Early prognosis of patients with sepsis-related acute kidney injury receiving continuous renal replacement therapy in the intensive care unit

doi:10.21203/rs.3.rs-5285694/v1

Objectives The aim of this study was to determine the clinical characteristics of patients with sepsis-induced acute kidney injury (SI-AKI) requiring continuous renal replacement therapy (CRRT) and their risk factors for mortality.

Methods This was a single-centre, retrospective, observational study that included 108 patients who underwent CRRT between 1 January 2022 and 31 December 2022 in the intensive care unit (ICU) of The Affiliated Wuxi People' s Hospital of Nanjing Medical University. The patients were divided into the SI-AKI group and the Non-SI-AKI group, and the 30-day prognosis of the two groups was investigated using the Kaplan-Meier survival curve, and the associated risk factors for death were investigated using multifactorial COX regression analysis.

Results Compared with the non-SI-AKI group, SI-AKI patients were older [72 (60, 78) vs. 60 (51, 70) years, P = 0.003], with higher SOFA score [9.0 (7.0, 10.0) vs. 6.0 (5.0, 7.0), P < 0.001] and APACHE II score [12.0 (10.0, 16.0) vs. 8.0 (7.0, 10.0), P < 0.001] were higher. During CRRT, patients with SI-AKI required mechanical ventilation for a longer period of time [11 (4, 23) days vs. 4 (1, 9) days, P < 0.001] and had a higher rate of extubation failure [21 (35.59%) vs. 7 (14.29%), P = 0.012]. In addition, patients with SI-AKI had worse 30-day outcomes and had lactate levels [HR 1.133, 95%CI 0.908, 1.415, P = 0.009] and extubation failures [HR 1.014, 95%CI 1.002, 1.090, P < 0.001] as risk factors for developing 30-day mortality.

Conclusions The early prognosis of SI-AKI patients treated with CRRT does not appear to be favorable, which may be related to the severity of the patient's disease. Lactate levels and the occurrence of failed extubation can increase the risk of 30-day mortality.

sepsis

acute kidney injury

continuous renal replacement therapy

lactate

extubation

Sepsis-induced acute kidney injury (SI-AKI) is a syndrome of acute dysfunction and organ damage that is associated with a poor long-term prognosis for patients^[1], which may ultimately lead to chronic kidney disease (CKD), and even increase the risk of patient death^[2]. Currently, SI-AKI is considered the leading cause of AKI in intensive care units (ICUs), severely affecting nearly 50% of patients with severe sepsis^[3], and is strongly associated with patient mortality and length of hospital stay^{[4, 5]}.

Based on the complex pathogenesis of SI-AKI, renal replacement therapy (RRT) has been used as an exceptional treatment to protect and improve renal function. However, the current treatment strategy for patients with SI-AKI is to consider sepsis or AKI separately, and its efficacy is controversial^[6]. Patients undergoing CRRT due to haemodynamic instability as a result of sepsis is a common and often lethal clinical scenario^[7]. The clinical characteristics, prognostic outcomes, and unique risk factors for mortality in SI-AKI patients undergoing CRRT are not fully understood. Therefore, the aim of this study was to investigate the early prognosis of SI-AKI patients treated with CRRT and the risk factors associated with death.

Sepsis is identified as a critical organ malfunction resulting from an imbalanced host reaction to infections (Sepsis 3.0)^[8].

AKI is defined based on the results of the Kidney Disease Improving Overall Prognosis (KDIGO) study^[9], in which patients with AKI could be categorized and differentiated using peak serum creatinine (SCr) and urine output. SCr had to have increased to ≥ 1.5 times the baseline within the previous 7 days; SCr increased by ≥ 0.3 mg/dL within 48 h; or urine output < 0.5 mL/kg/h for more than 6 h. The AKI patients could be classified and differentiated using peak SCr and urine output. SI-AKI is defined as the presence of both consensus sepsis criteria and AKI criteria when AKI occurs within 7 days of a diagnosis of sepsis according to Sepsis-associated acute kidney injury: consensus report of the 28th Acute Disease Quality Initiative workgroup^[10].

Extubation failure is defined as the need for re-tracheal intubation within 48 hours of tracheal extubation, or the need for tracheotomy after evaluation.

Renal function recovery is defined as not requiring renal replacement therapy within 90 days after discharge.

This was a single-centre, retrospective, observational study that included a total of 108 patients who underwent CRRT between 1 January 2022 and 31 December 2022 in ICU of the Affiliated Wuxi People' s Hospital of Nanjing Medical University. Inclusion Criteria: 1. Patients were ≥ 18 years old, 2. met the diagnosis of SI-AKI, and 3. had complete clinical data 48 hours prior to admission to the ICU. Exclusion criteria: 1. Pre-existing renal insufficiency; 2. Undergoing kidney-related surgery; 3. Not receiving nephrotoxic drugs before admission to the ICU. All patients were categorized into SI-AKI and non-SI-AKI groups according to the definition of SI-AKI.

The study protocol was reviewed by the ethics committee of our centre, which did not require informed consent due to the anonymous and retrospective nature of the study.

Because urine volume data were not available, only serum creatinine criteria were used to define AKI. The primary outcome was survival at 30 days, secondary outcomes were the total time the patient was treated with CRRT, mechanical ventilation status, length of stay in the intensive care unit, total length of stay, and recovery of renal function.

The main indications for patients to start CRRT are as follows: drug-refractory volume overload, electrolyte imbalance, metabolic acidosis, oliguria with progressive azotemia, and haemodynamic instability. Decisions about when to start or terminate CRRT and CRRT settings (target clearance, blood flow, dialysate/replacement fluid rate and anticoagulation) were made in consultation and discussion with nephrologists and intensivists. Femoral vein cannulation was preferred, followed by jugular vein. CRRT was initiated with a gradual increase in blood flow to 150 ml/min and a CRRT dose of 35–40 ml/kg/h to ensure that a CRRT dose of 35 ml/kg/h was administered.

Statistical analysis was performed using R, version 4.1.3 (R Foundation for Statistical Computing). Normally distributed measurements were expressed as mean ± standard deviation (SD), and comparisons between groups were made using the independent samples t test; skewed variables were expressed as median and interquartile spacing, and comparisons between groups were made using the Mann-Whitney U test. Count data were expressed as percentages, and comparisons between groups were made using the Chi-square test or Fisher's exact test. Multifactorial COX regression modeling analysis was used to explore the risk factors for the occurrence of 30 deaths in SI-AKI patients treated with CRRT. Survival data were estimated using Kaplan-Meier curves, and differences between groups were quantified using the Log-rank test. A two-sided P < 0.05 was considered statistically significant.

During the study period, we excluded 2 patients due to age < 18 years, 3 patients due to loss of clinical data, 2 patients due to endotracheal intubation before admission to the ICU, and 4 patients due to CRRT already performed before admission to the ICU. A total of 108 critically ill patients were enrolled in the study.

There were 59 patients in the SI-AKI group whose primary disease was mainly gastrointestinal (24, 40.68%), of whom 44 (74.58%) of all patients were male, and 49 patients in the Non-SI-AKI group whose primary disease was mainly respiratory (22, 44.90%), of whom 34 (69.39%) of all patients were male. Compared with the Non-SI-AKI group, the SI-AKI patients were older [72 (60, 78) years vs. 60 (51, 70) years, P = 0.003] and had more patients with NYHA IV [25 (42.37%) vs. 13 (26.53%), P < 0.001]. According to the assessment of disease severity, SOFA score [9.0 (7.0, 10.0) vs. 6.0 (5.0, 7.0), P < 0.001] and APACHE II score [12.0 (10.0, 16.0) vs. 8.0 (7.0, 10.0), P < 0.001] were higher in patients with SI-AKI. In laboratory indices and blood gas analyses before receiving CRRT, SI-AKI patients had slightly higher lymphocyte counts [0.7 (0.5, 1.2) × 10⁹/L vs. 0.5 (0.4, 1.0) × 10⁹/L, P = 0.030] and higher C-reactive protein levels [120 (67, 193) mg /L vs. 57 (14, 109) mg/L, P < 0.001], low creatinine levels [242 (158, 397) µmol/L vs. 546 (266, 823) µmol/L, P < 0.001], and poor PaO2/FIO2 [196 (141, 315) mmHg vs. 314 (220, 363) mmHg, P = 0.001]. During CRRT, patients with SI-AKI required mechanical ventilation for longer periods of time [11 (4, 23) days vs. 4 (1, 9) days, P < 0.001], had a greater rate of failure to extubate [21 (35.59%) vs. 7 (14.29%), P = 0.012]. See Table 1 for specific clinical information.

Table 1

Characteristics and occurrences of the study population in SI-AKI and Non-SI-AKI patients treated with CRRT.
	SI-AKI(n = 59)	Non-SI-AKI (n = 49)	P value
Sex, %			0.549
Male	44 (74.58%)	34 (69.39%)
Female	15 (25.42%)	15 (30.61%)
Age, year	72(60, 78)	60(51, 70)	0.003
BMI, kg/m²	23.1 ± 3.2	22.2 ± 3.3	0.152
Comorbidities, %
Hypertension			0.616
YES	37 (62.71%)	33 (67.35%)
NO	22 (37.29%)	16 (32.65%)
Diabetes mellitus	24(40.7%)	18(36.7%)	0.676
Yes	24 (40.68%)	18 (36.73%)
No	35 (59.32%)	31 (63.27%)
NYHA Ⅳ			<0.001
Yes	25 (42.37%)	6 (12.24%)
No	34 (57.63%)	43 (87.76%)
Hepatic Dysfunction			0.0864
Yes	25 (42.37%)	13 (26.53%)
No	34 (57.63%)	36 (73.47%)
Primary disease			-
Gastrointestinal	24 (40.68%)	15(30.61%)
Respiratory	20 (33.90%)	22 (44.90%)
Cardiovascular	10 (16.95%)	3 (6.12%)
Immunity	5 (8.47%)	9 (18.37%)
Score
SOFA	9.0 (7.0, 10.0)	6.0 (5.0, 7.0)	<0.001
APACHE Ⅱ	12.0 (10.0, 16.0)	8.0 (7.0, 10.0)	<0.001
Pre-CRRT
Laboratory data
Leukocytes (\(\:\times\:\)10⁹/L)	11.0(8.0, 18.0)	10.7(7.4, 15.3)	0.476
Neutrophil (\(\:\times\:\)10⁹/L)	9.0(5.9, 15.8)	9.4(6.5, 13.8)	0.720
Lymphocytes (\(\:\times\:\)10⁹/L)	0.7(0.5, 1.2)	0.5(0.4, 1.0)	0.030
Platelet (\(\:\times\:\)10⁹/L)	147 ± 12	148 ± 14	0.946
Hemoglobin (g/L)	88 (76, 110)	84 (75, 93)	0.377
C-reactive protein (mg/L)	120 (67, 193)	57 (14, 109)	< 0.001
Creatinine (µmol/L)	242(158, 397)	546(266, 823)	< 0.001
Urea (mmol/L)	19 (13, 33)	20 (14, 30)	0.904
Alanine aminotransferase (U/L)	22.5(12.5, 70.4)	17.9(10.7, 81.2)	0.657
Aspartate aminotransferase (U/L)	49 (28, 160)	33 (20, 150)	0.223
Arterial Blood Gas
PH	7.35 ± 0.08	7.39 ± 0.10	0.024
PaO2 (mmHg)	99 (81, 155)	129 (95, 164)	0.077
PaCO2 (mmHg)	35 (29, 44)	35 (31, 39)	0.966
PaO2/FIO2 (mmHg)	196 (141, 315)	314 (220, 363)	0.001
Lactate (mmol/L)	2.10 (1.15, 3.45)	1.40 (0.80, 3.50)	0.055
During CRRT
Mechanical ventilation time, day	11 (4, 23)	4 (1, 9)	< 0.001
Extubation failure, %	21 (35.59%)	7 (14.29%)	0.012
Clinical event, %
Thrombus at cannula			0.101
Yes	13 (22.03%)	5 (10.20%)
No	46 (77.97%)	44 (89.80%)
Hemorrhage			0.523
Yes	24 (40.68%)	17 (34.69%)
No	35 (59.32%)	32 (65.31%)
Atrial fibrillation			0.070
Yes	20 (33.90%)	9 (18.37%)
No	39 (66.10%)	40 (81.63%)
Pathogen, %
Klebsiella pneumoniaea	14(28.6%)	15(30.6%)	0.825
Acinetobacter baumannii	26(44.1%)	14(28.6%)	0.097
Pseudomonas aeruginosa	17(28.8%)	6(12.2%)	0.036
Staphylococcus	13(22.0%)	6(12.2%)	0.183
Fungal	14(23.7%)	9(18.4%)	0.498
Others	14(23.7%)	3(6.1%)	0.012

BMI Body, Mass Index; SOFA score, Sequential Organ Failure Assessment; APACHE Ⅱ, Acute Physiology and Chronic Health Evaluation Ⅱ; Others, Escherichia coli, Streptococcus pneumoniae, Haemophilus influenzae and Elizabeth bacteria, etc.

Table 2 analyzes the primary and secondary outcomes of critically ill patients treated with CRRT. In terms of 30-day prognosis, the death rate of SI-AKI patients was 61.02%, whereas the mortality rate of Non-SI-AKI patients was 28.57%. In addition, there was a significant difference between the two groups of patients on the K-M survival curve according to the 30-day prognosis shown in Fig. 1 (P = 0.002). Regarding secondary outcomes, there was no significant difference between the two groups in terms of length of hospitalization, recovery of renal function, and time to CRRT application (P > 0.05), but the length of ICU stay was longer in patients with SI-AKI [13 (7, 24) days vs. 8 (5, 16) days, P = 0.037].

Table 2

Outcomes of SI-AKI and Non-SI-AKI patients treated with CRRT
	SI-AKI(n = 59)	Non-SI-AKI (n = 49)	P value
Primary outcome
30-day mortality, %	36 (61.02%)	14 (28.57%)	< 0.001
Secondary outcome
ICU length of stay, day	13 (7, 24)	8 (5, 16)	0.037
Length of hospitalization, day	19 (11, 37)	24 (16, 38)	0.376
Renal recovery, %			0.118
Yes	33 (55.93%)	20 (40.82%)
No	26 (44.07%)	29 (59.18%)
Time of CRRT, hour	62(20.0-144.0)	44(22.5–84.1)	0.880

Renal function recovery; no need for kidney replacement therapy within 90 days after discharge.

In the univariate COX regression analysis (Table 3), it was found that C-reactive protein, creatinine levels, PaO2/FIO2, lactic acid levels, and extubation failure had an impact on the 30-day mortality of critically ill patients receiving CRRT treatment (P < 0.05). Through multivariate COX regression analysis, only the oxygenation index and extubation failure were found to increase the risk of 30-day mortality. Specifically, for each mmHg increase in the PaO2/FIO2, the patient's risk of death decreased by 0.008 times, while extubation failure increased the risk of death by 0.112 times.

Table 3

Univariate and multivariate cox regression models to analyse risk factors for the occurrence of 30-day mortality in critically ill patients treated with CRRT
	Univariable			Univariable
	HR	95% CI	p-value		HR	95% CI	p-value
Sex
Male	—	—	-	-		-	-
Female	1.410	0.778, 2.556	0.258	-		-	-
Age	1.014	0.995, 1.033	0.153	-		-	-
BMI	1.003	0.920, 1.093	0.949	-		-	-
Comorbidities
Hypertension
No	—	—	-	-		-	-
Yes	0.585	0.335, 1.024	0.060	-		-	-
Diabetes mellitus
No	-	-	-	-		-	-
Yes	0.853	0.479, 1.519	0.589	-		-	-
NYHA Ⅳ
No	-	-	-	-		-	-
Yes	1.601	0.898, 2.852	0.111	-		-	-
Hepatic Dysfunction
No	-	-	-	-		-	-
Yes	1.553	0.885, 2.725	0.125	-		-	-
Score
SOFA	1.070	0.953, 1.202	0.253	-		-	-
APACHE Ⅱ	1.064	0.991, 1.141	0.085	-		-	-
Laboratory data
Leukocytes, \(\:\times\:\)10⁹/L	1.014	0.979, 1.051	0.437	-		-	-
Neutrophil, \(\:\times\:\)10⁹/L	1.014	0.976, 1.054	0.486	-		-	-
Lymphocytes,\(\:\:\times\:\)10⁹/L	1.168	0.920, 1.483	0.201	-		-	-
Platelet, \(\:\times\:\)10⁹/L	0.997	0.993, 1.000	0.058	-		-	-
Hemoglobin, g/L	1.005	0.994, 1.016	0.396	-		-	-
C-reactive protein, mg/L	1.004	1.001, 1.007	0.017	0.998		0.993, 1.004	0.534
Creatinine, µmol/L	0.998	0.997, 0.999	0.001	0.999		0.997, 1.001	0.231
Urea, mmol/L	0.992	0.969, 1.015	0.472	-		-	-
Alanine aminotransferase, U/L	1.004	0.999, 1.009	0.157	-		-	-
Aspartate aminotransferase, U/L	1.000	1.000, 1.000	0.986	-		-	-
Arterial Blood Gas
PH	0.393	0.015, 10.541	0.578	-		-	-
PaO2, mmHg	0.997	0.992, 1.002	0.232	-		-	-
PaCO2, mmHg	0.988	0.964, 1.012	0.334	-		-	-
PaO2/FIO2, mmHg	0.997	0.994, 0.999	0.006	0.992		0.986, 0.998	0.010
Lactate, mmol/L	1.176	1.093, 1.265	< 0.001	1.084		0.945, 1.245	0.249
Mechanical ventilation time, day	1.980	0.960, 1.001	0.067	-		-	-
Extubation failure	1.266	1.113, 1.626	0.002	1.112		1.031, 1.403	< 0.001
HR, Hazard Ratio; CI, Confidence Interval

Table 4 demonstrates the risk factors for 30-day mortality in SI-AKI patients treated with CRRT. After multifactorial analysis, lactate [HR 1.133, 95%CI 0.908, 1.415, P = 0.009] and extubation failure [HR 1.014, 95%CI 1.002, 1.090, P < 0.001] were the independent risk factors for 30-day death in patients with SI-AKI.

Table 4

Univariate and multivariate COX regression models to analyse risk factors for 30-day mortality in SI-AKI patients treated with CRRT
	Univariable			Univariable
	HR	95% CI	p-value	HR	95% CI	p-value
Sex
Male	—	—	-	-	-	-
Female	1.337	0.644, 2.775	0.437	-	-	-
Age	1.005	0.984, 1.027	0.645	-	-	-
BMI	1.018	0.927, 1.118	0.709	-	-	-
Comorbidities
Hypertension
No	-	-	-	-	-	-
Yes	1.090	0.551, 2.155	0.804	-	-	-
Diabetes mellitus
No	-	-	-	-	-	-
Yes	0.824	0.417, 1.627	0.577	-	-	-
NYHA Ⅳ
No	-	-	-	-	-	-
Yes	1.120	0.580, 2.162	0.736	-	-	-
Hepatic Dysfunction
No	-	-	-	-	-	-
Yes	1.033	0.532, 2.007	0.923	-	-	-
Score
SOFA	1.996	1.063, 1.151	0.961	-	-	-
APACHE Ⅱ	1.954	1.036, 1.050	0.337	-	-	-
Laboratory data
Leukocytes, ×109/L	1.004	0.965, 1.044	0.846	-	-	-
Neutrophil, ×109/L	1.004	0.964, 1.046	0.839	-	-	-
Lymphocytes, ×109/L	1.108	0.844, 1.456	0.460	-	-	-
Platelet, ×109/L	0.999	0.994, 1.003	0.499	-	-	-
Hemoglobin, g/L	1.003	0.992, 1.015	0.545	-	-	-
C-reactive protein, mg/L	1.001	0.997, 1.005	0.518	-	-	-
Creatinine, µmol/L	1.000	0.998, 1.002	0.967	-	-	-
Urea, mmol/L	0.993	0.970, 1.016	0.538	-	-	-
Alanine aminotransferase, U/L	1.004	0.992, 1.016	0.495	-	-	-
Aspartate aminotransferase, U/L	1.000	1.000, 1.000	0.050	-	-	-
Arterial Blood Gas
PH	0.367	0.006, 22.671	0.634	-	-	-
PaO2, mmHg	0.999	0.994, 1.003	0.540	-	-	-
PaCO2, mmHg	0.988	0.961, 1.017	0.411	-	-	-
PaO2/FIO2, mmHg	0.998	0.995, 1.001	0.162	-	-	-
Lactate, mmol/L	1.119	1.029, 1.218	0.009	1.133	0.908, 1.415	0.009
Mechanical ventilation time, day	1.953	0.925, 0.982	0.002	1.005	0.977, 1.035	0.711
Extubation failure	1.137	1.033, 1.056	< 0.001	1.014	1.002, 1.090	< 0.001
HR, Hazard Ratio; CI, Confidence Interval

In this retrospective cohort study, we sought to describe the differences in clinical characteristics and prognostic outcomes between severe patients requiring CRRT for SI-AKI and those with Non-SI-AKI, and to explore their risk factors for mortality. We found that patients with SI-AKI were older, had more cardiac insufficiency, were more severely ill at ICU admission, had a more intense inflammatory response, and had a worse 30-day prognosis compared with patients with Non-SI-AKI. After multifactorial analysis, PaO2/FIO2 and extubation failure are risk factors for 30-day mortality in critically ill patients treated with CRRT, whereas lactate level and extubation failure are independent risk factors for 30-day mortality in SI-AKI patients treated with CRRT.

The occurrence of SI-AKI is complex and heterogeneous. Its mechanisms can arise directly from infection and related host responses, or they may be indirect consequences of sepsis or its treatment. Several pathophysiological mechanisms may interact and contribute to AKI in septic patients, including systemic and renal inflammation, microcirculatory dysfunction and macrocirculatory abnormalities, mitochondrial dysfunction, metabolic reprogramming, and dysregulation of the renin-angiotensin-aldosterone system (RAAS)^[11]. Impairment of the microcirculation is primarily associated with endothelial damage, microvascular thrombosis and inflammatory progression, ultimately leading to inadequate microcirculatory perfusion and increased renal vascular resistance^[12]. While focusing on microcirculatory alterations, fluctuations in the macrocirculation require extra attention, and haemodynamic changes in macrovascular dysfunction can also contribute to the development of SI-AKI, although it can occur independently of renal underperfusion^[13]. CRRT has been widely accepted as the method of choice for critically ill patients with haemodynamic instability because it provides slow, gentle and continuous renal support^[14]. Not only that, but CRRT allows for stable fluid removal over a longer period of time, and can be applied for prolonged periods of time to prevent fluid overload in patients with AKI when rapid rehydration is required to correct shock or to transfuse blood products^[15]. However, the efficacy of CRRT continues to be the subject of much controversy, for example, in a study by Nagata I and his team, no significant difference was found in in-hospital mortality between SI-AKI and Non-SI-AKI patients treated with CRRT (61.1% vs 56.3%, p = 0.42). A cohort study of critically ill patients admitted to 32 ICUs found no difference in 30-day mortality and a lower rate of RRT dependence in patients treated with CRRT compared with patients treated with intermittent hemodialysis phases (8.3% vs 16.5%)^[16].

In our study, lactate levels and extubation failure in SI-AKI patients were found to be risk factors for the occurrence of 30-day mortality. This may be related to impaired renal function and inability to remove lactate, which is rapidly effluxed from damaged renal cells to the plasma and extracellular space when SI-AKI occurs, resulting in elevated plasma lactate and reduced lactate clearance^[17]. Moreover, renal tubular epithelial cells can first generate energy through glycolysis rather than oxidative phosphorylation, which in turn leads to a massive conversion of pyruvate to lactate and lactate accumulation occurs^[18]. In a previous model of SI-AKI, a significantly elevated renal venous lactate/pyruvate ratio was found to parallel renal cortical microcirculatory dysfunction and progressively worsen during sepsis^[19]. In addition, the lactate-activated PD-1/PD-L1 pathway induces immunosuppression by inducing apoptosis of lymphocytes in SI-AKI, and can also inhibit the cytolytic activity of cytotoxic T cells and promote the production of the pro-inflammatory cytokine IL-17 by Th17 cells^{[20, 21]}; thus, patients with SI-AKI are prone to immunosuppression and a state of imbalance of anti-inflammatory-promotional levels in the body, which ultimately leads to the rapid disease progression. And in a clinical study, both lactate levels and lactate clearance after 24 hours of CRRT were found to be independently associated with mortality in patients with SI-AKI^[22]. We have also demonstrated that failed extubation is an independent risk factor for the occurrence of death within 30 days in patients, and previous literature suggests that the high mortality rate after failed extubation may be attributed to the higher severity of the disease at the time of extubation, but this is also refuted by studies in the literature, which have shown that failure of extubation adversely affects survival, independent of the severity of the underlying disease^{[23, 24]}. Failed extubation or reintubation itself can reduce a patient's chances of survival. In several studies, reintubation was significantly associated with ventilator-associated pneumonia^[25], and thus Arnaud W et al. suggested that reintubation may lead to a worsening of the clinical condition of the frail patient, which in turn increases the risk of death^[26].

Limitation

Our study has several limitations. First, it was a targeted retrospective study, reducing the reliability of the findings. Second, we did not follow patients' clinical indicators such as C-reactive protein and creatinine during CRRT, and third, the sample size was relatively small and needs to be interpreted with caution. Finally, more well-designed large-scale trials are needed to confirm our findings and to further complement the prognostic and mortality risk factors for septic AKI. However, to the best of our knowledge, the present study is one of the few studies exploring early prognostic and mortality risk factors in SI-AKI patients treated with CRRT.

In conclusion, the early prognosis of SI-AKI patients treated with CRRT does not appear to be favorable, which may be related to the severity of the patient's disease. In addition, patients' lactate levels and the occurrence of failed extubation can increase the risk of 30-day mortality. Numerous prospective studies are still needed to further explore this in the future.

Author Contributions

Jing Tian contributed substantially to the study concept and design, data analysis and interpretation. Jiayue Zhang was involved in drafting the manuscript and critically revising important intellectual content. Hongyang Xu was involved in key revisions of the manuscript and approval of the final version. All authors have read and agreed to the published version of the manuscript.

Acknowledgements

Not applicable.

Funding

None.

Clinical trial number

Not applicable.

Informed Consent Statement

Written informed consent from each patient was waived because our study was conducted using anonymized health care data, which met the IRBs minimal risk waiver criteria.

Data Availability Statement

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

Ethics declarations

Ethics approval and consent to participate

This study was performed in accordance with the ethical standards of the Helsinki Declaration and its later amendments. The study protocol was approved by the Human Ethics Committees of each study organization. As it was a retrospective study, the Human Ethics Committee of The Affiliated Wuxi People' s Hospital of Nanjing Medical University waived the need for informed consent in the study. All clinical data analyzed were obtained from pre-existing datasets at the hospital.

Conflicts of Interest

The authors declare no conflicts of interest.

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No competing interests reported.

Early prognosis of patients with sepsis-related acute kidney injury receiving continuous renal replacement therapy in the intensive care unit

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Abstract

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Introduction

Definition

Study population

Outcome Measures

CRRT protocol

Statistical analysis

Results

Discussion

Conclusions

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References

Additional Declarations

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