• Acute kidney injury
• Intensive care units
• Nephrology consultation
• Nephrology referral

• 2022R1C1C1009362 National Research Foundation of Korea

• Acute kidney injury
• meta-analysis
• risk factors
• severe acute pancreatitis
• systematic review

• Humans
• Acute Kidney Injury/etiology
• Acute Kidney Injury/epidemiology
• Acute Kidney Injury/diagnosis
• Risk Factors
• Pancreatitis/complications
• APACHE
• Severity of Illness Index
• Acute Disease
• Alcohol Drinking/adverse effects
• Risk Assessment

• Correlation coefficient
• Dense multi scale entropy
• Eigen-entropy
• Eigenvalue
• Multivariate time series classification
• Time series signatures

• 2122901 National Science Foundation (NSF) - Partnership for Innovation - "Avoiding Kidney Injuries"

• Acute kidney injury
• Neutrophil elastase inhibitor
• Oxidative stress
• Sepsis
• Sivelestat

• Acute kidney injury
• Cystatin C
• Intensive care unit
• Liver-type fatty acid-binding protein
• Mortality
• Neutrophil gelatinase-associated lipocalin

• Humans
• Lipocalin-2
• Cystatin C
• Prospective Studies
• Critical Illness
• Biomarkers
• Acute Kidney Injury/diagnosis
• Acute Kidney Injury/etiology
• Fatty Acid-Binding Proteins
• Liver

• Adult
• Humans
• beta-Lactamase Inhibitors/adverse effects
• beta-Lactams
• Carbapenems/therapeutic use
• Polymyxins
• Lactams
• Aminoglycosides/adverse effects
• Retrospective Studies
• Incidence
• Anti-Bacterial Agents/pharmacology
• Acute Kidney Injury/chemically induced

• Merck Sharp & Dohme LLC
• Merck & Co., Inc.

• Acute heart failure
• Emergency department
• Hospitalization
• Mortality
• Outcome
• Potassium
• Revisit

• Enteral nutrition
• acute kidney injury
• critical care
• sepsis

• Acute dialysis quality initiative
• Acute kidney injury
• Acute renal failure
• Hyperthermic intraperitoneal chemotherapy
• Intensive care unit
• Length of stay
• RIFLE

• acute kidney injury
• cisplatin
• drug-related side effects and adverse reactions

• Humans
• Acute Kidney Injury/chemically induced
• Acute Kidney Injury/diagnosis
• Biomarkers
• Cisplatin/adverse effects
• Cohort Studies
• Creatinine
• Retrospective Studies
• Head and Neck Neoplasms/complications
• Head and Neck Neoplasms/drug therapy

Acute Kidney injury is a major clinical problem associated with increased morbidity and mortality. Despite, intensive research the clinical outcome remains poor and apart from supportive therapy no other specific therapy exists. Single cell technologies have enabled us to get deeper insights into the transcriptome of individual cells in complex tissues like the kidney. With respect to kidney injury, this would allow us to better define the unique role of individual cell populations in the pathophysiology of acute kidney injury and progression to chronic kidney disease. In this mini review, we would like to give an overview and discuss the current major findings in the field of acute kidney injury through Single-Cell technologies.

• acute kidney injury
• chronic kidney disease
• single cell sequencing
• transcriptomics
• tubular regeneration

• COVID-19
• acute renal failure
• adult intensive & critical care

• Acute Kidney Injury/etiology
• Adult
• COVID-19/complications
• Critical Illness
• Hospital Mortality
• Humans
• Intensive Care Units
• Renal Insufficiency, Chronic/complications
• Renal Insufficiency, Chronic/epidemiology
• Retrospective Studies
• Risk Factors

• Humans
• Meropenem/therapeutic use
• Ceftazidime
• Retrospective Studies
• Ceftriaxone
• Tigecycline
• Drug Monitoring/methods
• Anti-Bacterial Agents/therapeutic use
• Piperacillin/therapeutic use
• Critical Care

• Critical Care Nephrology and Acute Kidney Injury Series
• acute kidney injury
• epidemiology

• Acute Disease
• Acute Kidney Injury/diagnosis
• Acute Kidney Injury/epidemiology
• Acute Kidney Injury/etiology
• Artificial Intelligence
• Biomarkers
• Critical Illness
• Female
• Humans
• Male

• T32 DK007569 NIDDK NIH HHS
• P30 DK114809 NIDDK NIH HHS
• National Institute of Diabetes and Digestive and Kidney Diseases

Increasing AKI diagnosis precision to refine the understanding of associated epidemiology and outcomes is a focus of recent critical care nephrology research. Timing of onset of acute kidney injury (AKI) during pediatric critical illness and impact on outcomes has not been fully explored.

This was a secondary analysis of the Assessment of Worldwide Acute Kidney Injury, Renal Angina and Epidemiology (AWARE) database. AKI was defined as per Kidney Disease: Improving Global Outcomes criteria. Early AKI was defined as diagnosed at ≤48 h after intensive care unit (ICU) admission, with any diagnosis >48 h denoted as late AKI. Transient AKI was defined as return to baseline serum creatinine ≤48 h of onset, and those without recovery fell into the persistent category. A second incidence of AKI ≥48 h after recovery was denoted as recurrent. Patients were subsequently sorted into distinct phenotypes as early-transient, late-transient, early-persistent, late-persistent and recurrent. Primary outcome was major adverse kidney events (MAKE) at 28 days (MAKE28) or at study exit, with secondary outcomes including AKI-free days, ICU length of stay and inpatient renal replacement therapy.

A total of 1262 patients had AKI and were included. Overall mortality rate was 6.4% (n = 81), with 34.2% (n = 432) fulfilling at least one MAKE28 criteria. The majority of patients fell in the early-transient cohort (n = 704, 55.8%). The early-persistent phenotype had the highest odds of MAKE28 (odds ratio 7.84, 95% confidence interval 5.45–11.3), and the highest mortality rate (18.8%). Oncologic and nephrologic/urologic comorbidities at AKI diagnosis were associated with MAKE28.

Temporal nature and trajectory of AKI during a critical care course are significantly associated with patient outcomes, with several subtypes at higher risk for poorer outcomes. Stratification of pediatric critical care-associated AKI into distinct phenotypes is possible and may become an important prognostic tool.

• acute kidney injury
• outcome
• pediatric critical care
• prognostication
• renal recovery

• acute kidney injury
• progenitor cell
• proximal tubular cell
• tubular regeneration

Sepsis is the most common contributing factor towards development of acute kidney injury (AKI), which is strongly associated to poor prognostic outcomes. There are numerous epidemiological studies about sepsis-associated acute kidney injury (S-AKI), however current literature is limited with the majority of studies being conducted only in the intensive care unit (ICU) setting. The aim of this study was to assess the epidemiology of S-AKI in all hospitalized in-patients.

This was a retrospective population-based study using a large regional population database in Beijing city from January, 2005 to December, 2017. It included patients with S-AKI. Patients with pre-existing end-stage kidney disease (ESKD), previous history of kidney transplantation, or being pregnant were excluded. Patients’ demographic characteristics, incidence, risk factors and outcomes of S-AKI were analyzed. The contrast between different time periods, different levels of hospitals, and types of the hospitals (traditional Chinese medicine hospitals (TCMHs) and western medicine hospitals (WMHs)) was also compared using Mann–Whitney U-test.

A total of 19,579 patients were included. The overall incidence of S-AKI in all in-patients was 48.1%. The significant risk factors by multivariate analysis for AKI included: age, male, being treated in a level-II hospital, pre-existing hypertension, chronic kidney disease (CKD), cirrhosis, atrial fibrillation (AF), ischemic heart disease (IHD), being admitted from emergency room, ICU admission, shock, pneumonia, intra-abdominal infection, bloodstream infection, respiratory insufficiency, acute liver injury, disseminated intravascular coagulation (DIC) and metabolic encephalopathy. The overall mortality rate in this cohort was 55%. The multivariate analysis showed that the significant risk factors for mortality included: age, being treated in a level-II hospital and TCMHs, being admitted from emergency room, pre-existing comorbidities (CKD, malignancy, cirrhosis and AF), shock, pneumonia, intra-abdominal infection, bloodstream infection, central nervous system (CNS) infection and respiratory insufficiency.

AKI is a common complication in patients with sepsis, and its incidence increases over time, especially when ICU admission is required. Exploring interventional strategies to address modifiable risk factors will be important to reduce incidence and mortality of S-AKI.

• epidemiology
• sepsis-associated acute kidney injury
• traditional Chinese medicine hospitals
• western medicine hospitals

• energy metabolism
• kidney injury
• mitochondria

• R01 HL145470 NHLBI NIH HHS
• IK2 BX004338 BLRD VA
• P30 DK079337 NIDDK NIH HHS
• I01 BX002175 BLRD VA
• R01 DK107852 NIDDK NIH HHS
• P30DK079337 NIDDK NIH HHS
• R01DK107852 NIDDK NIH HHS

Sepsis is the leading cause of acute kidney injury (AKI) and leads to increased morbidity and mortality in intensive care units. Current treatments for septic AKI are largely supportive and are not targeted towards its pathophysiology. Sepsis is commonly characterized by systemic inflammation and increased production of reactive oxygen species (ROS), particularly superoxide. Concomitantly released nitric oxide (NO) then reacts with superoxide, leading to the formation of reactive nitrogen species (RNS), predominantly peroxynitrite. Sepsis-induced ROS and RNS can reduce the bioavailability of NO, mediating renal microcirculatory abnormalities, localized tissue hypoxia and mitochondrial dysfunction, thereby initiating a propagating cycle of cellular injury culminating in AKI. In this review, we discuss the various sources of ROS during sepsis and their pathophysiological interactions with the immune system, microcirculation and mitochondria that can lead to the development of AKI. We also discuss the therapeutic utility of N-acetylcysteine and potential reasons for its efficacy in animal models of sepsis, and its inefficacy in ameliorating oxidative stress-induced organ dysfunction in human sepsis. Finally, we review the pre-clinical studies examining the antioxidant and pleiotropic actions of vitamin C that may be of benefit for mitigating septic AKI, including future implications for clinical sepsis.

• N-acetylcysteine
• hypoxia
• oxidative stress
• septic acute kidney injury
• vitamin C

• Acute kidney injury
• LCN2
• acute kidney failure
• lipocalin 2
• multiple trauma
• multiple-organ dysfunction syndrome
• multiple-organ failure
• neutrophil gelatinase-associated lipocalin

• ICD-10
• acute kidney injury
• diagnostic error
• laboratory alert value

There is no treatment for septic acute kidney injury (sAKI). The anti-inflammatory activity of prolonged-release pirfenidone (PR-PFD) could be beneficial in this clinical setting.

This study was a double-blind randomized clinical trial in sAKI patients with nephrology consultation at the Civil Hospital of Guadalajara, in addition to the usual treatment of AKI associated with sepsis; patients were randomized to receive either PR-PFD at 1,200 mg/day (group A) or 600 mg/day (group B) or a matched placebo for 7 consecutive days. The primary objective was the decrease in serum creatinine (sCr) and increase in urinary volume (UV); the secondary objectives were changes in serum electrolytes, acid-base status, and mortality.

Between August 2016 and August 2017, 88 patients were randomized. The mean age was 54 (17 ± SD) years, and 47% were male. The main site of infection was the lung (39.8%), septic shock was present in 39.1% of the cases, and the mean SOFA score was 8.8 points. 28 patients received PFD 1,200 mg, 30 patients received PFD 600 mg, and 30 patients received placebo. During the study, sCr did not differ among the groups. The reversion rate of sCr, UV, and mortality was not different among the groups (p=0.70, p=0.47, and p=0.38, respectively). Mild adverse events were not different among the groups.

PR-PFD did not improve the clinical course of sAKI and seemed to be safe in terms of adverse events. This trial is registered with NCT02530359.

This study aimed to develop and validate a model for mortality risk stratification of intensive care unit (ICU) patients with acute kidney injury (AKI) using the machine learning technique.

Eligible data were extracted from the Medical Information Mart for Intensive Care (MIMIC-III) database. Calibration, discrimination, and risk classification for mortality prediction were evaluated using conventional scoring systems and the new algorithm. A 10-fold cross-validation was performed. The predictive models were externally validated using the eICU database and also patients treated at the Second People’s Hospital of Shenzhen between January 2015 to October 2018.

For the new model, the areas under the receiver operating characteristic curves (AUROCs) for mortality during hospitalization and at 28 and 90 days after discharge were 0.91, 0.87, and 0.87, respectively, which were higher than for the Simplified Acute Physiology Score (SAPS II) and Sequential Organ Failure Assessment (SOFA). For external validation, the AUROC was 0.82 for in-hospital mortality, higher than SOFA, SAPS II, and Acute Physiology and Chronic Health Evaluation (APACHE) IV in the eICU database, but for the 28- and 90-day mortality, the new model had AUROCs (0.79 and 0.80, respectively) similar to that of SAPS II in the SZ2 database. The reclassification indexes were superior for the new model compared with the conventional scoring systems.

The new risk stratification model shows high performance in predicting mortality in ICU patients with AKI.

• Acute kidney injury (AKI)
• in-hospital mortality
• intensive care unit (ICU)
• machine learning
• severity score

To evaluate the transmembrane clearance (CL_TM) of apixaban during modeled in vitro continuous renal replacement therapy (CRRT), assess protein binding and circuit adsorption, and provide initial dosing recommendations.

Apixaban was added to the CRRT circuit and serial pre-filter bovine blood samples were collected along with post-filter blood and effluent samples. All experiments were performed in duplicate using continuous veno-venous hemofiltration (CVVH) and hemodialysis (CVVHD) modes, with varying filter types, flow rates, and point of CVVH replacement fluid dilution. Concentrations of apixaban and urea were quantified via liquid chromatography-tandem mass spectrometry. Plasma pharmacokinetic parameters for apixaban were estimated via noncompartmental analysis. CL_TM was calculated via the estimated area under the curve (AUC) and by the product of the sieving/saturation coefficient (SC/SA) and flow rate. Two and three-way analysis of variance (ANOVA) models were built to assess the effects of mode, filter type, flow rate, and point of dilution on CL_TM by each method. Optimal doses were suggested by matching the AUC observed in vitro to the systemic exposure demonstrated in Phase 2/3 studies of apixaban. Linear regression was utilized to provide dosing estimations for flow rates from 0.5–5 L/h.

Mean adsorption to the HF1400 and M150 filters differed significantly at 38 and 13%, respectively, while mean (± standard deviation, SD) percent protein binding was 70.81 ± 0.01%. Effect of CVVH point of dilution did not differ across filter types, although CL_TM was consistently significantly higher during CRRT with the HF1400 filter compared to the M150. The three-way ANOVA demonstrated improved fit when CL_TM values calculated by AUC were used (adjusted R² 0.87 vs. 0.52), and therefore, these values were used to generate optimal dosing recommendations. Linear regression revealed significant effects of filter type and flow rate on CL_TM by AUC, suggesting doses of 2.5–7.5 mg twice daily (BID) may be needed for flow rates ranging from 0.5–5 L/h, respectively.

For CRRT flow rates most commonly employed in clinical practice, the standard labeled 5 mg BID dose of apixaban is predicted to achieve target systemic exposure thresholds. The safety and efficacy of these proposed dosing regimens warrants further investigation in clinical studies.

The online version contains supplementary material available at 10.1186/s12882-021-02248-7.

• Apixaban
• CRRT
• CVVH
• CVVHD
• Dialysis
• Pharmacokinetics
• Renal replacement therapy
• Saturation coefficient
• Sieving coefficient
• Transmembrane clearance

• acute kidney injury
• microbiology
• sepsis

• Acute kidney injury (AKI)
• HRS-AKI
• IL-18
• KIM-1
• L-FABP
• acute tubular necrosis (ATN)
• biomarkers
• cystatin C
• decompensated cirrhosis
• hepatorenal syndrome (HRS)
• liver failure
• neutrophil gelatinase-associated lipocalin (NGAL)
• prerenal AKI
• review
• serum creatinine
• tubular injury

Acute kidney injury (AKI) carries a poor prognosis. Its incidence is increasing in the intensive care unit (ICU). Our purpose in this study is to develop and externally validate a model for predicting AKI in the ICU using patient data present prior to ICU admission.

We used data of 98 472 adult ICU admissions at Mayo Clinic between 1 January 2005 and 31 December 2017 and 51 801 encounters from Medical Information Mart for Intensive Care III (MIMIC-III) cohort. A gradient-boosting model was trained on 80% of the Mayo Clinic cohort using a set of features to predict AKI acquired in the ICU.

AKI was identified in 39 307 (39.9%) encounters in the Mayo Clinic cohort. Patients who developed AKI in the ICU were older and had higher ICU and in-hospital mortality compared to patients without AKI. A 30-feature model yielded an area under the receiver operating curve of 0.690 [95% confidence interval (CI) 0.682–0.697] in the Mayo Clinic cohort set and 0.656 (95% CI 0.648–0.664) in the MIMIC-III cohort.

Using machine learning, AKI among ICU patients can be predicted using information available prior to admission. This model is independent of ICU information, making it valuable for stratifying patients at admission.

• acute kidney injury
• critical care
• intensive care unit
• machine learning

Acute kidney injury (AKI) is the major complication of rhabdomyolysis. We aimed to identify the predictive factors for AKI and renal replacement therapy (RRT) requirement in poisoning-associated rhabdomyolysis. We conducted a cohort study including 273 successive poisoned patients (median age, 41 years) who developed rhabdomyolysis defined as creatine kinase (CK) >1000 IU/L. Factors associated with AKI and RRT requirement were identified using multivariate analyses. Poisonings mainly involved psychotropic drugs. AKI occurred in 88 patients (37%) including 43 patients (49%) who required RRT. Peak serum creatinine and CK were weakly correlated (R² = 0.17, p < 0.001). Death (13%) was more frequent after AKI onset (32% vs. 2%, p < 0.001). On admission, lithium overdose (OR, 44.4 (5.3–371.5)), serum calcium ≤2.1 mmol/L (OR, 14.3 (2.04–112.4)), female gender (OR, 5.5 (1.8–16.9)), serum phosphate ≥1.5 mmol/L (OR, 2.0 (1.0–4.2)), lactate ≥ 3.3 mmol/L (OR, 1.2 (1.1–1.4)), serum creatinine ≥ 125 µmol/L (OR, 1.05 (1.03–1.06)) and age (OR, 1.04 (1.01–1.07)) independently predicted AKI onset. Calcium-channel blocker overdose (OR, 14.2 (3.8–53.6)), serum phosphate ≥ 2.3 mmol/L (OR, 1.6 (1.1–2.6)), Glasgow score ≤ 5 (OR, 1.12; (1.02–1.25)), prothrombin index ≤ 71% (OR, 1.03; (1.01–1.05)) and serum creatinine ≥ 125 µmol/L (OR, 1.01; (1.00–1.01)) independently predicted RRT requirement. We identified the predictive factors for AKI and RRT requirement on admission to improve management in poisoned patients presenting rhabdomyolysis.

• acute kidney injury
• poisoning
• predictive factor
• renal replacement therapy
• rhabdomyolysis

• inflammation
• kidney
• mitochondria
• sepsis
• shock

• AKI
• Estrogen-like pathway
• In vivo imaging
• LPS
• Radix Achyranthis bidentata
• Salt-processed Achyranthis bidentata

• acute kidney injury
• metabolism
• mitochondria
• oxygenation

• Bacteraemia
• MIC
• Meropenem
• Susceptibility

• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/therapeutic use
• Bacteremia/drug therapy
• Bacteremia/mortality
• Enterobacteriaceae/drug effects
• Enterobacteriaceae Infections/drug therapy
• Enterobacteriaceae Infections/mortality
• Humans
• Meropenem/pharmacology
• Meropenem/therapeutic use
• Microbial Sensitivity Tests

Acute kidney injury (AKI) is a major problem for health systems being directly related to short and long-term morbidity and mortality. In the last years, the incidence of AKI has been increasing. AKI and chronic kidney disease (CKD) are closely interconnected, with a growing rate of CKD linked to repeated and severe episodes of AKI. AKI and CKD can occur also secondary to imbalanced oxidative stress (OS) reactions, inflammation, and apoptosis. The kidney is particularly sensitive to OS. OS is known as a crucial pathogenetic factor in cellular damage, with a direct role in initiation, development, and progression of AKI. The aim of this review is to focus on the pathogenetic role of OS in AKI in order to gain a better understanding. We exposed the potential relationships between OS and the perturbation of renal function and we also presented the redox-dependent factors that can contribute to early kidney injury. In the last decades, promising advances have been made in understanding the pathophysiology of AKI and its consequences, but more studies are needed in order to develop new therapies that can address OS and oxidative damage in early stages of AKI.

We searched PubMed for relevant articles published up to May 2019. In this review we incorporated data from different types of studies, including observational and experimental, both in vivo and in vitro, studies that provided information about OS in the pathophysiology of AKI.

The results show that OS plays a major key role in the initiation and development of AKI, providing the chance to find new targets that can be therapeutically addressed.

Acute kidney injury represents a major health issue that is still not fully understood. Research in this area still provides new useful data that can help obtain a better management of the patient. OS represents a major focus point in many studies, and a better understanding of its implications in AKI might offer the chance to fight new therapeutic strategies.

• Acute kidney injury
• Mithocondria
• Oxidative stress
• Physiopathology
• Reactive oxygen species

Few data showed the optimal blood pressure (BP) in noncritically ill patients with acute kidney injury (AKI) relative to mortality or severe AKI. We therefore sought to analyze the data that exist for the ideal target range for BP in noncritically ill patients with AKI.

We performed a retrospective cohort study involving 1,612 hospitalized patients who were diagnosed with AKI using the Kidney Disease: Improving Global Outcomes definition based on serum creatinine measurements for a period of 1 year. The average systolic BP (SBP) was categorized into 10-mmHg increments (within 48 hours after the development of AKI). The primary outcome was a composite of severe AKI or 90-day mortality.

The composite outcome rate in patients was 18.7% (302/1,612). The relationship between BP and the composite outcome followed a U-shaped curve, with an increased event rate observed at both low and high BP values. The average SBP after AKI predicted the composite outcome after adjusting for baseline variables (reference SBP: 120–129 mmHg; < 100 mmHg: hazard ratio [HR] 1.84, P = 0.015; 100–109 mmHg: HR 1.56, P = 0.038; 110–119 mmHg: HR 1.15, P = 0.483; 130–139 mmHg: HR 1.51, P = 0.045; ≥ 140 mmHg: HR 1.73, P = 0.005).

Among noncritically ill patients with AKI, a U-shaped curve association was observed between the average SBP within 48 hours after AKI and the composite primary outcome of this study, with the lowest event rate for SBP ranging from approximately 110 to 129 mmHg.

• cardiorenal syndrome
• myocardial motion
• strain
• three-dimensional speckle tracking echocardiography

• Biomechanical Phenomena
• Cardio-Renal Syndrome/diagnostic imaging
• Cardio-Renal Syndrome/physiopathology
• Echocardiography, Three-Dimensional/methods
• Humans
• Reproducibility of Results

Acute kidney injury (AKI) is a critical issue in cancer patients because it is not only a morbid complication but also able to interrupt timely diagnostic evaluation or planned optimal treatment. However, the impact of AKI on overall mortality in cancer patients remains unclear.

We conducted a retrospective cohort study of 67 986 cancer patients, from 2004 to 2013 to evaluate the relationship between AKI and all‐cause mortality. We used KDIGO AKI definition and grading system.

During 3.9 ± 3.1 years of follow‐up, 33.8% of the patients experienced AKI at least once. Among AKI events, stage 1, 2, and 3 was 71.0%, 13.8%, and 15.1%, respectively. AKI incidence was highest in hematologic malignancies, followed by urinary tract cancer, and hepatocellular carcinoma. Male sex, older age, underlying diabetes and hypertension, lower serum albumin and plasma hemoglobin, more frequent radio‐contrast exposure, entrance of clinical trials, and receiving chemotherapy were associated with AKI occurrence. AKI development was an independent risk factor for elevated mortality in cancer patients with dose‐responsive manner (Stage 1, hazard ratio [HR] 1.183, 95% confidence interval [CI] 1.145‐1.221, P < 0.001; Stage 2, HR 1.710, 95% CI 1.629‐1.796; Stage 3, HR 2.000, 95% CI 1.910‐2.095; No AKI, reference group) even after adjustment. This tendency was reproduced in various cancer types except thyroid cancer and in various treatment modalities, however, not shown in patients with baseline renal dysfunction.

AKI was an independent risk factor for all‐cause mortality in overall cancer patients with dose‐responsive manner.

• AKI stage
• acute kidney injury
• all-cause mortality
• cancer
• cancer treatment

Background

Acute kidney injury (AKI) is a frequently encountered clinical condition in hospitalized patients, particularly those admitted to intensive care units (ICU). AKI has its systemic sequelae and contributes to the morbidity of underlying diseases.

Methods

This descriptive case series aimed to determine the frequency of acute kidney injury in critically ill patients admitted to the ICU at Shifa International Hospital, Islamabad, according to the RIFLE (risk, injury, failure, loss, and end-stage) criteria. A total of 124 patients were enrolled in this study. RIFLE criteria were applied to determine the frequency of AKI in critically ill patients.

Results

The frequency of AKI was 68.55% and mortality was 18.55%. The severity of AKI was found to be significantly associated with mortality (p < 0.001).

Conclusion

AKI is very common in critically ill patients and contributes to the mortality and morbidity of the patients. Early identification of AKI can reduce mortality in critically ill patients.

• : akin
• acute kidney injury
• aki
• end stage renal disease
• kdigo
• oliguria
• rifle