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Abstract
Acute Kidney Injury (AKI) is a common complication of critical illness and is associated with high mortality and has a separate independent effect on the risk of death.
The definition of AKI was unclear till appearance of RIFLE classification. It defines 3 grades of severity of AKI which are (risk, injury, failure) based on changes in serum creatinine and urine output and also defines two clinical outcomes which are (loss, end stage). On the other hand Acute Kidney Injury Network criteria (AKIN) classify AKI into 3 stages of severity (stage 1, 2 and 3).
The incidence of AKI in hospitalized patients ranged from 2-5%, while the incidence of AKI in the ICU varies from 2.5 to 15 %, and mortality in this setting can be as high as 78% in patients who require dialysis. AKI carries high morbidity, increases the length of hospital stay, increases hospital costs and is an independent risk factor for poor outcome in critically ill patients.
The most important reported risk factors for developing AKI are the old age, infection, history of chronic heart failure, lymphoma, leukemia, DM, cancer, and connective tissue disease, Glasgow Coma Score (GCS) of less than 10, and liver cirrhosis.
Preventive strategies of AKI are categorized into non pharmacological strategies and pharmacological strategies. Non pharmacological strategies entail adequate hydration, maintaining renal perfusion pressure by using vasopressors as norepinephrine and minimizing nephrotoxin exposure. Pharmacological strategies include loop diuretics as furosemide, low dose dopamine, benzazepine derivative, mannitol, natriuretic peptides, adenosine antagonists as theophylline and N-Acetylcysteine (NAC).
The aim of the work is to screen critically ill patients admitted to ICU for acute kidney injury using RIFLE criteria.
The study carried out on 325 patients admitted to the Department of Critical Care Medicine, Main Alexandria University Hospital. All patients enrolled in this study were subjected to the following:-
1) Complete history taking from the patient or the relatives on admission and included demographic data, previous past medical and surgical history and previous drug history)
2) Clinical examination on admission with stress on level of consciousness, blood pressure, pulse rate, respiratory rate and temperature.
3) Laboratory investigations included serum urea and serum creatinine, e GFR by MDRD equation, serum sodium (Na) and potassium (K), white blood count and arterial blood gases)
4) The APACHE II score on admission: done for all patients using the 12 variables.
Follow up of those patients was done during their ICU stay till discharge or death (end points). Follow up serum urea and serum creatinine were done either daily for patients with risk factors or according to ICU protocol for patients with no risk factors. RIFLE stages were reassessed based on the percentage change of serum creatinine from the baseline value.
The characteristics of the whole group include the followings:
• The mean age of the whole group was 49.54±19.38 years and included 184 male (56.6%) and 141 female (43.4%).
• The mean of GCS of the whole group was 13.22±3.06.
• The mean of GFR of the whole group was 61.548±32.6761 ml/min/1.73 m2.
• The mean of APACHE II score of the whole group was 15.74±5.55.
The characteristics of the 4 subgroups at base line include the followings:
• The age in the no AKI subgroup was significantly lower in comparison to the failure subgroup (p=0 .016 respectively). This denotes the important role of old age as a risk factor for AKI.
• The GCS in no AKI subgroup was significantly higher in comparison to injury subgroup as well as failure subgroup (p=.002, .005 respectively). The GCS in risk subgroup was significantly higher in comparison to injury as well as failure subgroups (p=0.002, 0.020 respectively). This data could demonstrate the severity of illness as a risk factor for AKI.
• The GFR of failure subgroup was significantly lower in comparison to no AKI, risk and injury subgroups (p=0.000, 0.000, 0.018 respectively). This denotes the important role of premorbid kidney disease as a risk factor for AKI.
• The pH of no AKI subgroup was significantly higher in comparison to risk as well as failure subgroup (p=0.002, 0.000 respectively). The pH of injury subgroup was significantly higher in comparison to no AKI, risk and failure subgroups. (p=0.023, 0.000, 0.000 respectively).
• The PaCO2 of no AKI subgroup was significantly lower in comparison to risk as well as failure subgroups (p=0.017, 0.020 respectively).
• The APACHE II score of failure subgroup was significantly higher in comparison to no AKI, risk and injury subgroups (p=0.000, 0.000, 0.003 respectively).
The ICU stay of no AKI subgroup was significantly lower in comparison to injury as well as failure subgroups (p= 0.000, 0.010).
At the beginning, the no AKI were 269 patients and 27 patients progressed to class Risk and 10 patients to class Failure, and from 27 patients in class Risk only 4 patients progressed to class injury and from them 2 progressed to class failure.
The AKI were 56 patients; 16 in class Risk, 6 in class Injury and 34 in class Failure. from the 16 patients in class Risk 2 patients progressed to class Injury, and from the 6 patients in class Injury 2 progressed to class Risk and 2 to class Failure.
During the entire ICU stay, 232 patients remained with no AKI (71.38%), 93 patients had AKI (28.61%), 39 in Risk class (12%), 6 in Injury class (1.84%), and 48 in failure class (14.76%).
Characteristics of the 4 subgroups of AKI during their ICU stay (maximum RIFLE characteristics) include the followings:
The GCS of failure subgroup was significantly lower in comparison to no AKI subgroup (p=0.004).
The GFR of no AKI subgroup was significantly lower in comparison to risk subgroup (p=0.002). The GFR of failure subgroup was significantly lower in comparison to no AKI, risk and injury subgroups (p=0.000, 0.000, 0.001 respectively).
The pH of failure subgroup was significantly lower in comparison to no AKI as well as injury subgroups (p=0.000, 0.021 respectively).
The SaO2 of non AKI was significantly higher in comparison to risk as well as failure subgroups (p=0.004, 0.001).
The APACHE II score of failure subgroup was significantly higher in comparison to no AKI, risk and injury subgroups (p=0.000, 0.000, 0.014 respectively).
The ICU stay of no AKI subgroup was significantly lower in comparison to risk, injury and failure subgroups (p=0.000, 0.000, 0.000 respectively). The ICU stay of injury subgroup was significantly higher in comparison to risk as well as failure subgroups (p=0.006, 0.005 respectively).
In conclusion, we found that:
• Acute kidney injury (AKI) is a common health problem among our population as the incidence of hospital acquired AKI was 17.2% and that of ICU acquired AKI was 28.6% in our cohort.
• Acute kidney injury is a serious complication of critical illness which has a great impact on mortality in ICU with a mortality rate reaching up to 52% of our AKI cases.
• The most important risk factors for development of AKI among our series were drugs as NSAIDS, co-morbid conditions as diabetes mellitus, greater illness severity as assessed by high APACHE II score and low GCS, and the associated acute lung injury as shown by low SaO2, high PaCO2 and low PH.
• Among our cohort, patients with RIFLE class (R) were at high risk of progression to class (I) or class (F) as well as patients with RIFLE class (I) were at high risk of progression to class (F).
• Patients with class (I) and class (F) were older in age and had higher APACHE II score and longer ICU stay in comparison to the class (R).
• Patients who progress to higher RIFLE classes have higher mortality and longer ICU stay in comparison to patients who did not progress.
And we recommend:
• Larger studies are recommended stressing on the risk factors of AKI in ICU to develop risk stratification tools to identify patients at risk for AKI and thus they would benefit from close observation and renal protective strategies to prevent development of AKI.
• Scoring systems as APACHE II score should be applied in the ICU to have a prognostic evaluation of each patient as regards the development of AKI.
• Biomarkers that could be used for the early detection and follow up of AKI as Cystatin C, Neutrophil gelatinase-associated lipocalin (NGAL), Interleukin-18 (IL-18) and Kidney injury molecule 1 (KIM-1) are recommended for early diagnosis and management of AKI.
• Stressing on treatement of the cause of AKI as drug induced AKI as the first line in preventing AKI.