1 Acute Kidney Injury, part 1 Flashcards
Remarks on Acute Kidney Injury
For most causes of AKI, global or regional decrease in renal blood flow is the final common pathway. Recovery from AKI first depends on restoration of renal blood flow.
The most common cause of intrinsic AKI
ischemic injury or ischemic tubular necrosis (also historically called acute tubular nacrosis), when renal perfusion is decreased so much that the kidney parenchyma is affected.
This is virtually pathognomonic of obstruction
alternating oliguria and polyuria
Stage 1 AKI
Serum Crea ↑ 1.5x
or
Crea ↑ >0.3 mg/dL over <48 hours
or
GFR ↓ 25-50%
or
Urine output 0.5 mL/kg/h for 6 hours
Stage 2 AKI
Serum crea ↑ 2.0 - 3.0x
or
GFR ↓ 50-75%
or
0.5 mL/kg/h for 12 hours
Stage 3 AKI
Serum Crea ↑ >3.0x
or
Serum Crea >4 mg/dL (≥354 umol/L)
and acute ↑ >0.5 mg/dL (44 umol/L)
or
GFR ↓ >75%
or
0.3 mL/kg/h for 24 h
or
Anuria for 12 hours
Acute Kidney Loss
Complete loss of kidney function for >4 weeks
End-stage renal disease
Need for renal replacement therapy for >3 months
For AKI in the ED, the goals are
- Identify patients at risk for AKI
- Correct metabolic effects
- Decrease ongoing renal injury
- Prevent iatrogenic injury
Fastest screening test for hyperkalemia
ECG
But sensitivity for a level over 6.5 mmol/L is 14-60%
Peaked T waves are only seen in 34% of patients
This suggests bladder outlet obstruction
A large postvoid bladder residual volume (>125 mL)
Anuria is defined as
<100 mL of urine per day, and can be present with prerenal, postrenal, or intrinsic
Remarks on prerenal AKI
Prerenal AKI is also a common precursor to ischemic and nephrotoxic conditions, leading to intrinsic AKI
The most common cause of postrenal AKI
prostatic hypertrophy
most common cause of AKI in hospitalized patients
intrinsic kidney injury
Hospital AKI si due to toxic and ischemic insults in most cases.