scholarly journals Optimization of Acute Kidney Injury (AKI) Time Definitions Using the Electronic Health Record: A First Step in Automating In-Hospital AKI Detection

2021 ◽  
Vol 10 (15) ◽  
pp. 3304
Author(s):  
Joshua T. Swan ◽  
Linda W. Moore ◽  
Harlan G. Sparrow ◽  
Adaani E. Frost ◽  
A. Osama Gaber ◽  
...  

Kidney Disease: Improving Global Outcomes (KDIGO) acute kidney injury (AKI) definitions were evaluated for cases detected and their respective outcomes using expanded time windows to 168 h. AKI incidence and outcomes with expanded time intervals were identified in the electronic health records (EHRs) from 126,367 unique adult hospital admissions (2012–2014) and evaluated using multivariable logistic regression with bootstrap sampling. The incidence of AKI detected was 7.4% (n = 9357) using a 24-h time window for both serum creatinine (SCr) criterion 1a (≥0.30 mg/dL) and 1b (≥50%) increases from index SCr, with additional cases of AKI identified: 6963 from 24–48 h.; 2509 for criterion 1b from 48 h to 7 days; 3004 cases (expansion of criterion 1a and 1b from 48 to 168 h). Compared to patients without AKI, adjusted hospital days increased if AKI (criterion 1a and 1b) was observed using a 24-h observation window (5.5 days), 48-h expansion (3.4 days), 48-h to 7-day expansion (6.5 days), and 168-h expansion (3.9 days); all are p < 0.001. Similarly, the adjusted risk of in-hospital death increased if AKI was detected using a 24-h observation window (odds ratio (OR) = 16.9), 48-h expansion (OR = 5.5), 48-h to 7-day expansion (OR = 4.2), and 168-h expansion (OR = 1.6); all are p ≤ 0.01. Expanding the time windows for both AKI SCr criteria 1a and 1b standardizes and facilitates EHR AKI detection, while identifying additional clinically relevant cases of in-hospital AKI.

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Libin Xu ◽  
◽  
Yanhua Wu ◽  
Yuanhan Chen ◽  
Ruiying Li ◽  
...  

Abstract Background Although aging increases susceptibility to acute kidney injury (AKI), whether the AKI risk and the association between AKI and adverse outcomes are age-dependent remain unclear in older adults. The current study aimed to identify whether AKI risk was age-dependent in older adults and to investigate whether the association between AKI and mortality increased with increasing age. Methods Medical records from 47,012 adult hospital admissions, including 30,194 older adults aged 60 or older, in two tertiary general hospitals were studied retrospectively. AKI was identified based on changes in blood creatinine levels according to the Kidney Disease: Improving Global Outcomes criteria. Results Among the total population and 30,194 older adult patients, the raw incidences of AKI were 8.2 and 8.3%, respectively. The curve of the age-grouped AKI incidence was “U-shaped”, which revealed a positive relationship between the AKI incidence and age among the older adults aged 75 years or older. This trend of the age-AKI relationship was supported by further multivariable analysis. After adjusting for the Charlson Comorbidity Index score, the AKI was associated with in-hospital mortality; however, the associations did not increase with increasing age. Conclusion The AKI risk does not increase with age in older adults, except for those aged 75 and above. The association between AKI and in-hospital death did not increase in an age-dependent manner in older adults. Trial registration This study was retrospectively registered at clinicaltrials.gov (NCT03054142) on February 13, 2017.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Davis Kimweri ◽  
Julian Ategeka ◽  
Faustine Ceasor ◽  
Winnie Muyindike ◽  
Edwin Nuwagira ◽  
...  

Abstract Background Acute kidney injury (AKI) is a frequently encountered clinical condition in critically ill patients and is associated with increased morbidity and mortality. In our resource-limited setting (RLS), the most common cause of AKI is sepsis and volume depletion. Sepsis alone, accounts for up to 62 % of the AKI cases in HIV-positive patients. Objective The major goal of this study was to determine the incidence and risk predictors of AKI among HIV-infected patients admitted with sepsis at a tertiary hospital in Uganda. Methods In a prospective cohort study, we enrolled adult patients presenting with sepsis at Mbarara Regional Referral Hospital (MRRH) in southwestern Uganda between March and July 2020. Sepsis was determined using the qSOFA criteria. Patients presenting with CKD or AKI were excluded. Sociodemographic characteristics, physical examination findings, and baseline laboratory values were recorded in a data collection tool. The serum creatinine and urea were done at admission (0-hour) and at the 48-hour mark to determine the presence of AKI. We performed crude and multivariable binomial regression to establish the factors that predicted developing AKI in the first 48 h of admission. Variables with a p < 0.01 in the adjusted analysis were considered as significant predictors of AKI. Results Out of 384 patients screened, 73 (19 %) met our inclusion criteria. Their median age was 38 (IQR 29–46) years and 44 (60.3 %) were male. The median CD4 T-cell count was 67 (IQR 35–200) cells, median MUAC was 23 (IQR 21–27) cm and 54 (74.0 %) participants were on a regimen containing Tenofovir Disoproxil Fumarate (TDF). The incidence of AKI in 48 h was 19.2 % and in the adjusted analysis, thrombocytopenia (Platelet count < 150) (adjusted risk ratio 8.21: 95 % CI: 2.0–33.8, p = 0.004) was an independent predictor of AKI. Conclusions There is a high incidence of AKI among HIV-positive patients admitted with sepsis in Uganda. Thrombocytopenia at admission may be a significant risk factor for developing AKI. The association of thrombocytopenia in sepsis and AKI needs to be investigated.


2018 ◽  
Vol 34 (3) ◽  
pp. 401-407 ◽  
Author(s):  
Emily L Joyce ◽  
Dilhari R DeAlmeida ◽  
Dana Y Fuhrman ◽  
Priyanka Priyanka ◽  
John A Kellum

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Felix G. Meinel ◽  
Carlo N. De Cecco ◽  
U. Joseph Schoepf ◽  
Richard Katzberg

Contrast-induced acute kidney injury (CI-AKI) is commonly defined as a decline in kidney function occurring in a narrow time window after administration of iodinated contrast material. The incidence of AKI after contrast material administration greatly depends on the specific definition and cutoff values used. Although self-limiting in most cases, postcontrast AKI carries a risk of more permanent renal insufficiency, dialysis, and death. The risk of AKI from contrast material, in particular when administered intravenously for contrast-enhanced CT, has been exaggerated by older, noncontrolled studies due to background fluctuations in renal function. More recent evidence from controlled studies suggests that the risk is likely nonexistent in patients with normal renal function, but there may be a risk in patients with renal insufficiency. However, even in this patient population, the risk of CI-AKI is probably much smaller than traditionally assumed. Since volume expansion is the only preventive strategy with a convincing evidence base, liberal hydration should be encouraged to further minimize the risk. The benefits of the diagnostic information gained from contrast-enhanced examinations will still need to be balanced with the potential risk of CI-AKI for the individual patient and clinical scenario.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Nurhan Seyahi ◽  
...  

Abstract Background and Aims Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. There have been previous studies focusing on incidence and mortality of AKI in COVID-19 but none has made in depth analysis in relation to the background pathophysiology. Based on previous observations, we hypothesized that all AKIs seen in COVID-19 are not uniform and we aimed to analyze the etiologies and prognosis of AKI among hospitalized COVID-19 patients in relation to the time of AKI during different phases of the disease. Method A total of 1056 patients were admitted to the designated COVID-19 clinics from March to July in 2020. 77 Patients who were younger than 18 years old and 7 kidney transplant patients were excluded from the study. 427 of the remaining patients were confirmed by real time polymerase chain reaction (RT-PCR) test.). As eGFR below 60 mL/min/1,73 m2 was already shown to be related to mortality, these patients (44) were also excluded. As immunologic response is generally accepted to start with the second week of COVID-19 course, patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels, electrolytes, acid-base status and changes in the inflammatory markers were compared between the groups. A comparison between patients who survived and who died was also performed. Results 89 of the 383 included COVID-19 patients developed AKI. 24% of those who developed AKI died. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Additionally, patients who died had higher initial inflammatory marker levels and lower lymphocyte counts than those who survived. Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was as high as 44% for those who developed AKI after 7th day. Early AKI was related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Patients who died had significantly higher ferritin and d-dimer levels upon their hospital admissions (p=0,000). Electrolyte disturbances, metabolic acidosis and mortality were also higher in patients who developed AKI later. Hypernatremia (OR: 6,5, 95% CI: 3 – 13,9) and phosphorus disturbances (both hyperphosphatemia (OR: 3,3; 95%CI: 1,6 – 6,9) and hypophosphatemia (OR: 3,9; 95% CI: 2,0-7,9)) were related to mortality. Conclusion Findings of this study suggest that AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies


2021 ◽  
Author(s):  
Titik Setyawati ◽  
Ricky Aditya ◽  
Tinni Trihartini Maskoen

AKI is a syndrome consisting of several clinical conditions, due to sudden kidney dysfunction. Sepsis and septic shock are the causes of AKI and are known as Sepsis-Associated AKI (SA-AKI) and accounted for more than 50% of cases of AKI in the ICU, with poor prognosis. Acute Kidney Injury (AKI) is characterized by a sudden decline in kidney function for several hours/day, which results in the accumulation of creatinine, urea and other waste products. The most recent definition was formulated in the Kidney Disease consensus: Improving Global Outcome (KDIGO), published in 2012, where the AKI was established if the patient’s current clinical manifestation met several criteria: an increase in serum creatinine levels ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, an increase in serum creatinine for at least 1.5 times the baseline value within the previous 7 days; or urine volume ≤ 0.5 ml/kg body weight for 6 hours. The AKI pathophysiology includes ischemic vasodilation, endothelial leakage, necrosis in nephrons and microtrombus in capillaries. The management of sepsis associated with AKI consisted of fluid therapy, vasopressors, antibiotics and nephrotoxic substances, Renal Replacement Therapy (RRT) and diuretics. In the analysis of the BEST Kidney trial subgroup, the likelihood of hospital death was 50% higher in AKI sepsis compared to non-sepsis AKI. Understanding of sepsis and endotoxins that can cause SA-AKI is not yet fully known. Some evidence suggests that renal microcirculation hypoperfusion, lack of energy for cells, mitochondrial dysfunction, endothelial injury and cycle cell arrest can cause SA-AKI. Rapid identification of SA-AKI events, antibiotics and appropriate fluid therapy are crucial in the management of SA-AKI.


ESC CardioMed ◽  
2018 ◽  
pp. 2670-2673
Author(s):  
Susanna Price

Chronic kidney disease is a global health burden, with an estimated prevalence of 11–13%, with the majority of patients diagnosed as stage 3, and is an independent risk factor for cardiovascular disease. The incidence of acute kidney injury is increasing, and estimated to be present in one in five acute hospital admissions, and there is a bidirectional relationship between acute and chronic kidney disease. The relevance to the patient with cardiovascular disease relates to increased perioperative risk, as reduced kidney function is an independent risk factor for adverse postoperative cardiovascular outcomes including myocardial infarction, stroke, and progression of heart failure. Furthermore, patients undergoing cardiovascular investigations are at risk of developing acute kidney injury, in particular where iodinated contrast is administered. This chapter reviews the classification of renal disease and its impact on cardiovascular disease, as well as potential methods for reducing the development of contrast-induced acute kidney injury.


Author(s):  
Graham T. McMahon

Acute renal failure, now referred to as acute kidney injury (AKI), complicates 5–10% of general hospital admissions and is associated with increased morbidity and mortality and prolonged hospitalizations. The definition of AKI varies, but it is usually defined as an increase in serum creatinine concentration of 25–50% above the baseline, a decline in estimated glomerular filtration rate (eGFR) of 25–50%, or the need for renal replacement therapy. It is now recognized that changes in GFR are delayed manifestations of renal injury, and the development of urinary biomarkers may help to identify AKI earlier in the course of injury. The major causes of AKI in hospitalized patients include prerenal causes (~40%), postrenal causes (~5–10%), and intrinsic diseases affecting blood vessels, glomeruli, or tubules. Of the intrinsic causes, tubular disorders (acute tubular necrosis and acute interstitial nephritis) are the most common etiologies, accounting for 40–50% of all causes of AKI. Acute glomerulonephritis and vascular disorders are rare etiologies of AKI in hospitalized patients (〈5%).


2019 ◽  
Vol 8 (12) ◽  
pp. 2192 ◽  
Author(s):  
Nicola Cosentino ◽  
Stefano Genovese ◽  
Jeness Campodonico ◽  
Alice Bonomi ◽  
Claudia Lucci ◽  
...  

Background. Accumulating evidence suggests that inflammation plays a key role in acute kidney injury (AKI) pathogenesis. We explored the relationship between high-sensitivity C-reactive protein (hs-CRP) and AKI in acute myocardial infarction (AMI). Methods. We prospectively included 2,063 AMI patients in whom hs-CRP was measured at admission. AKI incidence and a clinical composite of in-hospital death, cardiogenic shock, and acute pulmonary edema were the study endpoints. Results. Two-hundred-thirty-four (11%) patients developed AKI. hs-CRP levels were higher in AKI patients (45 ± 87 vs. 16 ± 41 mg/L; p < 0.0001). The incidence and severity of AKI, as well as the rate of the composite endpoint, increased in parallel with hs-CRP quartiles (p for trend <0.0001 for all comparisons). A significant correlation was found between hs-CRP and the maximal increase of serum creatinine (R = 0.23; p < 0.0001). The AUC of hs-CRP for AKI prediction was 0.69 (p < 0.001). At reclassification analysis, addition of hs-CRP allowed to properly reclassify 14% of patients when added to creatinine and 8% of patients when added to a clinical model. Conclusions. In AMI, admission hs-CRP is closely associated with AKI development and severity, and with in-hospital outcomes. Future research should focus on whether prophylactic renal strategies in patients with high hs-CRP might prevent AKI and improve outcome.


Nephron ◽  
2020 ◽  
Vol 144 (10) ◽  
pp. 498-505
Author(s):  
Anna L. Barton ◽  
Sam B.M. Williams ◽  
Stephen J. Dickinson ◽  
Rob G. Parry ◽  
Adam Pollard

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