Acute Kidney Injury Flashcards
Acute kidney injury (AKI) definition
- rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine (Pcr), urea, etc.
- AKI ==> reduced clearance of nitrogenous waste ==> azotemia
Types of AKI
- pre-renal azotemia: decrease in GFR due to decreases in renal plasma flow and/or renal perfusion pressure
- intrinsic renal disease: decrease in GFR due to direct injury to the kidneys
- post-renal azotemia/obstructive nephropathy: decrease in GFR due to obstruction of urine flow
Uremia definition
- constellation of signs/symptoms of multiorgan dysfunction ==>
- caused by retention of uremic toxins + lack of renal hormones due to acute or chronic kidney injury
Symptoms of uremia
- nausea, vomiting
- abdominal pain, diarrhea
- weakness, fatigue
Azotemia definition
- Buildup of nitrogenous wastes in the blood
- Blood Urea Nitrogen (BUN) + serum creatinine are increased
Oliguria + Anuria definition
- Oliguria = urine volume <400 ml/24 hours in normal sized adult
- Anuria = urine volume <50 ml/24 hours in normal sized adult
General algorithm for AKI classification
- Pre-renal causes vs. (<= most common)
- Renal causes vs.
- vascular disorders
- glomerulonephritis
- interstitial nephritis
- tubular necrosis: ischemia vs. toxins vs. pigments
- Post-renal causes
Prerenal azotemia characteristics
- decrease in RBF ==> lower GFR
- most common cause of an abrupt fall in GFR in a hospitalized patient
- causes: hypovolemia + certain hypervolemic states ==> CHF or cirrhosis
- CHF/cirrhosis ==> low effective arterial blood volume (EABV) + reduced renal perfusion
- renal tubules fxn normally
Signs of prerenal azotemia
- urine sodium concentration = low = < 20 mEq/L
- urine creatinine concentration = high = Ucr/Pcr > 20
- fractional exrection of sodium
- FENa = (UNa/PNa) / (Ucr/Pcr) x 100
- FENa < 1% in prerenal
Postrenal Azotemia characteristics
- obstruction to urine flow ==> increase in intratubular pressure ==> low GFR
- prolonged obstruction ==> renal vasoconstriction
- usually bilateral ==> significant injury
- ==> anuria or intermittent urine flow
- ==> derangement of tubular fxn
Causes of postrenal azotemia
- obstruction of ureters
- extrauretal (e.g. carcinoma of the cervix, retroperitoneal fibrosis)
- intraureteral (e.g. stones, clots, etc)
- bladder outlet obstruction (e.g. bladder carcinoma, urinary infection)
- urethral obstruction (e.g. posterior urethral valves, prostatic hypertrophy)
Signs of postrenal azotemia
- impairment of tubular sodium reabsorption ==> high urinary sodium concentrations = >40 mEq/L
- impairment of water reabsorption ==> low urine creatinine concentrations (Ucr/Pcrratio < 10)
- FENa > 2%
- renal ultrasound shows hydronephrosis = expasion of the collecting system
- catheter test = bladder catheter following void ==> volume is “post-void residual”
Intrinsic renal disease characteristics
- 4 types: vessels, gleruli, interstitium, tubules
- most common = acute tubular necrosis (ATN) <== ischemia or nephrotoxin
- oliguric or nonoliguric
- complications: infections (<== decreased leukocyte fxn) and gastrointestinal tract hemorrhage (<== increased acid secretion)
Intrinsic renal diseases causing AKI
- vascular diseases: cholesterol emboli, renal vein thrombosis
- glomerular diseases: acute glomerulonephritis, hemolytic uremic syndrome
- interstitial diseases: acute interstitial nephritis, infection, myeloma kidney
- tubular diseases: ischemic or nephrotoxic acute tubular necrosis
Mechanism of decreased GFR in ATN
- vascular factors = decreases in renal blood flow + decreases in glomerular permeability (Kf)
- may produce failure of autoregulation of RBF
- tubular factors = tubular obstruction + backleak of glomerular filtrate
Hx/PE: evidence of prerenal AKI
- intravascular volume depletion:
- decrease in weight
- flat neck veins
- postural changes in BP/pulse
- signs of hypervolemia:
- edema, pulmonary rales, S3 gallop
Hx/PE: evidence of ATN/renal disease
- hx of exposure to renal insults:
- hypotension
- surgery w/large blood loss
- transfusion rxns
- exposure to radiocontrast dye
- cardiac cath
- evidence of rash and fever after exposure to ampicillin = allergic interstial nephritis (AIN)
Hx/PE: evidence of postrenal AKI
- evidence of urinary obstruction ==> anuria, intermittent anuria, swings in urine flow rate
- dysuria, hematuria
Urinalysis/sediment examination characteristics
- info on tonicity + levels of heme
- main components:
- macroscopic/gross exam = direct, visual observation
- dipstick chemical analysis = plastic strips w/rxn pads to biochem rxns
- microscopic exam = identifying formed elements
Rhabdomyolysis definition/characteristics
- muscle necrosis + release of intracellular muscle constituents (w/myoglobin)
- common cause of AKI, especially in trauma patients
- urine: heme w/out RBCs
Possible microscopic findings on urinalysis
- cells, casts, crystals
- cells = WBCs, RBCs, bacterial and epithelial cells
- casts = secreted mucoproteins “gel” w/in tubule
- hyaline casts = normal
- RBC/WBC = pathologic
- RBC=glomerulonephritis
- WBC=AIN
Urinalysis pattern: prerenal azotemia
Relatively high specific gravity, no heme pigment, normal sediment (i.e. any casts are waxy or finely granular).
Urinalysis pattern: glomerulonephritis
Variable tonicity, + heme pigment, sediment exam reveals RBC and RBC casts.
Urinalysis pattern: AIN
Isotonic urine, +/- heme pigment, white blood cell casts, eosinophils (with allergic interstitial nephritis)
Urinalysis findings: vascular disease
Variable tonicity, ± hematuria
Urinalysis findings: ATN
Typically isotonic, variable heme pigment (+ if from hemolysis or rhabdomyolysis). Sediment exam **will show pigmented coarsely granular casts and renal tubular epithelial cells (RTEs). **
Urinalysis findings: Obstruction
Tonicity usually isotonic or hypotonic, usually heme is negative unless superimposed infection. Micro may be totally benign or show evidence of superimposed infection (e.g. RBCs & WBCs).
UA patterns of SG, blood (dip), protein (dip), microscopic in various disease
Biochemical differences: Prerenal vs. ATN
Test
Prerenal
ATN
Urine Na
< 20
> 20
Ucr/Pcr
> 20
< 10
Uosm
increased
isosmotic
FENa
< 1
> 2
Complications of AKI
- volume overload (pulmonary edema)
- electrolyte abnormalities (hyperkalemia, acidosis)
- ==> uremia
- mortality is very high
- infections
- GI bleeding
Therapy of AKI
- prerenal: improve renal perfusion
- improve CO w/CHF
- replace intravascular volume w/hypovolemia
- postrenal: releave obstruction
- ATN:
- avoid risk factors e.g. prerenal azotemia or nephrotoxins
- tx fluid overload and electrolute disturbances
- renal replacemet therapy (dialysis)
