Introduction
Methods
Statement | Grade |
---|---|
What are interventions or modifiable risk factors which may mitigate respiratory dysfunction among patients with AKI? | |
1. We recommend adherence to KDIGO guidelines for AKI management, as it may translate into improved pulmonary outcomes | 1D |
2. We suggest conservative fluid management and selected use of diuretics or ultrafiltration (RRT) in patients with AKI on IMV to improve respiratory function and decrease duration of IMV in patients with ARF/ARDS | 2C |
3. We recommend delivery of RRT to mitigate the metabolic consequences of AKI particularly where acid–base derangement may affect ventilation | 1D |
What are interventions or modifiable risk factors to mitigate AKI among patients with ARF/ARDS not requiring mechanical ventilation? | |
1. We recommend treating patients with ARF/ARDS according to the KDIGO guidelines who are at risk of or with AKI | 1C |
2. We suggest at least daily measurement of serum creatinine and regular monitoring of urine output in patients with severe ARF/ARDS to detect development of AKI | 1B |
3. We recommend the implementation of adequate screening measures for early reorganization of pulmonary infections, followed by early initiation of appropriate antibiotic therapy, which is associated with lower risk of AKI | 1C |
What are the interventions or modifiable risk factors to mitigate AKI among patients with ARF/ARDS requiring mechanical ventilation? | |
1. We recommend monitoring of tidal volumes and ventilation pressures and application of lung protective ventilation strategies in patients receiving IMV to reduce the risk of new or worsening AKI | 1C |
2. We recommend monitoring and treatment of mechanically ventilated patients for hypotension, venous congestion, right heart failure, and intraabdominal hypertension, which can contribute to renal dysfunction | 1B |
3. We suggest avoiding—if possible—specific ancillary interventions known to be associated with AKI, including fluid overload, nephrotoxin exposure, and high doses of iNO | 2B |
What is the impact of RRT on lung function? | |
1. We suggest, that during RRT in patients with COPD with metabolic compensation, the correction of compensatory metabolic alkalosis should be as slow as tolerated, to avoid development of acidosis | 2D |
What is the impact of ECMO on kidney function? | |
1. We recommend close monitoring for haemolysis and markers of coagulation and inflammation | 1C |
2. We recommend that in patients undergoing ECMO, kidney function should be monitored routinely with at least daily serum creatinine measurements and fluid balance assessment | 1C |
Are combinations of extracorporeal lung and renal support protective for organ function? | |
1. We recommend initiation of CRRT should be based on absolute and relative indications for critically ill patients, given there is no evidence of benefit for combining ECMO therapy with pre-emptive use of CRRT | 1D |
2. We do not recommend the use of CRRT and/or haemoabsorption with the sole intention to clear pro-/anti-inflammatory mediators during ECMO | 1C |
Results
Epidemiology
Question: What is the association between AKI and ARF/ARDS?
Consensus statements
Rationale
Recommendations for research
Kidney–lung interactions
Question: What are the pathophysiological mechanisms of respiratory failure in patients with AKI?
Consensus statement
Rationale
Recommendation for research
Question: What are interventions or modifiable risk factors which may mitigate respiratory dysfunction among patients with AKI?
Consensus statements
Rationale
Recommendations for practice
Recommendations for research
Lung–kidney interactions
Question: What are the potential physiological and/or pathophysiological mechanisms of AKI in patients with ARF/ARDS?
Consensus statements
Rationale
Haemodynamic effects | Inflammatory/immune- mediated effects | Effects of altered acid–base status | Effects of impaired gas exchange | Neuro-hormonal effects | |
---|---|---|---|---|---|
Potential pathophysiological mechanisms | Effects of acute pulmonary disease on kidney function | ||||
Increased release of pro-inflammatory mediators (IL-6, TNF-α, IL-1 beta, TGF-β, substance P) [16‐19] Decreased release of anti-inflammatory mediators (IL-10) | Increased oxygen consumption in the proximal renal tubular system in respiratory acidosis [119] | Activation of RAAS [65] Increased aldosterone secretion [65] Reduction of ANP/BNP levels [65] Activation of the sympathetic nervous system [65] Release of non-osmotic vasopressin [48] | |||
Additional effects of positive pressure ventilation on kidney function | |||||
Excessive increase in intrathoracic pressure leading to: reduced venous return [64] reduced left ventricular preload [64] reduced cardiac output [64] | Effect of injurious ventilation: increased release of IL-6, PAI-1, TNFR-1 and TNFR-2 into systemic circulation [62] induction of renal epithelial cell apoptosis and dysregulation of extracellular ligands [63] | As above | Permissive Hypercapnia: as above Hyperoxaemia: lack of data | As above | |
Parameters to monitor lung–kidney interaction | CVP [47] MAP Renal perfusion pressure [77] PEEP [68] Inspiratory pressure [62] Intra-abdominal pressure [47] | Arterial pH [95] | BNP [67] |
Recommendations for research
Question: What additional mechanisms attributable to invasive mechanical ventilation may contribute to AKI?
Consensus statement
Rationale
Recommendation for research
Question: What are interventions or modifiable risk factors to mitigate AKI among patients with AFR/ARDS not requiring mechanical ventilation?
Consensus statement
Rationale
Recommendations for practice
Recommendations for research
Question: What are the interventions or modifiable risk factors to mitigate AKI among patients with ARF/ARDS requiring mechanical ventilation?
Consensus statements
Rationale
Therapeutic category | Intervention type | Patient population/number of patients/trial type | Results | Level of evidence |
---|---|---|---|---|
Ventilation strategies | Spontaneous breathing during APRV | Acute lung injury 12 patients [OT] | Improved renal blood flow and GFR with spontaneous breathing vs. controlled ventilation [76] | C |
Lung protective ventilation | ARDS 861 patients [RCT] | Less days with renal failure (defined as sCr ≥ 2 mg/dL) in the lung protective ventilation group [73] | B | |
Neuromuscular blockade and lung-protective ventilation | Early ARDS 340 patients [RCT] | Significantly more ventilator-free days (p = 0.04) and more days without renal failure (20.5 ± 10.1 vs. 18.1 ± 11.6 days; p = 0.05) [79] | B | |
1006 patients [RCT] | No effect on mortality and kidney failure free days by day 28 in another trial [80] | B | ||
Prone ventilation | ARDS 16 patients [OT] | No effect on renal blood flow index, glomerular filtration rate index, filtration fraction, urine volume, fractional sodium excretion, and osmolar and free water clearances [77] | C | |
Anti-inflammatories | Glucocorticoids ± mineralocorticoid | ARDS 91 patients [RCT] | Improvement in extra-pulmonary organ function, including a trend towards less AKI by day 7 (18% vs. 37%; p = 0.06) No effect on RRT [85] | C |
Fluids | Albumin and diuretics | ARDS 40 [RCT]/37 [RCT] patients | C | |
Conservative fluid management | ARDS 1000 patients [RCT] | Trend towards reduced need for RRT with fluid restrictive strategy [36] | C | |
2124 patients [RCT] | Less AKI with fluid restrictive strategy after correction for fluid balance [40] | C | ||
Furosemide and conservative fluid management | ARDS 1000 [RCT] | Trend towards reduced need for RRT (10% vs. 14%; p = 0.06) [36] | C | |
ARDS + AKI 306 [SG] patients | Reduced mortality in patients with AKI and ARDS [37] | C |