Risk factors, clinical features and outcome of new-onset acute kidney injury among critically ill patients: a database analysis based on prospective cohort study

Abstract

Background Acute kidney injury (AKI) newly-emerged in intensive care unit (ICU), has not been thoroughly studied in previous researches, is likely to differ from AKI developed before ICU admission. This study aimed to evaluate the incidence, risk factors, clinical features and outcome of new-onset AKI in critically ill patients. Methods The data of present study derived from a multicenter, prospective cohort study in17 Chinese ICUs (January 2014 - August 2015). The incidence, risk factors, clinical features and survival analysis of new-onset AKI were assessed. Results A total of 3374 adult critically ill patients were eligible. The incidence of new-onset AKI was 30.0 % (n = 1012). Factors associated with a higher risk of new-onset AKI included coronary heart disease, hypertension, chronic liver disease, use of nephrotoxic drugs, sepsis, SOFA score, APACHEII score and use of vasopressors. The new-onset AKI was an independent risk factor for 28-day mortality (adjusted hazard ratio, 1.643; 95 % CI, 1.370–1.948; P < 0.001). 220 (21.7 %) patients received renal replacement therapy (RRT), 71 (32.3 %) of them were successfully weaning from RRT. More than half of the new-onset AKI were transient AKI (renal recovery within 48 h). There was no statistical relationship between transient AKI and 28-day mortality (hazard ratio, 1.406; 95 % CI, 0.840–1.304; P = 0.686), while persistent AKI (non-renal recovery within 48 h) was strongly associated with 28-day mortality (adjusted hazard ratio, 1.486; 95 % CI, 1.137–1.943; P < 0.001). Conclusions New-onset AKI is common in ICU patients and is associated with significantly higher 28-day mortality. Only persistent AKI, but not transient AKI is associated with significantly higher 28-day mortality.

Clinical Value of Prognostic Nutritional Index and Neutrophil-to-Lymphocyte Ratio in Prediction of the Development of Sepsis-Induced Kidney Injury

“…With increasing age, the body's self-regulatory mechanism is perturbed, and the secretion of vasoactive substances decreases, resulting in a gradual decrease in the number of functional glomeruli, which eventually expedites the occurrence and progression of acute kidney injury. We included septic patients with chronic liver disease and complications such as abdominal effusion and lower extremity edema that resulted in decreased effective circulating blood volume, activation of the sympathetic adrenal medulla system, elevated catecholamine concentrations in the blood, and significantly decreased glomerular filtration rate, which eventually induced renal damage [ 27 , 28 ].…”

The Potential of miR-370-3p and miR-495-3p Serving as Biomarkers for Sepsis-Associated Acute Kidney Injury

“…In a US study including 192,980 patients with sepsis, 22% of patients with sepsis progressed to AKI, with a 38.2% mortality rate [ 4 ]. A multicenter prospective study with 1255 patients found that the incidence of AKI in the ICU was 31.6%, with sepsis accounting for 44.9% of patients [ 5 ]. Early diagnosis and timely intervention can improve the prognosis of invalids with SA-AKI [ 2 ].…”

Acute kidney injury in critically ill patients in the intensive care units

“…It is associated with increased risks of in-hospital mortality and long-term chronic kidney disease. Some patients had kidney injury before admission to the ICU and others developed AKI in the first 72 hours [1,2]. The time of onset of kidney injury implicates the difference in causes and severity of the disease, resulting in different clinical manifestations and outcomes.…”

“…The incidence of AKI in the ICU varies from 20% to as high as 80%. A rapid increase in aging population with multiple comorbidities contributes to high incidence [1][2][3].…”

“…Determination of the etiology and risk factors of AKI were the initial goals of our study. Furthermore, our aim was to determine the pre-renal (cardiorenal syndrome, including heart failure and venous congestion, hemorrhagic, hypovolemic and septic shock, abdominal compartment syndrome, kidney trans-bdominal compartment syndrome, kidney trans-, kidney trans-idney transplant, including delayed graft function, medication, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers), intra-renal [thrombotic microangiopathies, cholesterol embo-hrombotic microangiopathies, cholesterol embo-microangiopathies, cholesterol embo-, cholesterol embolism, anti-glomerular basement membrane disease and immune complexes and anti-neutrophilic cyto-neutrophilic cytoplasmic autoantibody vasculitis, sickle cell anemia, systemic infections and sepsis, pyelonephritis, drugrelated or heavy metal-related tubule necrosis, crys-tubule necrosis, crys-tubule necrosis, crystal-induced nephropathy, myoglobin (rhabdomyoly-myoglobin (rhabdomyoly-(rhabdomyoly-(rhabdomyolysis), contrast media, light chains (monoclonal gam-), contrast media, light chains (monoclonal gam-media, light chains (monoclonal gam-media, light chains (monoclonal gam-gam-ammopathies) and metabolites (acute urate nephropathy and acute oxalate nephropathy), acute cellular rejec-, acute cellular rejec-cute cellular rejection, acute interstitial nephritis, immune checkpoint inhibitor-related and cytokine release syndrome, Tcell therapy], and post-renal (urinary tract obstruc-, and post-renal (urinary tract obstruc-ost-renal (urinary tract obstruc-(urinary tract obstruc-urinary tract obstruction, bilateral ureteral obstruction, bladder dysfunc-obstruction, bladder dysfunction and urethral obstruction) causes of AKI [1,[9][10][11]. These data are very important for prevention of AKI as well as for treatment initiation, because some forms of AKI are reveresible if the treatment is started immediately after diagnosis.…”