Intrinsic Acute Kidney Injury Research Articles

Comparative Analysis between Urinary Calprotectin and Serum Creatinine for Early Detection of Intrinsic Acute Kidney Injury.

Background:Acute kidney injury (AKI) is a common and important clinical condition that may lead to chronic kidney disease if it is not diagnosed and treated in its early stages. Urinary calprotectin is a valuable recognized biomarker that can be used to differentiate prerenal and intrinsic AKI. However, till date only a few reports on urine calprotectin measurement in early diagnosis of intrinsic AKI are available. In this study, we compared the sensitivity and specificity of urinary calprotectin with those of serum creatinine in detecting early intrinsic AKI.Methods:Over 6 months period (April to October 2018), 81 of 408 patients admitted to the pediatric intensive care unit met the criteria of this cross-sectional study. Their serum creatinine and urinary calprotectin were measured on the first and third day of admission using Jaffe and Elisa radioimmunoassay methods, respectively. The AKI was defined according to the pRIFLE criteria.Results:Of the total 81 patients, 67 had the criteria of intrinsic AKI. Of these 62% were female and 38% were male. The mean age of the patients was 22 months. According to data analysis, the area under the curve of ROC of urinary calprotectin on day-1 to detect renal failure is 0.93 with the best cutoff point obtained at 530 ng/mL. The sensitivity, specificity, positive, and negative predictive values of urinary calprotectin levels in diagnosing AKI at this cutoff point are 92.5%, 92.8%, 98.4, and 72.2%, respectively. Besides, urinary calprotectin changes occur much earlier than the rising of serum creatinine.Conclusion:Urinary level of calprotectin is a very sensitive biomarker for early diagnosis of intrinsic AKI in children and it can be used in intensive care units or anywhere critically ill children admitted to detect intrinsic AKI. Besides, this study shows that urine calprotectin may be a more sensitive and specific biomarker than serum creatinine in the early phases of intrinsic AKI.

Injuria renal aguda: Características clínicas y epidemiológicas y función renal al alta en un hospital en Perú

Objetivo: Describir las características de la Injuria Renal Aguda (IRA) en pacientes hospitalizados en un hospital de tercer nivel de enero a abril del 2016. Material y métodos: Estudio descriptivo, transversal y retrospectivo que incluyó a los pacientes que ingresaron a los servicios de hospitalización de Medicina y Unidad de Cuidados Intensivos. El diagnóstico de IRA y su clasificación según severidad fueron establecidos según los criterios propuestos por Kidney Disease: Improving Global Outcomes. La función renal al alta fue evaluada mediante la estimación de la tasa de filtración glomerular (TFG). Resultados: La frecuencia general de IRA fue 64,83%. En el servicio de Medicina, la frecuencia fue 57,06% y en UCI, 88,14%. La mortalidad general fue 27,45%. Los pacientes con IRA presentaron anemia, diabetes y enfermedad renal crónica en 84,97%, 20,92% y 19,61%, respectivamente. Según severidad, la frecuencia general fue estadio 3: 46,41%, estadio 1: 30,07% y estadio 2: 23,53%. Las categorías de etiología probable más frecuentes fueron intrínseca (41,83%), pre-renal (27,45%) y multifactorial (15,03%). La mediana de TFG al alta en los pacientes que estuvieron en UCI fue 114,40 ml/min/1,73 m2 y en Medicina, 84,89 ml/min/1,73 m2. Según severidad, la menor mediana de TFG al alta se presentó en los pacientes con estadio 3 y, según etiología probable, aquellos que desarrollaron IRA intrínseca y multifactorial presentaron menor función renal al alta. Conclusiones: IRA es un trastorno frecuente en pacientes hospitalizados. La TFG al alta fue significativamente mayor en los pacientes en UCI que en aquellos en Medicina.

Comparison of clinicopathological patterns of renal tubular damage in dogs with acute kidney injury caused by leptospirosis and other aetiologies

In humans, leptospiral acute kidney injury (AKI) is characterised by tubulointerstitial involvement and renal electrolyte losses, impacting clinical presentation and case management. The aim of this study was to evaluate urine chemistry findings in dogs with leptospirosis in order to identify characteristic patterns of tubular damage associated with this disease. Dogs with intrinsic AKI caused by leptospirosis and by other aetiologies were prospectively enrolled. Clinical and clinicopathological variables, including serum and urine chemistry, fractional excretion (FE%) of electrolytes, and urinary neutrophil gelatinase-associated lipocalin (NGAL), were evaluated in both groups and compared statistically.Dogs with leptospirosis (n = 38) had significantly higher serum creatinine concentration than dogs with AKI caused by other aetiologies (n = 37). Serum potassium and glucose concentrations were comparable between groups. Dogs with leptospiral AKI had significantly higher FE of potassium (median 100%, range 20–480 vs. median 68%, range 5–300; P = 0.048), as well as higher magnitude of glucosuria (urine glucose to creatinine ratio, median 0.64, range 0–26 vs. median 0.22, range 0–13; P = 0.023) and frequency of positive glucose dipstick reaction (59% vs. 18%; P = 0.002), than dogs with AKI of other aetiologies. Additional markers of tubular damage considered in this study, including FE of other electrolytes and urinary NGAL, did not differ between groups. In conclusion, when compared to other aetiologies of intrinsic AKI, canine leptospirosis was characterised by increased glucosuria and kaliuresis.

Combined use of GM2AP and TCP1-eta urinary levels predicts recovery from intrinsic acute kidney injury

Deficient recovery from acute kidney injury (AKI) has immediate and long-term health, clinical and economic consequences. Pre-emptive recovery estimation may improve nephrology referral, optimize decision making, enrollment in trials, and provide key information for subsequent clinical handling and follow-up. For this purpose, new biomarkers are needed that predict outcome during the AKI episode. We hypothesized that damage pattern-specific biomarkers are expected to more closely associate to outcome within distinct subpopulations (i.e. those affected by specific pathological processes determining a specific outcome), as biomarker pleiotropy (i.e. associated to phenomena unrelated to AKI) introduced by unselected, heterogeneous populations may blur statistics. A panel of urinary biomarkers was measured in patients with AKI and their capacity to associate to normal or abnormal recovery was studied in the whole cohort or after sub-classification by AKI etiology, namely pre-renal and intrinsic AKI. A combination of urinary GM2AP and TCP1-eta best associates with recovery from AKI, specifically within the sub-population of renal AKI patients. This two-step strategy generates a multidimensional space in which patients with specific characteristics (i.e. renal AKI patients with good or bad prognosis) can be identified based on a collection of biomarkers working serially, applying pathophysiology-driven criteria to estimate AKI recovery, to facilitate pre-emptive and personalized handling.

Urinary neutrophil gelatinase-associated lipocalin determines short-term mortality and type of acute kidney injury in cirrhosis.

Background and AimAcute kidney injury increases mortality in cirrhotic patients by four fold. This study aimed to determine the usefulness of urinary neutrophil gelatinase‐associated lipocalin (uNGAL) for differential diagnosis for acute kidney injury and for predicting short‐term mortality in cirrhotic patients.MethodsWe enrolled 94 patients of decompensated cirrhosis. uNGAL was measured upon hospital admission in all patients. Patients with urinary tract infection and anuria were excluded. Patients were followed for 30 days or until death.ResultsTen (9%) patients had normal kidney function, 9 (11.37%) stable chronic kidney disease, 32 (29.50%) prerenal azotemia, 33 (36.37%) hepatorenal syndrome (HRS), and 10 (13.64%) intrinsic acute kidney injury (iAKI). Prerenal azotemia had lower median uNGAL values compared to HRS and iAKI (95.50 vs 465.00 vs 1217.50, P < 0.001). uNGAL levels were significantly higher in patients who died within 30 days (717.17 ± 494.26 vs 331.65 ± 313.65 ng/mL, P −0.0017). On univariate analysis, serum creatinine (sCr), uNGAL, Model for End‐Stage Liver Disease (MELD) score on admission, and length of stay were significant, and on multivariate analysis, uNGAL and hepatic encephalopathy (HE) were significant in predicting mortality.ConclusionsuNGAL at baseline serves as an early marker in differentiating HRS, prerenal AKI, and iAKI in cirrhotic patients, where sCr values are not useful. Patients with higher uNGAL levels had higher transplant‐free mortality at 30 days.

Red Blood Cell Distribution Width and Neutrophil-to-Lymphocyte Ratio in Predicting Adverse Outcomes of Acute Kidney Injury in Hospitalized Patients

Background: Acute kidney injury (AKI) is a common clinical condition with high morbidity and mortality. Early risk stratification by identifying patients at risk for death or dialysis requirement has important therapeutic implications for timely interventions. Objective: The aim of this study was to examine the association of routine blood test parameters, specifically red blood cell distribution width (RDW) and neutrophil-to-lymphocyte ratio (NLR), with the AKI patient outcomes. Methods: All adult patients hospitalized from January 1, 2016, to June 30, 2016, in the Second Xiangya Hospital of Central South University were surveyed. Demographic characteristics, laboratory measurements, comorbidities, and outcomes of a total of 1,188 adult AKI patients were analyzed. Results: The incidence of AKI was 1.8% (1,188/65,329). The all-cause mortality was 16.0% (190/1,188). The multivariable relative risk of AKI mortality comparing high RDW with low RDW was 1.84 and the risk comparing high NLR with low NLR was 2.54. RDW and NLR combination showed additive values in stratifying high-risk patients, and the predictive power was comparable to the use of serum creatinine for staging AKI. In subgroup analyses, high RDW predicted prerenal AKI mortality better than intrinsic AKI. High RDW and NLR also independently predicted renal replacement therapy (RRT) requirement in AKI patients. In contrast, WBC count and platelet-to-lymphocyte ratio did not show obvious correlations with death and RRT requirement in AKI patients. Conclusion: The results support the potential usefulness of RDW and NLR in risk stratification of AKI patients, providing additional prognostic information for treatment and supportive care.

Profile of Acute Kidney Injury in Patients with Decompensated Cirrhosis at a Tertiary-Care Center in Uttarakhand, India

Objectives: To study the clinical profile and predictors of acute kidney injury (AKI) in patients with decompensated cirrhosis. Materials and Methods: This observational study was conducted at Himalayan Institute of Medical Sciences, Dehradun, India, on 175 consecutive patients with decompensated cirrhosis. Patients were studied for AKI as per International Club of Ascites-AKI criteria. Results: The prevalence of AKI was 40.6%, with prerenal AKI 67.6%, hepatorenal syndrome (HRS) 23.8%, intrinsic renal AKI 7%, and postrenal AKI 1.4%. Mean arterial pressure (MAP), platelet count, and serum albumin were significantly lower and total leucocyte count (TLC), blood urea nitrogen, serum creatinine (SCr), total bilirubin, aspartate aminotransferase, international normalized ratio, Child-Turcotte-Pugh (CTP) score, and model for end-stage liver disease (MELD) score higher in cirrhosis patients with AKI than without AKI (p < 0.05 each). MAP, hemoglobin, TLC, and SCr were significantly different in various types of AKI (p < 0.05 each). AKI had a significant association with CTP score, alcohol, spontaneous bacterial peritonitis (SBP), sepsis, and shock (p < 0.05 each). Type of AKI had significant association with SBP, sepsis, and shock (p < 0.05 each). Mortality occurred in 33.8% patients with AKI with 64.7% mortality in patients with HRS. Outcome had significant association with AKI, stage and type of AKI (p < 0.05 each). Multivariate analysis showed SBP, sepsis, and shock as independent predictors of AKI (p < 0.05 each). Conclusions: AKI occurred commonly in patients with decompensated cirrhosis. Prerenal AKI and HRS were the most common types of AKI. SBP, sepsis, and shock were important predictors of AKI.

Urine neutrophil gelatinase‐associated lipocalin to diagnose and characterize acute kidney injury in dogs

BackgroundUrine neutrophil gelatinase‐associated lipocalin (NGAL) is a promising biomarker of acute kidney injury (AKI) in dogs.ObjectivesTo evaluate the utility of urinary NGAL for characterizing AKI according to volume responsiveness, presence of inflammation and sepsis, and prognosis.AnimalsDogs with AKI (n = 76) and healthy controls (n = 10).MethodsProspective study. Clinical and clinicopathologic data including absolute urine NGAL concentration (uNGAL) and NGAL normalized to urine creatinine concentration (uNGALC) were measured upon admission. Dogs were graded according to International Renal Interest Society (IRIS) AKI guidelines and compared based on AKI features: volume‐responsive (VR‐) AKI vs. intrinsic (I‐) AKI based on IRIS criteria; VR‐AKI and I‐AKI based on urine chemistry; inflammatory versus noninflammatory; septic versus nonseptic; and survivors versus nonsurvivors. Nonparametric statistics were calculated, and significance set at P < .05.ResultsUrinary NGAL was significantly higher in dogs with AKI compared to controls, regardless of AKI grade. Urinary NGAL did not differ between dogs with VR‐AKI and I‐AKI based on IRIS criteria, whereas higher uNGALC was recorded in dogs with I‐AKI based on urine chemistry. Urinary NGAL was significantly higher in dogs with inflammatory AKI, whereas no difference with respect to sepsis or outcome was identified.Conclusions and Clinical ImportanceUrinary NGAL is a sensitive marker for AKI in dogs, but its specificity is affected by systemic inflammation. Increased urinary NGAL in both I‐AKI and VR‐AKI also suggests the presence of tubular damage in transient AKI. Combining urine chemistry data with IRIS criteria could facilitate AKI characterization in dogs.

SAT-149 BIOMARKERS OF MACROPHAGE POLARIZATION ASSOCIATE ETIOLOGIC CAUSES AND ACTIVITY OF INTRINSIC ACUTE KIDNEY INJURIES

Macrophage polarization is a major contributing factor in acute kidney injury (AKI). We aim to check the value of urine sCD163 and urine sediment macrophage subtypes in differentiating etiologic causes of various intrinsic renal AKI in a large cohort. A total of 205 patients with renal intrinsic acute kidney injuries verified by renal biopsy were enrolled. Uninary sCD163 was quantified using enzyme-linked immunosorbent assay, macrophage subtypes in urine sediments and in renal biopsy samples were determined by immunostaining. Compared to healthy controls (0 pg/ml) and AKI due to interstitial or tubular injuries (median 55.1 pg/ml), the level of urinary sCD163 was markedly higher in glomerulopathy, especially in diffuse proliferative glomerulonephritis (median 285.8 pg/ml, P<0.001) and significantly correlated with the proportion of cellular crescents formation (P=0.043). Urine sediment analysis of macrophage M1/M2 ratio could differentiate acute tubulointerstitial nephritis (M1/M2>2.35, with sensitivity of 98% and specificity of 100%) from crescentic glomerulonephritis (M1/M2<0.27, with sensitivity of 100% and specificity of 69%). Urinary sCD163 levels and urine M2 subtype positively correlated with infiltrated M2 macrophage in glomeruli, whereas urine M1 subtype positively correlated with infiltrated M1 macrophage in interstitium.View Large Image Figure ViewerDownload Hi-res image Download (PPT)View Large Image Figure ViewerDownload Hi-res image Download (PPT) Markers of macrophage polarization associate etiologic causes and activity of intrinsic AKI, which could be viewed as the noninvasive “liquid biopsy” in the presence of various intrinsic kidney diseases.

Urine macrophages reflect kidney macrophage content during acute tubular interstitial and glomerular injury

Macrophage polarization is a major contributing factor in acute kidney injury (AKI). We aim to determine its biomarker value in differentiating etiologic causes of various intrinsic renal AKI. A total of 205 patients with renal intrinsic AKI were enrolled. Urinary sCD163 was quantified and macrophage subtypes in urine and in renal biopsy were determined. Compared to healthy controls and AKI due to interstitial or tubular injuries (0 pg/μmol), urinary sCD163 was markedly higher in glomerulopathy, especially in diffuse proliferative glomerulonephritis (275.5 pg/μmol) and significantly correlated with cellular crescent formation. Urine sediment analysis of M1/M2 ratio could differentiate acute tubulointerstitial nephritis (M1/M2 > 2.35) from crescentic glomerulonephritis (M1/M2 < 0.27). Urinary sCD163 levels and M2 subtype positively correlated with infiltrated M2 in the glomeruli, whereas urine M1 positively correlated with infiltrated M1 in the interstitium. Of note, urinary sCD163 showed better diagnositic performance in differentiating disease etiologies compared to tradiational urinary biomarkers of AKI (NGAL and KIM-1) and markers of myeloid cells (CD11b) and pan macrophages (CD68). Thus markers of macrophage polarization could be viewed as the noninvasive “liquid biopsy” in the presence of various intrinsic kidney diseases.

Meta-Analysis: Urinary Calprotectin for Discrimination of Intrinsic and Prerenal Acute Kidney Injury.

Background: Urinary calprotectin is a novel biomarker that distinguishes between intrinsic or prerenal acute kidney injury (AKI) in different studies. However, these studies were based on different populations and different AKI criteria. We evaluated the diagnostic accuracy of urinary calprotectin and compared its diagnostic performance in different AKI criteria and study populations. Method: In accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we searched PubMed, Embase, and the Cochrane database up to September 2018. The diagnostic performance of urinary calprotectin (sensitivity, specificity, predictive ratio, and cutoff point) was extracted and evaluated. Result: This study included six studies with a total of 502 patients. The pooled sensitivity and specificity were 0.90 and 0.93, respectively. The pooled positive likelihood ratio (LR) was 15.15, and the negative LR was 0.11. The symmetric summary receiver operating characteristic (symmetric SROC) with pooled diagnostic accuracy was 0.9667. The relative diagnostic odds ratio (RDOC) of the adult to pediatric population and RDOCs of different acute kidney injury criteria showed no significant difference in their diagnostic accuracy. Conclusion: Urinary calprotectin is a good diagnostic tool for the discrimination of intrinsic and prerenal AKI under careful inspection after exclusion of urinary tract infection and urogenital malignancies. Its performance is not affected by different AKI criteria and adult or pediatric populations.

The role of sphingolipids in acute kidney injury.

Acute kidney injury (AKI) is most simply defined as the rapid loss of kidney function in a matter of hours to days. AKI can manifest in a number of ways including pre-renal, post-renal, or intrinsic AKI. During acute kidney injury, multiple pathogenic processes are activated including inflammation, cell death, and the generation of reactive oxygen species, just to name a few. Sphingolipids are known to play a role in a number of the pathogenic pathways involved in the pathogenesis of many types of AKI, which suggests a role for sphingolipids in AKI. This short review will discuss the evidence for a role for sphingolipids in AKI.

Immunopathogenesis of Acute Kidney Injury.

Pathophysiologically, the classification of acute kidney injury (AKI) can be divided into three categories: (1) prerenal, (2) intrinsic, and (3) postrenal. Emerging evidence supports the involvement of renal tubular epithelial cells and the innate and adaptive arms of the immune system in the pathogenesis of intrinsic AKI. Pro-inflammatory damage-associated molecular patterns, pathogen-associated molecular patterns, hypoxia inducible factors, toll-like receptors, complement system, oxidative stress, adhesion molecules, cell death, resident renal dendritic cells, neutrophils, T and B lymphocytes, macrophages, natural killer T cells, cytokines, and secreted chemokines contribute to the immunopathogenesis of AKI. However, other immune cells and pathways such as M2 macrophages, regulatory T cells, progranulin, and autophagy exhibit anti-inflammatory properties and facilitate kidney tissue repair after AKI. Thus, therapies for AKI include agents such as anti-inflammatory (e.g., recombinant alkaline phosphatase), antioxidants (iron chelators), and apoptosis inhibitors. In preclinical toxicity studies, drug-induced kidney injury can be seen after exposure to a nephrotoxicant test article due to immune mechanisms and dysregulation of innate, and/or adaptive cellular immunity. The focus of this review will be on intrinsic AKI, as it relates to the immune and renal systems cross talks focusing on the cellular and pathophysiologic mechanisms of AKI.

Comparative study of clinico-biochemical profile and outcome of acute kidney injury in outborn and inborn neonates

Background: Acute Kidney Injury (AKI) is one of the major clinical problem in hospitalised neonates having variable outcomes. Prognosis depends on early diagnosis, associated risk factors and type of renal failure. The present study was undertaken to evaluate and compare risk factors, biochemical derangements and outcome of AKI in outborn and inborn neonates.Methods: For this hospital based prospective study 100 neonates were enrolled who were admitted in the NICU, diagnosed as AKI who had serum creatinine &gt;1.5mg/dl. Study was done for 1 year from June 2016 onwards.Results: A large majority (72.3%) cases were outborn neonates (extramural) whereas (27.7%) cases were inborn neonates (intramural). Most of (79.8%) cases were term and were admitted during summer months. In outborn, type of AKI in descending order was prerenal (64.7%), renal (33.8%) and postrenal (1.5%) while in inborn neonates, cases were equally (50%) divided in between renal and prerenal. Among outborn neonates risk factors for AKI was dehydration (44%), sepsis (28%) and shock (16%) whereas in inborn, perinatal asphyxia (31%), dehydration (27%), shock (23%) and sepsis (11.5%) were risk factors. In outborn 36.8% cases were oliguric whereas in inborn 53.9% cases were oliguric.Conclusions: The maximum cases of AKI were outborn neonates in which outborn dehydration was the commonest cause while in inborn neonates perinatal asphyxia was the commonest cause. Sepsis and shock were other causes in both groups. Presence of oliguria, intrinsic AKI and shock carried poor prognosis.

Fractional excretion of electrolytes in volume-responsive and intrinsic acute kidney injury in dogs: Diagnostic and prognostic implications.

BackgroundThe value of fractional excretion (FE) of electrolytes to characterize and prognosticate acute kidney injury (AKI) is poorly documented in dogs.ObjectivesTo evaluate the diagnostic and prognostic roles of FE of electrolytes in dogs with AKI.AnimalsDogs (n = 135) with AKI treated with standard care (February 2014‐December 2016).MethodsProspective study. Clinical and laboratory variables including FE of electrolytes, were measured upon admission. Dogs were graded according to the AKI‐IRIS guidelines and grouped according to AKI features (volume‐responsive, VR‐AKI; intrinsic, I‐AKI) and outcome (survivors/non‐survivors). Group comparison and regression analyses with hazard ratios (HR) evaluation for I‐AKI and mortality were performed. P < .05 was considered significant.ResultsFifty‐two of 135 (39%) dogs had VR‐AKI, 69/135 (51%) I‐AKI and 14/135 (10%) were unclassified. I‐AKI dogs had significantly higher FE of electrolytes, for example, FE of sodium (FENa, %) 2.39 (range 0.04‐75.81) than VR‐AKI ones 0.24 (range 0.01‐2.21; P < .001). Overall, case fatality was 41% (55/135). Increased FE of electrolytes were detected in nonsurvivors, for example, FENa 1.60 (range 0.03‐75.81) compared with survivors 0.60 (range 0.01‐50.45; P = .004). Several risk factors for death were identified, including AKI‐IRIS grade (HR = 1.39, P = .002), FE of electrolytes, for example, FENa (HR = 1.03, P < .001), and urinary output (HR = 5.06, P < .001).Conclusions and Clinical ImportanceFractional excretion of electrolytes performed well in the early differentiation between VR‐AKI and I‐AKI, were related to outcome, and could be useful tools to manage AKI dogs in clinical practice.

Clinical profile of hypernatremic dehydration in neonates with special emphasis to acute kidney injury

Background: Hypernatremic dehydration is common among breast fed babies due to various reasons. Unless diagnosed early and treated properly, dehydration fever or hypernatremic dehydration is devastating condition. Hypernatremia itself or its improper treatment can cause neurological damage. Dehydration can lead to pre-renal injury which can further progress in to intrinsic renal failure, complicating the management. We present clinical profile of hypernatremic dehydration with emphasis to kidney injury among neonates. Materials and Methods: It is prospective study conducted at tertiary care neonatal intensive care unit. Babies presenting with various symptoms were screened for hypernatremia, excluding other diseases. Kidney injury is assessed using fractional excretion of sodium. Results: out of 69 neonates 30 neonates with hypernatremia were selected with male: female ratio of 1:1.14. Majority of the babies 46.7% (n=14) presented within 1st week of life with fever being the most common symptom. Exclusively breastfed neonates (63.3%) were significant in number compared to other forms of feeding like mixed feeding (23.3) or exclusively formula fed babies. Prerenal acute kidney injury (AKI) was seen in 11 babies (36.7%), whereas 7(23.3%) had intrinsic renal AKI, 12 (40%) babies had normal renal function. Pre-renal AKI was predominant renal injury among all the three grades of hypernatremia. Conclusions: Hypernatremic dehydration is important preventable, treatable dangerous condition in neonates. Central nervous system is most commonly affected, but acute renal failure is also an important complication. Early diagnosis and proper treatment gives good outcome, sometimes renal failure complicates the management.

Acute Kidney Injury in Elderly Population: A Prospective Observational Study

Background/Aims: Acute kidney injury (AKI) has been reported as a recognized condition among the elderly population; however, its clinical epidemiology is still poorly evaluated. We propose to evaluate the epidemiological profile of AKI in hospitalized elderly patients and the variables associated with renal replacement therapy (RRT) dependency at discharge after an episode of AKI. Methods: This prospective observational study enrolled 286 elderly patients (aged ≥60 years), who had a diagnosis of AKI and were admitted to a tertiary care hospital. Clinical data were analyzed, which included RRT indication, referral time to nephrologist support, standby period in the emergency care units (ECU) before a transfer to an intensive care unit, staff criteria used to indicate palliative care, and the incidence of patients who stayed on chronic dialysis for at least 6 months after discharge. Results: The overall hospital mortality was 56.3%. Acute Kidney Injury Network (AKIN) 3 at the time of admission was significantly higher in patients who underwent RRT. Intrinsic AKI (p < 0.001), AKIN 3 (p < 0.001), RRT (p < 0.001), and increased length of stay in ECUs (p = 0.01) all had a significantly higher prevalence among non-survivors. On multivariate analysis, however, only renal aetiology (intrinsic AKI) was independently associated with mortality (OR 2.88; 95% CI [1.29–6.13]). Approximately 85% of the discharged patients (n = 125) were dialysis free and 36.4% of them who had a previous diagnosis of chronic kidney disease (CKD) upon admission had a worse renal function. Age, AKIN 3, RRT, prior history of CKD, diabetes mellitus, and the number of hemodialysis sessions showed to have an impact on dialysis dependence. Furthermore, 24 of 161 patients who had a dialysis indication were placed on palliative care. Conclusions: The severity of AKI and the need for RRT were risk factors for mortality and dependence on dialysis. Antecedents of CKD seem to be associated with a poor renal outcome following an AKI episode. Starting RRT had an impact on the clinical decision to enroll these patients into palliative care.

Incidence and Risk Factors of in-hospital mortality from AKI after non-cardiovascular operation: A nationwide Survey in China

This study aimed to describe the mortality and risk factors of in-hospital mortality from acute kidney injury (AKI) after non-cardiovascular operation in China based on a nationwide survey about AKI. The study sample was drawn from ISN AKF 0by25 China Consortiums, which is a nationwide, cross-sectional survey from 22 provinces in mainland China. AKI after non-cardiovascular operation was identified according to the 2012 KDIGO AKI creatinine criteria or expanded criteria. In total, 3468 cases were identified as hospital-acquired AKI (HA-AKI). Of these, 1059 cases were defined as AKI after major non-cardiovascular surgery. Post-operative AKI and non-operative AKI were similar in aetiology and in the need for RRT intervention. The all-cause in-hospital mortality was 17.0% (180 of 1059) among patients with AKI after a major surgery. Older age (OR = 1.14, p = 0.046), more severe comorbidities (OR = 9.29, p < 0.001), a history of CVD (OR = 1.85, p = 0.007), more severe peak AKI stage, and being located in the northwest region of China (OR = 2.47, p = 0.012) were all significantly associated with increased in-hospital mortality risk in AKI patients who underwent an operation. AKI after a non-cardiovascular operation has become a huge medical burden in China. The features of operative AKI varied substantially in different regions of China. Increased attention must be paid to the occurrence of potential intrinsic renal AKI when patients are exposed to nephrotoxic factors or comorbidities.

Urinary Neutrophil Gelatinase Associated Lipocalcin—A Novel Diagnostic and Prognostic Biomarker of Hours in Acute Kidney Injury in Cirrhosis

Background and Aim: Acute kidney injury (AKI) is prone to increase mortality in patients with cirrhosis. Identification of kidney failure etiology and recognition of those at the highest mortality risk remains a challenge. We aimed to determine an accuracy of uNGAL for diagnosing HRS in cirrhosis and association in predicting mortality at 30 days in AKI in cirrhosis. Methods: We Prospectively enrolled patients with cirrhosis at single institute from western India. Patients were investigated for uNGAL by CMIA method upon hospital admission (within 24 h or after development of AKI). FeNa calculated from urine and serum creatinine and urinary sodium values. Patients with urinary tract infection and anuria were excluded. Kidney failure type was determined blinded to NGAL measurements. Patients were followed for 30 days and 90 days. Results: We enrolled 45 patients of cirrhosis. Four (8.6%) patients had normal kidney function, 5 (12%) stable chronic kidney disease, 14 (33.33%) prerenal azotemia, 16(38.09%) HRS and 6 (14.2%) intrinsic acute kidney injury (iAKI). Patients with HRS had mean uNGAL levels of 432.45 ng/ml intermediate between prerenal azotemia mean 256 ng/ml, and iAKI [1389 ng/ml]. 12 patients died at 30 days. Patients with intrinsic AKI had highest uNGAl level. Level of uNGAL correlated with MELD levels. Eleven patients had hepatic encephalopathy and 6 had SBP. Patients with SBP had higher mean NGAL values (1234 ng/ml) than patients with hepatic encephalopathy (552 ng/ml).though serum creatine values were same in HRS or prerenal AKI, uNGAL can differentiate early between two conditions. FeNa levels does not differentiate between prerenal and HRS group. Conclusion: uNGAL level and Fe Na can serve as early marker in differentiating HRS and prerenal AKI early than serum creatinine. Patients with higher urinary NGAL level has higher transplant free mortality at 30 days. The authors have none to declare.

Diagnostic performance of serum blood urea nitrogen to creatinine ratio for distinguishing prerenal from intrinsic acute kidney injury in the emergency department

BackgroundThe blood urea nitrogen to creatinine ratio (BCR) has been used since the early 1940s to help clinicians differentiate between prerenal acute kidney injury (PR AKI) and intrinsic AKI (I AKI). This ratio is simple to use and often put forward as a reliable diagnostic tool even though little scientific evidence supports this. The aim of this study was to determine whether BCR is a reliable tool for distinguishing PR AKI from I AKI.MethodsWe conducted a retrospective observational study over a 13 months period, in the Emergency Department (ED) of Nantes University Hospital. Eligible for inclusion were all adult patients consecutively admitted to the ED with a creatinine >133 μmol/L (1.5 mg/dL).ResultsSixty thousand one hundred sixty patients were consecutively admitted to the ED. 2756 patients had plasma creatinine levels in excess of 133 μmol/L, 1653 were excluded, leaving 1103 patients for definitive inclusion.Mean age was 75.7 ± 14.8 years old, 498 (45%) patients had PR AKI and 605 (55%) I AKI. BCR was 90.55 ± 39.32 and 91.29 ± 39.79 in PR AKI and I AKI groups respectively. There was no statistical difference between mean BCR of the PR AKI and I AKI groups, p = 0.758. The area under the ROC curve was 0.5 indicating that BCR had no capacity to discriminate between PR AKI and I AKI.ConclusionsOur study is the largest to investigate the diagnostic performance of BCR. BCR is not a reliable parameter for distinguishing prerenal AKI from intrinsic AKI.