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.
Contrast-induced nephropathy is defined by
a relatively small change in serum creatinine (25% increase from baseline or an absolute increase of 0.5 mg/dL [44 umol/L] 48 to 72 hours after infusion)
Remarks on contrast-induced nephropathy
Studies found no differences in mortality, development of chronic kidney disease, or need for dialysis or renal transplantation in the future between contrast-exposed patients and unexposed patients.
Prevention of worsening renal function due to contrast exposure continues to serve as an indication for hydration prior to contrast-enhanced imaging for patients with preexisting chronic kidney disease
Most common causes of crystal-induced AKI
Elevated uric acid levels in the setting of tumor lysis syndrome
and some medications - in particular, acyclovir, sulfonamides, indinavir, and triamterene
Remarks on ACE inhibitors and NSAIDS
ACEi cause a preferential efferent arteriolar vasodilation in the renal glomerulus
NSAIDS cause afferent renal arteriole vasoconstriction (decreasing both GFR and renal blood flow)
This drug class may cause rhabdomyolysis
Statins
The most common antiviral implicated in AKI
antiretrovirals
acyclovir
valacyclovir
Nephrotic syndrome
Proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia
Nephritic syndrome
Hematuria, RBC casts
Oliguria
Hypertension
