Introduction
Materials and methods
Patients
Data collection
Characteristics | All patients (N = 137) | AKI − (N = 68) | AKI + (N = 69) | P value |
---|---|---|---|---|
Age (years) | 71.1 (56.3 to 79.8) | 68.5 (49.8 to 77.5) | 73.4 (60.3 to 80.7) | 0.044 |
Males | 60 (45) | 35 (41.5) | 42 (60.9) | 0.38 |
Comorbidities | ||||
COPD | 12 (9) | 9 (13) | 3 (4) | 0.06 |
Diabetes mellitus | 20 (15) | 7 (10) | 13 (19) | 0.16 |
Hypertension | 59 (43) | 23 (34) | 36 (52) | 0.03 |
Heart failure | 19 (14) | 7 (10) | 12 (17) | 0.23 |
CAD | 16 (12) | 6 (9) | 10 (14) | 0.3 |
Liver disease | 10 (7) | 4 (6) | 6 (9) | 0.53 |
Cancer | 39 (28) | 19 (30) | 20 (29) | 0.89 |
Medication before admission | ||||
NSAIDs | 7 (5) | 3 (4) | 4 (6) | 0.71 |
Diuretics | 28 (20) | 11 (16) | 17 (25) | 0.22 |
Statins | 24 (17) | 9 (13) | 15 (22) | 0.19 |
Steroids | 9 (7) | 3 (4) | 6 (9) | 0.32 |
β-blockers | 29 (2) | 12 (18) | 17 (25) | 0.32 |
Antiplatelet therapy | 27 (20) | 13 (19) | 14 (10) | 0.86 |
Organ failure | ||||
Mechanical ventilation | 118 (86) | 55 (81) | 63 (91) | 0.08 |
SAPS II | 50 (39 to 60) | 45 (33 to 52) | 57 (46 to 67) | <0.0001 |
Norepinephrine | 131 (96) | 65 (95) | 66 (95) | 0.82 |
Epinephrine | 17 (12) | 4 (6) | 13 (19) | 0.02 |
Dobutamine | 4 (3) | 3 (4) | 1 (1) | 0.3 |
Dose of norepinephrineb | 0.44 (0.20 to 0.73) | 0.31 (0.16 to 0.54) | 0.56 (0.30 to 0.95) | 0.0005 |
Dose of epinephrineb | 0.31 (0.14 to 0.40) | 0.23 (0.15 to 0.32) | 0.31 (0.12 to 42) | 0.70 |
Dose of dobutamineb | 5 (5 to 5) | 5 (5 to 5) | 5 (5 to 5) | 1 |
Hydrocortisone | 19 (14) | 2 (10.5) | 17 (25.4) | 0.17 |
Lactate (mmol/L) | 2.8 (1.9 to 4.8) | 2.7 (1.8 to 3.9) | 3 (2.1 to 6.2) | 0.06 |
Serum creatinine (μmol/L) | 141.5 (83 to 215.8) | 88 (68 to 143.2) | 185 (134 to 255) | <0.0001 |
Bilirubin (mg/ml) | 16 (9 to 27.8) | 14 (8 to 21.8) | 16 (11 to 33) | 0.04 |
Platelet count (g/ml) | 65 (30.8 to 98.2) | 63 (28.8 to 89.2) | 67 (31 to 102) | 0.45 |
Hemoglobin (g/dl) | 10.3 (9.4 to 12) | 10.3 (9.9 to 12) | 10.4 (9.3 to 12.1) | 0.39 |
Base deficit (mmol/L) | −7.7 (−11.3 to −3.4) | −5 (−8.9 to −2.3) | −8.8 (−13 to −5.8) | 0.0006 |
Fluid balance (ml) | 3,480 (1,945 to 5,351) | 2,905 (1,350 to 4,717.5) | 3,591.5 (2,597.5 to 5,714) | 0.008 |
Origin of sepsis | ||||
Abdomen | 78 (57) | 37 (54) | 41 (59) | 0.55 |
Lung | 28 (20) | 16 (23) | 12 (17) | 0.37 |
Urinary tract | 9 (7) | 3 (4) | 6 (9) | 0.31 |
Soft tissue | 8 (6) | 5 (7) | 3 (4) | 0.45 |
Other | 20 (15) | 11 (16) | 9 (13) | 0.6 |
Nephrotoxic agents | ||||
Contrast media | 82 (61) | 41 (60) | 41 (60) | 0.21 |
Vancomycin | 53 (39) | 29 (43) | 24 (35) | 0.31 |
Aminoglycosides | 9 (7) | 5 (7) | 4 (6) | 0.71 |
Colloids | 108 (79) | 47 (69) | 61 (88) | 0.005 |
Parameters | AKI − (N = 68) | AKI + (N = 69) | P value |
---|---|---|---|
CO (mean) | 4.6 (3.6 to 6.2) | 4.9 (3.8 to 6.7) | 0.41 |
CO (LLR) | 3.7 (3 to 5.4) | 3.8 (2.9 to 4.8) | 0.76 |
CO (ULR) | 5.7 (3.9 to 7.1) | 6 (5.1 to 8.1) | 0.14 |
ScvO2 (mean) | 74.5 (71.7 to 78.4) | 74.5 (67.3 to 77.5) | 0.26 |
SvcO2 (LLR) | 71 (65 to 75) | 67 (60.1 to 72.3) | 0.058 |
SvcO2 (ULR) | 80 (76 to 84.2) | 80 (75.6 to 84) | 0.92 |
SAP (mean) | 110.2 (101.4 to 117) | 108.5 (100.5 to 119) | 0.94 |
SAP (LLR) | 88.5 (80 to 98) | 89 (77 to 100) | 0.8 |
SAP (ULR) | 128 (116 to 142) | 130 (117 to 143) | 0.74 |
DAP (mean) | 54.8 (50.4 to 59.5) | 51.5 (46.5 to 56) | 0.028 |
DAP (LLR) | 45 (40 to 50) | 42 (37 to 46) | 0.15 |
DAP (ULR) | 64.5 (57.8 to 69.2) | 60 (55 to 66) | 0.022 |
MAP (mean) | 73 (69.2 to 79.1) | 72 (65.5 to 77) | 0.16 |
MAP (LLR) | 61.7 (53 to 65.5) | 58 (52 to 65) | 0.26 |
MAP (ULR) | 87.5 (81 to 94) | 84 (76 to 95) | 0.18 |
CVP (mean) | 8.5 (7 to 11.1) | 11 (8.5 to 13) | 0.00031 |
CVP (LLR) | 4.5 (3 to 6.2) | 7 (3 to 8) | 0.0042 |
CVP (ULR) | 13 (10 to 16) | 15 (12 to 18) | 0.00055 |
Definition
Statistical analysis
Primary endpoint
Secondary endpoint
Results
Patients’ characteristics
Relation between acute kidney injury and systemic hemodynamics
Outcomes
Discussion
Conclusions
Key messages
-
AKI progresses in about 50% of septic patients despite hemodynamic optimization.
-
We observed a weak association between systemic hemodynamic parameters and AKI in septic patients.
-
Higher mean CVP in the first 24 hours was linearly associated with increasing risk of new or persistent AKI across all observed CVP values.
-
The association of elevated CVP with AKI suggests a role of venous congestion in the development of AKI.
-
The paradigm that targeting high CVP may reduce the occurrence of AKI should be revised.