associated parameters (UNa/UK, UNa/UCr) and urinary creatinine were also significant in logistic regression. Discussion Urinary biomarkers are not well defined parameters in heart failure patients but these parameters may be more dynamic than serum parameters as spot urine sodium. Our data indicates that poor response group has a more prerenal phenotype than good response group.Table 1.Urine biomarker definitionsTable 2.Results

Fractional Excretion of Urea for the Differential Diagnosis of AKI: A Systematic Review and Meta-Analysis with Comparison to Fractional Excretion of Sodium

Fractional Excretion of Urea for the Differential Diagnosis of AKI: A Systematic Review and Meta-Analysis with Comparison to Fractional Excretion of Sodium

THU280 Acute Interstitial Nephritis- A Complication Of Semaglutide Use

Abstract Disclosure: M. Alsayed Hasan: None. J. Doroshow: None. Background: With the widespread use of glucagon-like peptide 1 (GLP-1) agonists in diabetes, several cases have been reported of GLP-1 induced acute interstitial nephritis (AIN) with variable recovery in kidney function (1). Although it is a rare side effect, the primary management requires early identification and removal of the offending agent. Clinical Case: A 75-year-old male presented with a week of nausea, vomiting, abdominal pain, and reduced urine output. He was started on semaglutide 4 months prior to admission when his creatinine was 1.16 mg/dL. Initial lab abnormalities included an elevated blood urea nitrogen 119 mg/dL (n 8-20 mg/dL), elevated creatinine 13.8 mg/dL (n 0.7-1.3 mg/dL), anion gap acidosis with a CO2 of 15 mEq/L (n 22-32 mEq/L) and an anion gap of 18 (n&amp;lt;12), lipase 659 U/L (n 20-51 U/L). His urinalysis demonstrated too numerous to count red blood cells, 4-10 white blood cells, rare eosinophils and no casts or crystals. Urine culture was negative. The fractional excretion of sodium and urea were 5.56% and 56% respectively, consistent with intrinsic renal disease. CT of the abdomen and pelvis demonstrated peri-pancreatic inflammation. A follow up renal ultrasound showed normal echotexture with no hydronephrosis or renal calculi. His picture was concerning for pancreatitis and pre-renal/acute tubular necrosis from diuretic use and vomiting. Despite aggressive fluid resuscitation, there was minimal improvement in his creatinine. Further work up for his renal injury was negative for monoclonal antibodies on protein electrophoresis and immunofixation. An autoimmune work up was negative for antinuclear antibody, anti-double stranded DNA, antineutrophil cytoplasmic (ANCA) myeloperoxidase IgG, anti-proteinase 3 ANCA IgG, glomerular basement membrane antibody, hepatitis B and C antibodies, and HIV. Complements and immunoglobin G subclasses were normal. A renal biopsy was performed which showed active interstitial inflammation with eosinophils consistent with allergic interstitial nephritis without an immune complex mediated glomerular lesion. He was started on intravenous methyl prednisone for 3 days followed by a prednisone taper. His home metformin, ramipril and hydrochlorothiazide were discontinued on discharge. He was eventually started on mycophenolate as the creatinine did not return to baseline with steroids. Conclusion: AIN is a rare, yet serious complication of GLP-1 use that requires early identification and discontinuation of the medication. A rapid or unexplained decline in renal function after starting a GLP-1 should be evaluated early on with concern for AIN once volume depletion is ruled out (1). Reference: (1) Chaudhury N., Liarakos A., Gopalakrishnan K., Ayub W., Murthy N., Rao R. Antidiabetic medication-induced acute interstitial nephritis: case report and literature search. British Journal of Diabetes. 2021;21(2);228-32. Presentation: Thursday, June 15, 2023

Evaluation of simple diagnostic parameters in acute kidney injury in hospitalized patients—diagnostic recommendations for non-nephrologists

Acute kidney injury (AKI) is very common in hospitalized patients, affecting patient’s mortality and morbidity. Major causes are prerenal AKI and acute tubular necrosis (ATN). Even though a variety of parameters/indices exist, their reliability and practicability are controversial: in fact, there is a need for a simple diagnostic approach for AKI in in-patients with parameters easily obtained in any hospital. The objective of the study was: (1) to assess reliability of simple laboratory parameters/indices to differentiate pre-/intrarenal AKI; (2) to evaluate the most reliable and feasible parameters/indices; and (3) to identify the possible impact of confounding factors. Retrospectively, in-patients with AKI hospitalized in 2020 in a university nephrology department were included. Spot urine and 24-h collection urine was analyzed with urine sodium (UNa), urine specific gravity (USG), fractional excretion of sodium (FENa), fractional excretion of urea (FEUrea), urine osmolality (UOsm), urine to plasma creatinine ratio (UCr/PCr) and renal failure index (RFI). Overall, 431 patients were included. UNa, UOsm, USG and RFI showed high specificity > 85% for prerenal AKI, UNa and RFI provided good specificity for ATN. Loop diuretics, ACE inhibitors/AT1 blockers or pre-existing chronic kidney disease had no impact. In patients with AKI, UNa, USG and RFI: (1) proved to be very specific for prerenal AKI and showed high sensitivity for ATN; (2) can be easily determined using serum and spot urine; and (3) are not confounded by medication or comorbidities. These parameters/indices are helpful to identify the aetiology of AKI and to guide therapy, thereby improving patients’ safety and outcome.

#3594 CHANGES IN ALBUMINURIA AND KIDNEY FUNCTION AFTER 8 WEEK HIGH-INTENSITY INTERVAL TRAINING PROGRAM IN 2ND AND 3RD TRIMESTER OF PHYSIOLOGICAL PREGNANCY

Abstract Background and Aims Physical exercise is the best prophylaxis of many disorders and should be continued during uncomplicated pregnancy. Several studies suggested that most pregnant women had no contraindications to perform intensive exercises. In recently published studies the beneficial effect of high-intensity interval training (HIIT) on both mental health and reduction of excessive weight gain during pregnancy has been demonstrated. The knowledge regarding kidney function after exercise in pregnancy is very scarce and only few studies concerning this topic were published. The aim of this study was to estimate changes in markers of kidney function in healthy pregnant exercising women. Changes after single intensive exercise and after 8 week training program were analyzed. Method The group of 36 women in 2nd and 3rd trimester of pregnancy were recruited to the study. At the beginning of the study all participants had normal kidney function (serum creatinine level below 0.6 mg/dl) and albuminuria (uACR below 30 mg/g) in rest. 19 women participated in 8-week HIIT program and 17 women in 8-week educational program (EDU group). Before and after 8 week training and education programs a progressive maximal exercise test on cyclometer was performed. Several biochemical measurements were performed. Results Women from both groups revealed mild changes concerning kidney function in rest, typical for physiological pregnancy (e.g. low sodium, creatinine and uric acid levels). After progressive maximal exercise test some unexpected findings were found: the fractional excretion of urea and uric acid increased (FeUrea from 41.25 to 50.05%; FeUA from 7.18 to 8.04%) and serum uric acid decreased significantly (sUA from 3.35 to 3.28mg/dL). Other changes after short exercise were typical: significant increase of uACR (from 5.12 to 9.43mg/g), serum creatinine (from 0.52 to 0.56mg/dL) and urea (from 16.45 to 21.65 mg/dL), among others. The 8-week HIIT training program did not change kidney function in rest. In both groups a significant increase of eCrCl and sUA were observed. The interesting observation was that uACR increased significantly only in EDU group. Conclusion Changes in kidney function after short intensive exercise in pregnancy were typical for healthy subjects, but there was no negative impact on markers of renal hypoperfusion. It was probably related to increased renal blood flow occurring in healthy pregnancy. The supervised 8-week HIIT training program had no negative impact on kidney function. The possible positive impact of this training on albuminuria was suggested.

Fractional Excretion of Sodium and Urea are Useful Tools in the Evaluation of AKI: PRO.

This is an Early Access article. Please select the PDF button, above, to view it. Be sure to also read the CON: 10.34067/KID.0002512022 and the COMMENTARY: 10.34067/KID.0002502022.

Fractional Excretion of Sodium and Urea are Useful Tools in the Evaluation of AKI: COMMENTARY.

This is an Early Access article. Please select the PDF button, above, to view it. Be sure to also read the PRO: 10.34067/KID.0002492022 and the CON: 10.34067/KID.0002512022

Fractional Excretion of Sodium and Urea are Useful Tools in the Evaluation of AKI: CON.

This is an Early Access article. Please select the PDF button, above, to view it. Be sure to also read the PRO: 10.34067/KID.0002492022 and the COMMENTARY: 10.34067/KID.0002502022

MO422: Strong Positive Association Between GFR and the Urine-To-Plasma Urea Concentration Ratio in Patients With Sickle Cell Disease. Possible Functional Meaning

Abstract BACKGROUND AND AIMS Sickle cell disease (SCD) induces a decline in urine concentration and progressive deterioration of kidney (K) function. Hyperfiltration is often observed before this decline, and plasma urea is low. Oral urea or hydroxyurea improves the condition of these patients (pts). These observations draw the attention to renal urea handling in SCD. Studies suggest that addition of urea into the loop of Henle may indirectly modify NaCl concentration at the macula densa and induce a rise in glomerular filtration rate (GFR) by depressing the tubule-glomerular feedback (TGF) [1]. The urine-to-plasma urea concentration ratio (U/P urea) is a novel marker associated with GFR and the progression of disease in ADPKD [2]. The present study addresses the relationship of U/P urea with GFR in SCD pts. METHOD A total of 184 homozygous SCD pts referred to our department were included. They underwent extensive evaluation including measured GFR (mGFR) (51Cr EDTA clearance) and plasma and 24-h urine chemistries. The association between mGFR and U/P urea was tested using univariate, and multivariate stepwise regression analyses. RESULTS Mean age was 35.6 ± 2.8 years (mean ± SD) and body mass index (BMI) 22.2 ± 0.3 kg/m2. Mean mGFR was 107 ± 3 ml/min x 1.73m2. Hyperfiltration was observed in 37% of pts. Urine volume (UV) 1.71 ± 0.75 L/24h. Urea excretion 267 ± 151 mmol/24h. In 13% of pts fractional excretion of urea (FEurea) exceeded 50%. U/P urea (42 ± 20) varied from 6 to 112. It was not associated with 24-h urea excretion but showed a negative association with UV (P &amp;lt; 0.007). mGFR was strongly and positively associated with U/P urea (r = 0.58, P &amp;lt; 0.0001) but not with U/P osmolarity (see Figure and Table). mGFR was also associated with U/P creatinine although more weakly (r = 0.266, p &amp;lt; 0.0001) and with BMI and negatively associated with age, MAP and serum creatinine (creat). After adjustment for U/P creat, the association between mGFR and U/P urea remained highly significant, whereas, after adjustment for U/P urea, the association between mGFR and U/P creat disappeared. In multivariate regression, mGFR remained strongly associated with U/P urea. CONCLUSION Our data show a strong association between mGFR and U/P urea that remains highly significant after multivariate analysis. i) This suggests that a specific estimated GFR equation for SCD patients including the U/P urea ratio could be clinically more relevant than CKD-EPI equations. ii) A specific mechanism may link GFR and intrarenal urea handling, as U/P urea but not U/P osmolarity appears to be involved. Urea could play a role, indirectly, in the regulation of GFR [1]. In SCD, the longer transit time of the blood in vasa recta may favour countercurrent exchanges and lead to a greater addition of urea in loops of Henle (increasing the U/P urea ratio) and thus increasing GFR by reducing TGF. Sickled red cells and resulting in slower blood flow in the medulla may selectively influence urea handling, participating in high FEurea and GFR often observed in SCD pts. iii) As is the case in ADPKD, more attention should be given to longitudinal studies to the relationship between U/P urea and kidney disease progression in SCD pts.

The Adaptive Renal Response for Volume Homeostasis During 2 Weeks of Dapagliflozin Treatment in People With Type 2 Diabetes and Preserved Renal Function on a Sodium-Controlled Diet

IntroductionProximal tubule sodium uptake is diminished following sodium glucose cotransporter 2 (SGLT2) inhibition. We previously showed that during SGLT2 inhibition, the kidneys adapt by increasing sodium uptake at distal tubular segments, thereby maintaining body sodium balance. Despite continuous glycosuria, we detected no increased urine volumes. We therefore assessed the adaptive renal responses to prevent excessive fluid loss.MethodsWe conducted a mechanistic open-label study in people with type 2 diabetes mellitus with preserved kidney function, who received a standardized sodium intake (150 mmol/d) to evaluate the effects of dapagliflozin on renin-angiotensin-aldosterone system (RAAS) hormones, volume-related biomarkers, urinary albumin-to-creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR), at start of treatment (day 4), end of treatment (day 14), and follow-up (day 18).ResultsA total of 14 people were enrolled. Plasma renin and angiotensin II and urinary aldosterone and angiotensinogen were acutely and persistently increased during treatment with dapagliflozin. Plasma copeptin level was numerically increased after 4 days (21%). Similarly, fractional urea excretion was significantly decreased at start of treatment (−17%). Free water clearance was significantly decreased after 4 days (−74%) and 14 days (−41%). All changes reversed after dapagliflozin discontinuation.ConclusionDapagliflozin-induced osmotic diuresis triggers kidney adaptive mechanisms to maintain volume and sodium balance in people with type 2 diabetes and preserved kidney function. ClinicalTrials.gov (identification: NCT03152084).

Assessment of Proximal Tubular Function by Tubular Maximum Phosphate Reabsorption Capacity in Heart Failure.

The estimated glomerular filtration rate (eGFR) is a crucial parameter in heart failure. Much less is known about the importance of tubular function. We addressed the effect of tubular maximum phosphate reabsorption capacity (TmP/GFR), a parameter of proximal tubular function, in patients with heart failure. We established TmP/GFR (Bijvoet formula) in 2085 patients with heart failure and studied its association with deterioration of kidney function (>25% eGFR decrease from baseline) and plasma neutrophil gelatinase-associated lipocalin (NGAL) doubling (baseline to 9 months) using logistic regression analysis and clinical outcomes using Cox proportional hazards regression. Additionally, we evaluated the effect of sodium-glucose transport protein 2 (SGLT2) inhibition by empagliflozin on tubular maximum phosphate reabsorption capacity in 78 patients with acute heart failure using analysis of covariance. Low TmP/GFR (<0.80 mmol/L) was observed in 1392 (67%) and 21 (27%) patients. Patients with lower TmP/GFR had more advanced heart failure, lower eGFR, and higher levels of tubular damage markers. The main determinant of lower TmP/GFR was higher fractional excretion of urea (P<0.001). Lower TmP/GFR was independently associated with higher risk of plasma NGAL doubling (odds ratio, 2.20; 95% confidence interval, 1.05 to 4.66; P=0.04) but not with deterioration of kidney function. Lower TmP/GFR was associated with higher risk of all-cause mortality (hazard ratio, 2.80; 95% confidence interval, 1.37 to 5.73; P=0.005), heart failure hospitalization (hazard ratio, 2.29; 95% confidence interval, 1.08 to 4.88; P=0.03), and their combination (hazard ratio, 1.89; 95% confidence interval, 1.07 to 3.36; P=0.03) after multivariable adjustment. Empagliflozin significantly increased TmP/GFR compared with placebo after 1 day (P=0.004) but not after adjustment for eGFR change. TmP/GFR, a measure of proximal tubular function, is frequently reduced in heart failure, especially in patients with more advanced heart failure. Lower TmP/GFR is furthermore associated with future risk of plasma NGAL doubling and worse clinical outcomes, independent of glomerular function.

Kidney functions adaptations of professional soccer players in response to an entire game season.

This study investigated the renal function of soccer players after an entire game-season. Thirty-five athletes recruited to play for the Macae Futebol Clube were invited for this study, of which 18 athletes completed the entire game season. Blood and 24-hour urine were collected at the beginning (Pre-Season) and the end of the game season (Post-Season). Kidney functions were assessed by calculating the urinary excretion, clearance, and fractional excretion of the selected solutes. Plasma creatinine, sodium, total protein, and osmolality were lower in the Post-Season . In contrast, plasma urea was higher in the Post-Season period. Urinary excretion of urea was reduced while albumin excretion was higher in comparison to Pre-Season. The clearances of creatinine, total proteins, and albumin were higher in the Post-Season period. In accordance, the fractional excretion of albumin increased. On the other hand, the clearance and fractional excretion of urea was lower in the Post-Season period. These results show that soccer-associated exercise throughout the entire game-season induces kidney functions adaptations that may prevent dehydration in these athletes through increased urea reabsorption to conserve water. In addition, this data corroborates to increased glomerular permeability to plasma proteins, such as albumin, that soccer players may experience.

Utility of Fractional Excretion of Urea in Diagnosing Etiology of AKI in Cirrhosis

Background: Acute kidney injury is present in a third of hospitalized patients with cirrhosis. AKI in cirrhosis can be functional (Pre renal azotemia and Hepatorenal syndrome) or structural (Acute tubular necrosis). Distinguishing the precise etiology of AKI in cirrhosis remains a clinical challenge. Fractional excretion of sodium as a marker of functional AKI has several limitations.

Utility of Fractional Excretion of Urea (FeUrea) for differentiating AKI phenotypes in patients with cirrhosis and ascites.

Background and Aim: Acute renal failure (AKI) is a common complication of decompensated cirrhosis and confers a poor prognosis. AKI in these patients may result from functional decrease in renal function as in prerenal azotaemia (PRA) and Hepato-renal syndrome (HRS) or due to structural renal abnormalities as in acute tubular necrosis (ATN). These phenotypes of AKI have therapeutic and prognostic implications. However, in clinical practice, approaches to determine the cause of AKI in these patients are suboptimal.

The Significance of “Fractional Excretion of Urea” in The Differential Diagnosis of Acute Kidney Injury in Cirrhotic Patients

Abstract Background Patients with cirrhosis are more susceptible to develop AKI than the non-cirrhotic individuals. AKI has an estimated prevalence of approximately 20% to 50% among hospitalized patients with cirrhosis. Physicians caring for patients with cirrhosis should recognize the acute or chronic character of renal disease, the causes of renal injury, the clinical conditions leading concomitantly to AKI and liver dysfunction, and the prognostic factors associated with the progression of AKI. Hypovolemia (due to diuretics, hemorrhage and diarrhea), acute tubular necrosis (ATN), sepsis, nephrotoxic agents (such as nonsteroidal anti-inflammatory drugs, aminoglycosides and/or radiological contrasts) and hepatorenal syndrome (HRS)-type 1 are the most common causes of AKI in cirrhotic patients. Objective To evaluate the sensitivity of fractional excretion of urea (FEUrea) vas a diagnostic biomarker for different causes of acute kidney injury in liver cirrhosis. Patients and Methods This study was conducted in co-operation between Tropical Medicine Department, Ain-Shams University and the Gastroenterology and Hepatology Department, Theodor Bilharz Research Institute between July 2019 to January 2020. It included 70 adult Egyptian patients admitted for treatment of complications of cirrhosis who fulfilled the eligibility criteria and compared to 10 cirrhotic patients without renal impairment. All patients were subjected to; full history taking, thorough clinical examination, laboratory investigations, Child-Pugh score was calculated for admission and urine samples were collected for urinary urea and creatinine levels to calculate FEUrea. Results Concerning the gender distribution in this study, male to female percent was 40 (57.10%) males and 30 (42.90%) females for gender, respectively. As regards to the causes of AKI, there were 24 (34.30%) PRA, 7 (10.00%) HRS and 39 (55.70%) ATN for final diagnosis. In the current study, there was significant difference (P = 0.0001; P &amp;lt; 0.05) in FE urea % among PRA, HRS and ATN groups (26.28±2.89, 11.76±3.44, and 47.37±10.53, respectively). Findings showed a higher FEUrea cut-off for ATN (&amp;gt;33%) compared to lower cut-off values for PRA (&amp;lt;33% and &amp;gt;21%) and HRS (&amp;lt;21%). Conclusion FEUrea was found to be an excellent simple tool for the differential diagnosis of AKI in patients with decompensated cirrhosis and ascites. FEUrea has also proven to be a useful “tubular injury” marker by differentiating ATN from non-ATN with high diagnostic accuracy (Sensitivity and Specificity exceeding &amp;gt;90%). FEUrea was found to be a good alternative and noninvasive tool for differentiating causes of AKI in cirrhotic patients instead of other non-available or expensive markers.

Fractional Excretion of Sodium and Urea in Differentiating Acute Kidney Injury Phenotypes in Decompensated Cirrhosis

Prerenal acute kidney injury (prerenal AKI), hepatorenal syndrome (HRS-AKI), and acute tubular necrosis (ATN-AKI) are the various phenotypes of acute kidney injury, which are described in decompensated cirrhosis. It has therapeutic and prognostic implications. We aimed to evaluate the diagnostic utility of fractional excretion of sodium and urea (FENa and FEUrea) for differentiating AKI phenotypes. A prospective analysis was performed in 200 patients with decompensated cirrhosis with AKI to derive receiver operating curve, optimal cut-off, sensitivity, and specificity. These findings were validated in an independent cohort (n=50) to differentiate ATN-AKI, HRS-AKI, and prerenal AKI. The incidence of prerenal AKI, HRS-AKI, and ATN-AKI were 37.5%, 34%, and 28.5% in the derivation cohort and 28%, 38%, and 34% in the validation cohort respectively. The median FENa was significantly different in various phenotypes of AKI in the derivation and validation cohort (P 0.001); FEUrea was significantly different in the derivation cohort (P 0.0001), not in the validation cohort (P 0.106). The AUC for FENa (cut-off, sensitivity/specificity) was 86.6% (0.567, 89/71) and for FEUrea was 60.3% (34.73, 70/58) for ATN-AKI vs. non-ATN-AKI. The area under the curve for FENa to differentiate between HRS-AKI vs. non-HRS-AKI was 74.5%. FEUrea could not differentiate HRS-AKI vs. non-HRS-AKI (AUC 60.4%) satisfactorily. FENa and FEUrea were unable to differentiate between prerenal AKI and HRS-AKI (AUC <70%). Among cirrhotics FENa at admission is a simple, commonly available clinical tool that can be used to differentiate structural AKI from prerenal AKI and HRS-AKI. The newly derived lowered cut-off value of FENa makes the diagnosis of ATN-AKI easier, faster and thus obviates the need for extensive workup in a significant proportion of patients. FENa appears better than FEUrea in decompensated cirrhosis with AKI.

High mean arterial pressure target to improve sepsis-associated acute kidney injury in patients with prior hypertension: a feasibility study

BackgroundThe optimal mean arterial pressure (MAP) in cases of septic shock is still a matter of debate in patients with prior hypertension. An MAP between 75 and 85 mmHg can improve glomerular filtration rate (GFR) but its effect on tubular function is unknown. We assessed the effects of high MAP level on glomerular and tubular renal function in two intensive care units of a teaching hospital. Inclusion criteria were patients with a history of chronic hypertension and developing AKI in the first 24 h of septic shock. Data were collected during two 6 h periods of MAP regimen administered consecutively after haemodynamic stabilisation in an order depending on the patient's admission unit: a high-target period (80–85 mmHg) and a low-target period (65–70 mmHg). The primary endpoint was the creatinine clearance (CrCl) calculated from urine and serum samples at the end of each MAP period by the UV/P formula.Results26 patients were included. Higher urine output (+0.2 (95%:0, 0.4) mL/kg/h; P = 0.04), urine sodium (+6 (95% CI 0.2, 13) mmol/L; P = 0.04) and lower serum creatinine (− 10 (95% CI − 17, − 3) µmol/L; P = 0.03) were observed during the high-MAP period as compared to the low-MAP period, resulting in a higher CrCl (+25 (95% CI 11, 39) mL/mn; P = 0.002). The urine creatinine, urine–plasma creatinine ratio, urine osmolality, fractional excretion of sodium and urea showed no significant variation. The KDIGO stage at inclusion only interacted with serum creatinine variation and low level of sodium excretion at inclusion did not interact with these results.ConclusionsIn the early stage of sepsis-associated AKI, a high-MAP target in patients with a history of hypertension was associated with a higher CrCl, but did not affect the kidneys' ability to concentrate urine, which may reflect no effect on tubular function.

AACC Guidance Document on Laboratory Investigation of Acute Kidney Injury.

Acute kidney injury (AKI) is a sudden episode of kidney damage or failure affecting up to 15% of hospitalized patients and is associated with serious short- and long-term complications, mortality, and health care costs. Current practices to diagnose and stage AKI are variable and do not factor in our improved understanding of the biological and analytical variability of creatinine. In addition, the emergence of biomarkers, for example, cystatin C, insulin-like growth factor binding protein 7, and tissue inhibitor of metalloproteinases 2, and electronic notification tools for earlier detection of AKI, highlights the need for updated recommendations to address these developments. This AACC Academy guidance document is intended to provide laboratorians and clinicians up-to-date information regarding current best practices for the laboratory investigation of AKI. Topics covered include: clinical indications for further investigating potential AKI, analytical considerations for creatinine assays, the impact of biological variability on diagnostic thresholds, defining "baseline" creatinine, role of traditional markers (urine sodium, fractional excretion of sodium, fractional excretion of urea, and blood urea-to-creatinine ratio), urinary microscopic examination, new biomarkers, improving AKI-associated test utilization, and the utility of automated AKI alerts. The previous decade brought us a significant number of new studies characterizing the performance of existing and new biomarkers, as well as potential new tools for early detection and notification of AKI. This guidance document is intended to inform clinicians and laboratorians on the best practices for the laboratory investigation of AKI, based on expert recommendations where the preponderance of evidence is available.

Acute Kidney Injury in a Case of Multiorgan Failure, Disseminated Intravascular Coagulation and Purpura Fulminans

Introduction Purpura fulminans (PF) is a life-threatening syndrome consisting of Disseminated Intravascular Coagulation (DIC), thrombotic occlusion of small- and medium-sized blood vessels with skin necrosis. Although there are few studies in the literature, only a minority of them discuss renal manifestations. Case Report We present a case of a 57-year-old Caucasian female with acute kidney injury (AKI) in the setting of multiorgan failure (MOF), DIC and PF. She presented with fever, exudative drainage from her port site, and skin changes concerning for bacteremia. Empiric antibiotics were started after blood, urine, and wound cultures were obtained. None of the cultures grew any organisms. Fever resolved after port removal. She exhibited thrombocytopenia, leukopenia, and neutropenia. Urinalysis showed hyaline casts and a fractional excretion of urea (FeUrea) ≤35% indicating a pre-renal state. Her hospital course was complicated by atrial fibrillation, acute hypoxic respiratory failure requiring mechanical ventilation, and hypovolemic shock requiring pressor support. Further, complicated by multiorgan failure including non-oliguric AKI and heart failure with reduced ejection fraction (HFrEF) of ≤65%. Acute skin findings included dusky, purple macules and patches involving all digits of both hands as well as gangrenous changes on the face and toes. It prompted further investigation by Hematology and Dermatology. Skin biopsy showed early leukocytoclastic vasculitis changes. Her laboratory markers were suggestive of DIC and Purpura Fulminans.