Introduction: why focus on recovery?
Pathophysiology of recovery
Clinical definition of renal recovery
Pitfalls in evaluation of recovery
Assessment of baseline function
Defining the population
Timing of recovery assessment
Defining recovery
Future directions
Measurement of creatinine clearance
Measurement of renal functional reserve
Patient-related risk factors | Age Race ethnicity Genetic factors Chronic kidney disease Comorbidity |
Severity of acute disease | High illness severity Haemodynamic instability Medical admission |
Severity of AKI | Higher KDIGO stage |
Kinetic eGFR
Real-time GFR monitoring
Biomarkers for (non)recovery
AKI biomarker | Characteristics | Clinical setting | Outcome |
---|---|---|---|
Angiotensinogen | 453 amino acid protein; precursor of angiotensin I | Acute CRS Cardiac surgery ICU | AKI progression |
Cystatin C | 13 kDa cysteine protease inhibitor produced by all nucleated human cells; undergoes glomerular filtration | ICU | RRT |
Hepatocyte growth factor | Antifibrotic cytokine produced by mesenchymal cells and involved in tubular cell regeneration after AKI | ICU | RRT |
IGFBP7 TIMP-2 | 29 kDa and 21 kDa proteins involved in cell cycle arrest; released into urine after tubular cell stress | ICU Cardiac surgery | RRT |
IL-18 | 18 kDa pro-inflammatory cytokine; regulates innate and adaptive immunity; released into urine after proximal tubular cell injury | ICU Acute CRS Cardiac surgery Renal transplantation | AKI progression RRT DGF |
KIM-1 | 39 kDa transmembrane glycoprotein involved in tubular regeneration; released into urine following ischaemic or nephrotoxic tubular cell damage | ICU Hospitalised patients Renal transplantation | AKI progression Need for RRT DGF |
L-FABP | 14 kDa intracellular lipid chaperone produced in proximal tubular cells; aids in regulation of fatty acid uptake and intracellular transport; excretion into urine after tubular injury | ICU Cardiac surgery | AKI progression RRT |
MicroRNA | Endogenous single-stranded molecules of non-coding nucleotides; upregulated following tubular cell injury and cell proliferation; detectable in plasma and urine | ICU Cardiac surgery | AKI progression RRT |
NAG | >130 kDa lysosomal enzyme; produced in proximal and distal tubular cells; released into urine after tubular cell injury | Hospitalised patients | RRT |
NGAL | At least three different types: Monomeric 25 kDa glycoprotein produced by neutrophils and epithelial cells, including renal tubules Homodimeric 45 kDa protein produced by neutrophils Heterodimeric 135 kDa protein produced by renal tubular cells released into urine following systemic production or tubular injury | ICU Cardiac surgery Acute CRS Renal transplantation | AKI progression RRT DGF |
Potential markers of tubular function
Epidemiology of renal outcome after AKI
Short-term renal outcome
Long-term renal outcome
AKI stage | Absolute risk (%)/at time | Hazard ratio, HR (95% CI) over time |
---|---|---|
AKI (all stages) vs. non-AKI | 2% vs. 0.08%/1 year [62] 3.9% vs. 0.3%/5 year | HR 3.1 (1.9–5.0) per 100 patient-years [10] |
RRT-treated AKI | 180 days: 8.5% [6] 1 year: 20% [64] 5 years: 11.7% (cumulative risk) [6] 7 years: 3.4% (new ESKD) [66] | Up to 180 days: HR 105 (78–148) vs. critically ill [6] From 80 days to 5 years: HR 6.2(4.7–8.1) vs. critically ill [6] |