Acute Kidney Injury
Last Modified: 2016-03-08
Definition of Acute Kidney Injury (AKI)
Abrupt loss of kidney function
Retention or urea and other waste products
Dysregulation of extracellular volume and electrolytes
Lab values used in monitoring of kidney function
Urine Electrolytes (FENA, etc)
Discuss the FENa
Tells us if the body is holding onto water
Low = dehydration
Diuretics, specifically loops, throw off our ability to interpret FENa
What are limitations of the Cockcroft-Gault method of estimating CrCl
Developed in healthy male patients
Not as accurate in patients with decreased renal function
Not accurate in patients with changing SCr
What is the Cockcroft-Gault Equation
CrCl = [(140-age)*IBW]/(72*SCr)
0.85 factor is female
Do we use Adjusted BW if >120%IBW for CG?
No, we are wanting lean body mass.
However, you do use Actual BW if <IBW
When is MDRD a better indicator of renal function than CG?
Patients with decreased GFR
Understimates GFR if >60ml/min
Do not use MDRD for dosing
In which of the following would CrCl likely be underestimated?
· Body Builder
Body builders will have more muscle, so they will have a high Scr, wo we will have an underestimated CrCl
What is RIFLE, in respect to AKI?
Assessment of different degrees of injury
What are imputs into determination of the RIFLE stage?
What are the main differences between RIFLE and AKIN
AKIN in 3 stages
AKIN does not use GFR decrease
AKIN only accounts for changes within 48 hours
A change in SCr affects CrCl more at (low/high) GFR
High GFR (low SCr)
Remember that CrCl is inversely proportional to SCr
What is the effect (MOA) of prostaglandins on renal perfusion?
Vasodilation of the AFFERENT arteriole
Lets in more blood flow to the glomerulus
What is the effect (MOA) of NSAIDS on renal perfusion?
Blocking the production of prostaglandins
Blocking the vasodilation of the AFFERENT arteriole
Reducing the blood flow to the glomerulus
What is the effect (MOA) of Angiotensin II on renal perfusion?
Vasoconstriction of the EFFERENT arteriole
Increase glomerular gradient pressure (increased UOP)
What effect would an ACE-I, ARB, or direct Renin Inhibitor have on renal profusion?
Blocking the production of Angiotensin II
Blocking the Vasoconstriction of the EFFERENT arteriole
Decrease glomerular gradient pressure (decreased UOP)
Lab Values for Pre-Renal AKI
BUN/SCr > 20:1
OsmUrine >500 Osm
Urine Casts: Hyaline casts or none
Physical Exam finding for Pre-Renal AKI
Dehydration (Poor skin turgor, Dry mucus membranes)
Tx of Pre-Renal AKI
DC NSAIDS/ACE-I/ARB (switch)
Hold BP medication
Monitoring for patients with Pre-Renal AKI
Electrolytes [K (biggest concern), Na, Ca, Mg]
Types of Intrinsic AKI
Acute Tubular Necrosis (ATN) either ischemic or nephrotoxic
Acute Interstitial nephritis (AIN)
Lab Values associated with Intrinsic AKI
Osmurine <350 (low)
Muddy brown casts (microscopic)
Non-modifiable Risk factors for CIN
Older age (.75)
Pre-existing Renal failure (GFR <60)
Modifiable Risk Factors for CIN
Volume/Type of Contrast
Low Serum Albumin
ACE-I (hold 5 t1/2 before if possible)
NSAID (hold 5 t1/2 before if possible)
DC metformin (to prevent lactic acidosis, 48h before/after)
DC other nephrotoxic medications if possible
Choice of contrast dye
Volume load (NaHCO3 or NS, day before/day after)
Consider NAC (≥2 Risk Factors, battle oxidative stress)
S/Sx and Labs for AIN
Fever, rash, arthralgia
Management of AIN
DC offending agent (list as allergy!!!)
Supportive Care (may need TEMPORARY dialysis)
PO Steroids if no change after DC offending agent
S/Sx and Labs for Glomerulonephritis (GN)
RBC casts in urine
Acute GN Tx
ACE-I, ARB, or nondihydropyridine CCB
Low protein diet (Short Term)
ACE-I and/or ARB (caution – avoid pre-renal)
Lab Values for Post-Renal AKI
Distended Bladder or enlarged prostate
Tx for Post-Renal AKI
DC contributory medications
Indications for Acute Dialysis
E: Electrolyte Disturbance
U: Uremic (high BUN)
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