Intrinsic Acute Kidney Injury Research Articles

Point-of-care ultrasonography in acute kidney injury

Point-of-care ultrasonography (POCUS) is emerging as a valuable tool in nephrology, providing real-time insights into the etiology of acute kidney injury (AKI). This narrative review explores POCUS applications in AKI, emphasizing its role in diagnostic kidney ultrasound and comprehensive hemodynamic assessments. AKI, prevalent in hospitalized patients, poses significant morbidity and mortality risks. POCUS aids in unraveling AKI’s multifaceted origins, categorizing it into hemodynamic, obstructive, and intrinsic renal causes. We discuss the utility of POCUS in urinary obstruction by identifying hydronephrosis and detecting stones and providing prompt diagnostic assistance. In intrinsic AKI, POCUS has limited utility but can potentially differentiate between acute and chronic kidney disease and identify infectious complications. POCUS-assisted hemodynamic AKI assessment involves thorough evaluation of the cardiac, lung, and end organ venous congestion. As technology advances, the role of POCUS in the diagnosis and management of AKI is likely to increase, offering a portable, cost-effective, and radiation-free bedside diagnostic modality. This also has the potential to improve patient outcomes. However, proper training in techniques of POCUS and an understanding of the limitations of POCUS are essential elements in ensuring its optimal and appropriate use in the right clinical context.

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.

Clinical Presentation, Pathological Spectrum, and Outcomes of Alcoholic Cirrhosis-Related Immunoglobulin A Nephropathy

BackgroundIgA nephropathy associated with cirrhosis is frequent but often overlooked as largely considered silent. Until now, little has been known about their presentation and outcomes. MethodsWe conducted a retrospective multicenter study on patients with kidney biopsy-proven cirrhosis-related IgA nephropathy (cirrhosis-IgAN), diagnosed between 2009 and 2022. We mixed them up with 83 primary IgA nephropathy (pIgAN) diagnosed during the same period, using a partitioning clustering approach, to determine common clinicopathological profiles. ResultsAll the 46 patients with cirrhosis-related IgA nephropathy had an excessive alcoholic consumption. Clinical presentation was severe with acute kidney injury (AKI) in 79%, alternative causes of AKI was found in 62% of cases. Three clinicopathological clusters were identified: one represented chronic involvement, the second could be assimilated to mild disease, and the third corresponded to a MPGN pattern and was associated with heavy proteinuria and intrinsic AKI (without alternative causes). While the two first were equally distributed between pIgAN and cirrhosis-IgAN, the third was more frequent in patients with cirrhosis. The cumulative mortality rate in cirrhosis-IgAN was 26% and 46% at 1-year and 3-years. Steroid exposure and moderate/severe AKI were associated with higher mortality and steroid exposure was associated with the occurrence of severe infection. ConclusionOur results suggest that high AKI incidence is related to extrinsic causes in most cases but can also be driven by IgA-dominant MPGN in a subset of patients. Steroid use was associated with infectious disease and mortality. Further studies are needed to clarify the place of immunosuppressive treatment in cirrhosis-IgAN patients.

Incidence Of Acute Kidney Injury In Mild, Moderate And Severe Cases Of Coronavirus Disease

Objective: The purpose of this research was to determine the incidence of Acute Kidney Injury (AKI) in COVID-19-affected patients Methods: This retrospective cohort study was conducted at Ziauddin Hospital Clifton Campus from June to December 2020. Adult patients with AKI or acute-on-chronic kidney disease (ACKD) were included in a retrospective study. Patients infected with SARS-CoV2 and renal involvement were directed towards the ICU/Nephrology departments which have the expertise to perform laboratory analysis, radiography and institution of treatment. Supplemental oxygen use was documented. The research also assessed information about therapy (antivirals, immunomodulators, RRT) and results (renal function recovery or death). Results: After excluding patients with obstructive AKI, a total of 180 (mean age 50.1 years) of 104 males and 76 females were included in the research. 120 patients were found to have prerenal, and 60 had intrinsic AKI with significant differences between mild, moderate, and severe cases (p=0.004). Acute kidney injury (AKI) survivors had a complete recovery rate of 70%, a partial recovery rate of 22%, and a hemodialysis dependency rate of 8%. Conclusion: Patients with severe COVID-19 infection often develop more severe AKI, and those in the severe or critical stages often exhibit proteinuria and dipstick hematuria. Long-term follow-up for COVID-19 patients should be done to evaluate its influence on renal outcome, and larger samples are required to elucidate the association between COVID-19 and renal damage. Keywords: Coronavirus Disease, Renal Replacement Therapy, proteinuria, dipstick hematuria

Identification of Pre-Renal and Intrinsic Acute Kidney Injury by Anamnestic and Biochemical Criteria: Distinct Association with Urinary Injury Biomarkers.

Acute kidney injury (AKI) is a syndrome of sudden renal excretory dysfunction with severe health consequences. AKI etiology influences prognosis, with pre-renal showing a more favorable evolution than intrinsic AKI. Because the international diagnostic criteria (i.e., based on plasma creatinine) provide no etiological distinction, anamnestic and additional biochemical criteria complement AKI diagnosis. Traditional, etiology-defining biochemical parameters, including the fractional excretion of sodium, the urinary-to-plasma creatinine ratio and the renal failure index are individually limited by confounding factors such as diuretics. To minimize distortion, we generated a composite biochemical criterion based on the congruency of at least two of the three biochemical ratios. Patients showing at least two ratios indicative of intrinsic AKI were classified within this category, and those with at least two pre-renal ratios were considered as pre-renal AKI patients. In this study, we demonstrate that the identification of intrinsic AKI by a collection of urinary injury biomarkers reflective of tubular damage, including NGAL and KIM-1, more closely and robustly coincide with the biochemical than with the anamnestic classification. Because there is no gold standard method for the etiological classification of AKI, the mutual reinforcement provided by the biochemical criterion and urinary biomarkers supports an etiological diagnosis based on objective diagnostic parameters.

Assessment of Urinary Calprotectin in Early Diagnosis of Intrinsic Acute Kidney Injury in Critically Ill Children at Zagazig University Hospitals

Assessment of Urinary Calprotectin in Early Diagnosis of Intrinsic Acute Kidney Injury in Critically Ill Children at Zagazig University Hospitals

Clinical and pathological characteristics of patients with acute kidney injury in Japan in whom kidney biopsy was performed: a cross-sectional analysis of the Japan Renal Biopsy Registry (J‑RBR).

Acute kidney injury (AKI) is a worldwide concern and it leads to a poor prognosis or end-stage kidney disease. The purpose of this study was to clarify the characteristics of patients with AKI in whom kidney biopsy was performed using data of the Japan Renal Biopsy Registry (J-RBR). We screened 38,351 cases that were registered in the J-RBR from 2007 to 2018. We obtained data for 383 patients with AKI based on clinical diagnosis for analysis 1 and data for 714 patients with acute interstitial nephritis (AIN) or acute tubular necrosis (ATN) based on pathological diagnosis for analysis 2. Of the cases screened, 383 patients with AKI (1.0%) were included in analysis 1. The main pathological diagnoses of AKI were AIN, ATN, chronic interstitial nephritis, nephro-sclerosis and crescentic glomerulonephritis. Of the cases screened, 589 patients with AIN (1.5%) and 110 patients with ATN (0.3%) were included in analysis 2. The main clinical diagnoses of AIN were AKI, rapidly progressive glomerulonephritis (RPGN), chronic nephritic syndrome (CNS) and drug-induced nephropathy (DIN), whereas those of ATN were AKI, RPGN, DIN and CNS. ATN patients had a higher serum creatinine level than that of AIN patients. Our results revealed that cases in the J-RBR included 1.0% of AKI cases based on clinical diagnosis and 1.5% and 0.3% of AIN and ATN cases, respectively, based on pathological diagnosis. In patients with suspected intrinsic AKI, kidney biopsy should be performed for diagnosis of the precise etiology and selection of appropriate treatment.

Urinary KIM-1 Correlates with the Subclinical Sequelae of Tubular Damage Persisting after the Apparent Functional Recovery from Intrinsic Acute Kidney Injury.

Acute kidney injury (AKI) poses an increased risk factor for new AKI episodes, progression to chronic kidney disease, and death. A worsened evolution has been linked to an incomplete renal repair beyond the apparent functional recovery based on plasma creatinine (pCr) normalization. However, structural sequelae pass largely unnoticed due to the absence of specific diagnostic tools. The urinary kidney injury molecule 1 (KIM-1) participates in renal tissue damage and repair and is proposed as a biomarker of early and subclinical AKI. Thus, we study in this paper the evolution of KIM-1 urinary excretion alongside renal tissue sequelae after an intrinsic AKI episode induced by cisplatin in Wistar rats. Creatinine clearance, pCr, proteinuria and the fractional excretion of Na+ and glucose were used to monitor renal function. Renal tissue damage was blindly scored in kidney specimens stained with hematoxylin–eosin and periodic acid–Schiff. KIM-1 urinary excretion and renal mRNA expression were also assessed. Finally, we analyzed urinary KIM-1 in patients apparently recovered from AKI. Our results show that, after the normalization of the standard markers of glomerular filtration and tubular function, the extent of persistent histological findings of tissue repair correlates with the renal expression and urinary level of KIM-1 in rats. In addition, KIM-1 is also elevated in the urine of a significant fraction of patients apparently recovered from an AKI. Besides its potential utility in the early and subclinical diagnosis of renal damage, this study suggests a new application of urinary KIM-1 in the non-invasive follow-up of renal repair after AKI.

The Urinary Level of Injury Biomarkers Is Not Univocally Reflective of the Extent of Toxic Renal Tubular Injury in Rats.

Nephrotoxicity is a major cause of intrinsic acute kidney injury (AKI). Because renal tissue damage may occur independently of a reduction in glomerular filtration rate and of elevations in plasma creatinine concentration, so-called injury biomarkers have been proposed to form part of diagnostic criteria as reflective of tubular damage independently of renal function status. We studied whether the urinary level of NGAL, KIM-1, GM2AP, t-gelsolin, and REGIIIb informed on the extent of tubular damage in rat models of nephrotoxicity, regardless of the etiology, moment of observation, and underlying pathophysiology. At a time of overt AKI, urinary biomarkers were measured by Western blot or ELISA, and tubular necrosis was scored from histological specimens stained with hematoxylin and eosin. Correlation and regression studies revealed that only weak relations existed between biomarkers and tubular damage. Due to high interindividual variability in the extent of damage for any given biomarker level, urinary injury biomarkers did not necessarily reflect the extent of the underlying tissue injury in individual rats. We contended, in this work, that further pathophysiological contextualization is necessary to understand the diagnostic significance of injury biomarkers before they can be used for renal tubular damage severity stratification in the context of nephrotoxic and, in general, intrinsic AKI.

Early fluid management affects short-term mortality in patients with end-stage kidney disease undergoing chronic hemodialysis and requiring continuous renal replacement therapy

BackgroundEarly fluid management is considered a key element affecting mortality in critically ill patients requiring continuous renal replacement therapy (CRRT). Most studies have primarily focused on patients with intrinsic acute kidney injury requiring CRRT, although end-stage kidney disease (ESKD) patients generally exhibit greater vulnerability. We investigated the association between fluid balance and short-term mortality outcomes in ESKD patients undergoing chronic hemodialysis and requiring CRRT.MethodsThis retrospective study included 110 chronic hemodialysis patients who received CRRT between 2017 and 2019 at Ewha Womans University Mokdong Hospital. The amounts of daily input and output, and cumulative 3-day and 7-day input and output, were assessed from the initiation of CRRT. The participants were classified into two groups based on 7-day and 14-day mortalities. Cox regression analyses were carried out on the basis of the amounts of daily input and output, cumulative input and output, and cumulative fluid balance.ResultsDuring follow-up, 7-day and 14-day mortalities were observed in 24 (21.8%) and 34 (30.9%) patients. The patients were stratified into two groups (14-day survivors vs. non-survivors), and there were no significant differences in demographic characteristics between the two groups. However, diabetes mellitus was more common among survivors than among non-survivors. Univariate analyses showed that the amounts of daily output at 48, and 72 h, and 3-day cumulative input and output, were significantly associated with 7-day mortality risk regardless of the cumulative fluid balance (HR: 0.28, 95% CI: 0.12–0.70, p = 0.01 for daily output at 48 h; HR: 0.34, 95% CI: 0.13–0.85, p = 0.02 for daily output at 72 h.; HR: 0.72, 95% CI: 0.61–0.86, p = 0.01 for 3-day cumulative input; HR: 0.65, 95% CI: 0.41–0.90, p = 0.01 for 3-day cumulative output). Adjusted multivariate analyses showed that the lower 3-day cumulative output is an independent risk factor for 7-day and 14-day mortality.ConclusionsIn our study, increased cumulative output were significantly associated with reduced short-term mortality risk in chronic hemodialysis patients undergoing CRRT regardless of cumulative fluid balance. Further prospective studies to investigate the association between fluid balance and mortality in ESRD patients requiring CRRT are warranted.

Prevalence of Renal Failure in Children and the Need for Dialysis in Paediatric Nephrology in a Developing Country

Background: Renal failure is among the major visceral failures responsible for morbidity and mortality in children. Epidemiological data on renal failure in children are limited in sub-Saharan Africa, including Senegal. We conducted this study to assess the prevalence of renal failure (RF) and the need for dialysis in the paediatric nephrology unit. Patients and methods: This was a retrospective and descriptive study in the pediatric nephrology unit from 1st January 2020 to 30 June 2021, including children with acute or chronic RF. The need for dialysis was judged to be met by its effectiveness in face of an indication. The data collected were analysed on sphinx plus 2017 software. Results: The prevalence of RF was 60% (n/N = 132/220). RF was acute in 59% (n/N = 78/132) of cases. The mean age was 6.53 ± 4.77 years with a sex ratio of 1.8. The mean serum creatinine level was 27.22 mg/L (240.9 μmol/L) and BUN at 0.85 g/L. The aetiologies were dominated by prerenal AKI (Acute Kidney Injury) complicating nephrotic syndrome (NS) in 37.2% (n/N = 29/78) and dehydration due to stomach flu in 17.6% (n/N = 9/51). Acute post-infectious glomerulonephritis including group A streptococcus and plasmodium falciparum accounted for 16.7% (n = 13/78) of intrinsic AKI. The need for dialysis was unmet in 50% (n/N = 7/14) with a mortality of 14.1% (n/N = 11/78). The mean age of the patients with chronic RF was 8.68 ± 4.74 years with a sex ratio of 2.6. The mean serum creatinine level was 36.56 mg/L (323.5 μmol/L) and the BUN level was 0.99 g/L. Half of the children were classified as having CKD stage II (early stage). The aetiologies were dominated by primary focal and segmental glomerulosclerosis (FSGS), 53.7% (n/N = 29/54), renal hypoplasia, 22.2% (n/N = 12/54) and reflux nephropathy, 29.4% (n/N = 5/17). The need for dialysis was unmet in 46.1% (n/N = 6/13). The overall mortality of chronic kidney disease (CKD) with RF was 29.6% (n/N = 8/27). Conclusion: The prevalence of RF was high in the unit. Most aetiologies of AKI were accessible to prevention. Only half of the children had access to free dialysis, hence the need for a dedicated pilot dialysis centre.

47-Year-Old Woman With Bilateral Flank Pain

47-Year-Old Woman With Bilateral Flank Pain

TDAG51 induces renal interstitial fibrosis through modulation of TGF-\u03b2 receptor 1 in chronic kidney disease

Chronic kidney disease (CKD) is characterized by the gradual loss of renal function and is a major public health concern. Risk factors for CKD include hypertension and proteinuria, both of which are associated with endoplasmic reticulum (ER) stress. ER stress-induced TDAG51 protein expression is increased at an early time point in mice with CKD. Based on these findings, wild-type and TDAG51 knock-out (TDKO) mice were used in an angiotensin II/deoxycorticosterone acetate/salt model of CKD. Both wild-type and TDKO mice developed hypertension, increased proteinuria and albuminuria, glomerular injury, and tubular damage. However, TDKO mice were protected from apoptosis and renal interstitial fibrosis. Human proximal tubular cells were used to demonstrate that TDAG51 expression induces apoptosis through a CHOP-dependent mechanism. Further, a mouse model of intrinsic acute kidney injury demonstrated that CHOP is required for ER stress-mediated apoptosis. Renal fibroblasts were used to demonstrate that TGF-β induces collagen production through an IRE1-dependent mechanism; cells treated with a TGF-β receptor 1 inhibitor prevented XBP1 splicing, a downstream consequence of IRE1 activation. Interestingly, TDKO mice express significantly less TGF-β receptor 1, thus, preventing TGF-β-mediated XBP1 splicing. In conclusion, TDAG51 induces apoptosis in the kidney through a CHOP-dependent mechanism, while contributing to renal interstitial fibrosis through a TGF-β-IRE1-XBP1 pathway.

Iron deficiency exacerbates cisplatin- or rhabdomyolysis-induced acute kidney injury through promoting iron-catalyzed oxidative damage

Iron deficiency is the most common micronutrient deficiency worldwide. While iron deficiency is known to suppress embryonic organogenesis, its effect on the adult organ in the context of clinically relevant damage has not been considered. Here we report that iron deficiency is a risk factor for nephrotoxic intrinsic acute kidney injury of the nephron (iAKI). Iron deficiency exacerbated cisplatin-induced iAKI by markedly increasing non-heme catalytic iron and Nox4 protein which together catalyze production of hydroxyl radicals followed by protein and DNA oxidation, apoptosis and ferroptosis. Crosstalk between non-heme catalytic iron/Nox4 and downstream oxidative damage generated a mutual amplification cycle that facilitated rapid progression of cisplatin-induced iAKI. Iron deficiency also exacerbated a second model of iAKI, rhabdomyolysis, via increasing catalytic heme-iron. Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence. Our data suggests that correcting iron deficiency and/or targeting specific catalytic iron species are strategies to mitigate iAKI in a wide range of patients with diverse forms of kidney injury.

MO426HANTA HEMORRHAGIC FEVER WITH RENAL SYNDROME CAUSED BY HANTAAN SEROTIPE IN BALKAN PENINSULA - AN UNESPECTED FINDING

Abstract Background and Aims Hantavirus infection is a zoonosis rare in the Balkan Peninsula but with increasing frequency and geographic spread, causing two major syndromes, depending on the viral serotype: hemorrhagic fever with renal syndrome (HFRS) and cardiopulmonary syndrome (CPS). Because there is no specific treatment or vaccine for this condition, the key for minimizing the progression to chronic kidney disease, secondary hypertension or death is early diagnosis and prompt therapy. This paper presents a case of HFSR in which needle kidney biopsy played a major role in diagnosis and draws attention on this zoonosis that might be highly underdiagnosed in Balkan Peninsula. Method A 26-year-old female with no medical history was admitted in our department with acute kidney injury (AKI), nephritic syndrome with nephrotic range proteinuria, high blood pressure, hepatic cytolysis, severe thrombocytopenia, anemia and leukocytosis, elevated LDH, normal haptoglobin, positive Coombs test (Table 1). Immunological testing (C3, C4, ANA, ANCA, antiGBM), viral infection markers (hepatitis B/C, HIV, Epstein-Barr, Cytomegalovirus), IgA/M/G were all negative and ADAMTS13 activity was normal. Abdominal sonography showed both kidneys of normal size and shape. A kidney biopsy was performed. The biopsy specimen showed macroscopic features of hemorrhage in the renal medulla. In immunofluorescence the staining was negative for IgA, IgG, IgM, C1q, C3c, k and λ chains, albumin and fibrinogen. Light microscopy (LM) revealed normal glomeruli and arterioles, dilated proximal tubules with resorption droplets at the apical pole and erythrocytes in the lumen, important interstitial hemorrhage in the medulla, with no inflammation or interstitial fibrosis. The electron microscopy (EM) showed segmental foot process effacement, endotheliosis of the peritubular capillaries, rare plasmocytes and macrophages in the interstitium (Figure 1). The aspect of hemorrhagic interstitial nephritis suggested Hantavirus infection. Serological testing revealed both IgM and IgG antibodies for the Hantaan serotype (HTNV). The final diagnosis was HTNV hemorrhagic interstitial nephritis with intrinsic AKI and secondary hypertension. MO426 Figure 1: A, B LM, Toluidine Blue staining. Normal glomerulus. Resorption droplets in the proximal tubular cells. C, D LM, Toluidine Blue staining. Extensive interstitial hemorrhage in medulla, tubulitis. E EM. Interstitial extravasation of erythrocytes. F EM. Endothelial swelling, foot process effacement. Results The patient was treated with oral methylprednisolone 16mg/d for 2 weeks, with progressive tampering of the dose and removal after 2 months. She received antihypertensive and antiproteinuric treatment with ramipril. The evolution was good, with creatinine and liver enzymes returning to normal. Conclusion HFRS belongs to a group of rare zoonoses in Balkan Peninsula, the most involved serotypes being Dobrava and Puumala. This case had positive serology for HTNV usually being found in China and Russia, but our patient didn’t travel abroad before she got ill, so we can’t consider the case as being an imported infection. That highlights a possible underdiagnosis of the disease in this region and also the need to re-evaluate geographic distribution of different strains and changes in ecological aspects given that they may pose a major risk to public health. The disease begins with flu-like symptoms and progresses to AKI with severe thrombocytopenia, anemia and coagulation disorders, being easily mistaken for haemolytic uremic syndrome. In a region with sporadic cases, we face diagnosis difficulties related especially to the absence of initial diagnosis suspicion, so we emphasize the need to include this pathology in the differential diagnosis algorithm of diseases evolving with thrombocytopenia, anemia, hepatic cytolysis and renal injury.

SARS-CoV-2 Renal Impairment in Critical Care: An Observational Study of 42 Cases (Kidney COVID).

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to 5% to 16% hospitalization in intensive care units (ICU) and is associated with 23% to 75% of kidney impairments, including acute kidney injury (AKI). The current work aims to precisely characterize the renal impairment associated to SARS-CoV-2 in ICU patients. Forty-two patients consecutively admitted to the ICU of a French university hospital who tested positive for SARS-CoV-2 between 25 March 2020, and 29 April 2020, were included and classified in categories according to their renal function. Complete renal profiles and evolution during ICU stay were fully characterized in 34 patients. Univariate analyses were performed to determine risk factors associated with AKI. In a second step, we conducted a logistic regression model with inverse probability of treatment weighting (IPTW) analyses to assess major comorbidities as predictors of AKI. Thirty-two patients (94.1%) met diagnostic criteria for intrinsic renal injury with a mixed pattern of tubular and glomerular injuries within the first week of ICU admission, which lasted upon discharge. During their ICU stay, 24 patients (57.1%) presented AKI which was associated with increased mortality (p = 0.007), hemodynamic failure (p = 0.022), and more altered clearance at hospital discharge (p = 0.001). AKI occurrence was associated with lower pH (p = 0.024), higher PaCO2 (CO2 partial pressure in the arterial blood) (p = 0.027), PEEP (positive end-expiratory pressure) (p = 0.027), procalcitonin (p = 0.015), and CRP (C-reactive protein) (p = 0.045) on ICU admission. AKI was found to be independently associated with chronic kidney disease (adjusted OR (odd ratio) 5.97 (2.1–19.69), p = 0.00149). Critical SARS-CoV-2 infection is associated with persistent intrinsic renal injury and AKI, which is a risk factor of mortality. Mechanical ventilation settings seem to be a critical factor of kidney impairment.

CHILD-TURCOTTE-PUGH /ALBUMINURIA AS A PREDICTOR OF ACUTE KIDNEY INJURY AMONG HOSPITALIZED PATIENTS WITH LIVER CIRRHOSIS

Background: The incidence of acute kidney injury (AKI) in cirrhotic patients about fifteen percent of hospitalized cirrhotic patient, Prediction of AKI indicated in all patients with liver cirrhosis. Albuminuria in cirrhotic patient can predict AKI. Objective: To assess the role of Child-Turcotte Pugh/Albuminuria (CTP-Alb), in prediction of AKI among hospitalized patients with liver cirrhosis. Patients and Methods: After departmental ethics committee approval and patient consents were obtained, 60 patients with liver cirrhosis screened for AKI during hospital admission at hepatogastroenterology unit, Department of Internal Medicine in Al-Hussein Hospital, Al-Azhar University, and The study was carried out during the period from September 2019 and September 2020, The diagnosis of liver cirrhosis based on clinical, biochemical and ultrasonography findings. Patients with Fib-4 ≥ 3.5 in the absence of liver decomposition were categorized as compensated liver cirrhosis. Severity of liver disease was assessed using the CTP score, model for end stage liver disease (MELD) score and CTP-Alb score. Diagnosis of acute kidney injury was based on the changes in serum creatinine. The baseline renal assessment at first day of hospital admission was included serum creatinine, estimated glomerular filtration rate (eGFR), albumin/creatinine ratio, and abdominal ultrasonography. AKI was categorized as hepatorenal syndrome (HRS), pre-renal azotemia, post-renal azotemia or intrinsic acute kidney injury. Results: A total of 60 patients included. They were 40 (66.66%) males and 20 (33.34%) females. Their mean age was 50 ± 33 years, of them 8 (13.33%) patients developed AKI during hospital admission with their mean age was 60.6 ± 10.9 years. They were 5 (62.5%) males and 3 (37.5%) females, Hypoalbuminemia, Child score at admission and Child-albuminuria score at admission were identified as independent risk factors for AKI by multivariate analysis (p < 0.05). Conclusion: Thirteen percent of cirrhotic patients developed AKI during hospital admission according to our results. The majority of patients were child C in our series; CTP/Albuminuria score, Hypoalbuminemia and ACLF has promising sensitivity, specificity and accuracy in prediction of AKI in hospitalized cirrhotic patient.

POS-015 BIOPSY PROVEN ACUTE TUBULAR NECROSIS: SPECTRUM AND PROGNOSIS

Acute tubular necrosis (ATN) is the most common cause of intrinsic acute kidney injury (IAKI) (80%).kidney biopsy is usually not performed in intrinsic renal AKI. It is reserved when clinical assessement and or laboratory investigations oe evolutive data are suggestive of other causes of IAKI. The evolution of ATN is generally favorable with restitution ad integrum after regeneration of the tubules and parallel functional recovery in a few days to a few weeks. The aim of this study is to document the evolutionary features of biopsy proven ATN in our population.

POS-040 DIAGNOSTIC VALUE OF URINE MICROSCOPY IN PREDICTING OUTCOME OF HOSPITALIZED PATIENTS WITH ACUTE KIDNEY INJURY: A SINGLE-CENTER PROSPECTIVE STUDY

Acute kidney injury (AKI) is common in hospitalized and critically ill patients and has an important modifying effect on mortality, kidney recovery and health resources. Evaluation of the urine sediment is often viewed as a complementary measure for providing additional insight into the diagnosis and severity of AKI; however, it has not formally been integrated in consensus definitions. This is a prospective observational cohort study aimed at identifying the diagnostic value of urine microscopy of in-patients admitted at Perpetual Succour Hospital from May 2016 to May 2017 with AKI, specifically intrinsic and prerenal AKI in relation to predicting outcome such as worsening AKI, need for in-hospital dialysis, or in-hospital death. Eligible patients had clinical data and serum creatinine levels extracted. Urine samples were collected, and each had a dipstick test done. A single investigator did the evaluation of urine sediment. A urine microscopy scoring system was derived based from the number of granular casts, muddy-brown casts and renal tubular epithelial cells. The urine microscopy score was correlated to mortality, worsening or recovery of renal function, and need for renal replacement therapy (RRT). A total of 102 patients were eligible. The average age was 63.47 years old, and majority were males (59.8%). Sepsis was the most common cause of AKI (48%) followed by Cardiorenal Syndrome (20.6%). Most patients were hypertensive and diabetic (33.3%). As for patients’ creatinine results, their average baseline was 1.93 mg/dl with an eGFR of 43.32 ml/min. Creatinine levels during urine microscopy averaged at 4.72 + 2.97, and upon discharge, creatinine levels were 2.39 + 1.93 with corresponding eGFR of 39.94 + 34.75 ml/min. The urine microscopy score did not show a statistically significant association with regards to greater need for dialysis and its discontinuation (p value of 0.131 and 0.500 respectively). However, there is a trend towards an association with the patient’s mortality, though not statistically significant (p value= 0.084). Tests of correlations using Pearsons test showed that the relationship between urine microscopy scoring system and rise in creatinine percentage from baseline (r = 0.075, p = 0.475), as well as between the percent decrease in creatinine (r = 0.105, p = 0.349) were weak and not statistically significant. The presence of hematuria on patient’s outcome showed that the presence of RBC >10/hpf was significantly associated with the need for RRT (p= 0.015) and mortality (p= 0.039). Also, the presence of Renal Tubular Cells was significantly associated with dialysis (p= 0.002), while its absence was associated with no need for RRT (p= 0.002). Most importantly, the absence of Renal Tubular cells was significantly associated with renal recovery (p= 0.047). Moreover, there is a trend towards the association of the presence of Muddy Brown Casts and mortality (p=0.066). The presence of Renal tubular epithelial cells, muddy brown casts and hematuria are associated with mortality and need for RRT. More importantly, there is a trend towards an association of a higher urine microscopy score with mortality. Septic AKI seems to have higher urine microscopy scores; this finding may imply that the urine microscopy scoring system may be most useful in septic AKI in predicting outcome.

Risk Factors, Clinical Characteristics, and Prognosis of Acute Kidney Injury in Hospitalized COVID-19 Patients: A Retrospective Cohort Study

Background: Acute kidney injury (AKI) is a serious complication of COVID-19. Methods: Records of hospitalized adult patients with confirmed SARS-CoV-2 infection from 1 March to 31 May 2020 were retrospectively reviewed. Results: Of 283 patients, AKI occurred in 40.6%. From multivariate analyses, the risk factors of AKI in COVID-19 can be divided into: (1) demographics/co-morbidities (male, increasing age, diabetes, chronic kidney disease); (2) other organ involvements (transaminitis, elevated troponin I, ST segment/T wave change on electrocardiography); (3) elevated biomarkers (ferritin, lactate dehydrogenase); (4) possible bacterial co-infection (leukocytosis, elevated procalcitonin); (5) need for advanced oxygen delivery (non-invasive positive pressure ventilation, mechanical ventilation); and (6) other critical features (ICU admission, need for vasopressors, acute respiratory distress syndrome). Most AKIs were due to pre-renal (70.4%) and intrinsic (34.8%) causes. Renal replacement therapy was more common in intrinsic AKI. Both pre-renal (HR 3.2; 95% CI 1.7–5.9) and intrinsic AKI (HR 7.7; 95% CI 3.6–16.3) were associated with higher mortality. Male, stage 3 AKI, higher baseline and peak serum creatinine and blood urea nitrogen were prevalent in intrinsic AKI. Urine analysis and the fractional excretion of sodium and urea were not helpful in distinguishing intrinsic AKI from other causes. Conclusions: AKI is very common in COVID-19 and is associated with higher mortality. Characterization of AKI is warranted due to its diverse nature and clinical outcome.