AKI Flashcards
What is AKI?
Acute Kidney Injury
abrupt decline in kidney function in 7 days or less
What is AKD?
Between 7 and 90 days after an AKI event before CKD
AKI Stage 1 Scr
1.5 - 1.9 times baselines
OR
>/= 0.3 mg/dl increase
AKI Stage 1 UO
< 0.5 ml/kg/hr for 6 - 12 hours
AKI Stage 2 SCr
2.0 - 2.9 times baseline
AKI Stage 2 UO
<0.5 ml/kg/hr >/= 12
AKI Stage 3 SCr
3.0 times baseline
OR
>/= 4.0 increase
OR
Initiation of renal replacement therapy
OR
In pts <18 y/o dec in GFR <35MLMIN
AKI Stage 3 UO
<0.3 ml/kg/hr FOR >/=24 hrs
OR
Anuria for >/= 12 hrs
AKI Functional Damage
- Increase in biomarkers (SCr, BUN)
- Change in glomerular/tubular function
- Absence of true damage to kidney
AKI Kidney Damage
- Presence of glomerular/tubular injury
- Identified by novel biomarkers
- NGAL (proximal tubule)
- TIMP2 and IGFBP7 (cell cycle arrest)
- KIM 1 (proximal tubule)
Risk Factors of AKI
- Age >65 years
- African American ethnicity
- CKD
- DM
- Nephrotxin use
- Decreased effective circulatory volume (HF, cirrhosis, blood loss)
Gen Prevention of AKI
- Maintain euvolemia and normal Elytes
- isotonic crystalloids
- balanced crystalloids maybe vs saline
- Maintain organ perfusion (MAP > 65 mmHg)
- Vasopressors
- Avoid nephrotoxins
- Aminoglycosides, amphotericin, iodinated contrast, vancomycin, etc)
Prevention of Contrast Induced AKI
- Isotonic Na containing crystalloids
- 1 ml/kg/hr 12 hrs prior and post - Na bicarbonate (harm potential)
- N-acetylcysteine (mod data;no benefit)
- Vitamin D
***Decreasing data
Diuretics in AKI
- No benefit
- To manage edema or HyperK
- Resistance common
- increase dose
Dopamine in AKI
- Increase renal blood flow and urine output
- “renal dose dopamine” - 1 - 3 mcg/kg/min
- No change in AKI outcome
- Increases risk of arrhythmias and hypotension
Fenoldapam
Oral dopamine receptor agonist studied and shown no benefit with increased risk of hypotension
AKI Treatment (Supportive Care)
Maintain fluid, elytes, acid/base homeostasis
BP management
Avoid nephrotoxic meds
Kidney replacement therapy
Nutritional support
Treatment of hemodynamic AKI
Intravascular volume repletion
(Goal: >0.5 ml/kg/hr)
Temp hold meds: ACEi/ARB/NSAIDs/SGLT2is, calcineurin inhbitors
(Restart when kidney back baseline)
Diagnosis of Pre-Renal AKI
FeNa <1%
OR
FeUrea <35% (on loop diuretic)
Treatment of Pre-Renal AKI
Intravascular volume repletion
(Goal: >0.5 ml/kg/hr)
Temp hold meds: Thiazide and loop diuretics
(Restart when kidney back baseline)
Treatment of Intrinsic AKI
If med caused - stop med and DO NOT RESTART
Glomerulonephritis
Acute Tubular Necrosis
Tubulointerstitial nephritis
Vasculitis
Glomerulonephritis Treatment
Immunosuppresion
Acute Tubular Necrosis Treatment
Supportive Care
Tubulointerstitial nephritis Treatment
Glucocorticoids
- Prednisone 0.5 - 1 mg/kg/day x 3-8 weeks then taper
Vasculitis Treatment
Immunosuppression
Treatment of Post-Renal AKI
Relieve obstruction
- Acute: Foley catheter, nephrostomy tube
- Chronic: treat underlying cause (BPH, cancer)
Kidney Replacement Therapy
treatment for severe/prolonged AKI
- CKRT -continuous kidney replacement therapy
- IHD -intermittent hemodialysis
How to assess kidney function in AKI
DO NOT USE SCr
Use Urine Output
SCr in AKI kidney function assessment
DO NOT USE SCr
- Lags behind GFR by 1- 2 days
- EARLY AKI - OVERestimates GFR
- RECOVERY phase - UNDERestimates GFR
Urine output in AKI kidney function assessment
No drug dosing guidelines
oliguric vs non-oliguric is benchmark
Anuria = GFR <10 ml/min
Initiation and Extension Phase Assessment
need higher doses of hydrophilic drugs (ABx) due to to large Vd
Maintenance Phase Assessment
may rely on SCr calculation for GFR
Recovery Phase Assessment
increase doses of renally eliminated drugs
