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CVPR: Renal > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Acute kidney injury (AKI) definition

A
  • rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine (Pcr), urea, etc.
  • AKI ==> reduced clearance of nitrogenous waste ==> azotemia
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2
Q

Types of AKI

A
  • 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
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3
Q

Uremia definition

A
  • constellation of signs/symptoms of multiorgan dysfunction ==>
  • caused by retention of uremic toxins + lack of renal hormones due to acute or chronic kidney injury
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4
Q

Symptoms of uremia

A
  • nausea, vomiting
  • abdominal pain, diarrhea
  • weakness, fatigue
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5
Q

Azotemia definition

A
  • Buildup of nitrogenous wastes in the blood
  • Blood Urea Nitrogen (BUN) + serum creatinine are increased
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6
Q

Oliguria + Anuria definition

A
  • Oliguria = urine volume <400 ml/24 hours in normal sized adult
  • Anuria = urine volume <50 ml/24 hours in normal sized adult
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7
Q

General algorithm for AKI classification

A
  • Pre-renal causes vs. (<= most common)
  • Renal causes vs.
    • vascular disorders
    • glomerulonephritis
    • interstitial nephritis
    • tubular necrosis: ischemia vs. toxins vs. pigments
  • Post-renal causes
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8
Q

Prerenal azotemia characteristics

A
  • 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
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9
Q

Signs of prerenal azotemia

A
  • 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
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10
Q

Postrenal Azotemia characteristics

A
  • 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
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11
Q

Causes of postrenal azotemia

A
  • 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)
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12
Q

Signs of postrenal azotemia

A
  • 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”
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13
Q

Intrinsic renal disease characteristics

A
  • 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)
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14
Q

Intrinsic renal diseases causing AKI

A
  • 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
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15
Q

Mechanism of decreased GFR in ATN

A
  • 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
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16
Q

Hx/PE: evidence of prerenal AKI

A
  • intravascular volume depletion:
    • decrease in weight
    • flat neck veins
    • postural changes in BP/pulse
  • signs of hypervolemia:
    • edema, pulmonary rales, S3 gallop
17
Q

Hx/PE: evidence of ATN/renal disease

A
  • 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)
18
Q

Hx/PE: evidence of postrenal AKI

A
  • evidence of urinary obstruction ==> anuria, intermittent anuria, swings in urine flow rate
  • dysuria, hematuria
19
Q

Urinalysis/sediment examination characteristics

A
  • 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
20
Q

Rhabdomyolysis definition/characteristics

A
  • muscle necrosis + release of intracellular muscle constituents (w/myoglobin)
  • common cause of AKI, especially in trauma patients
  • urine: heme w/out RBCs
21
Q

Possible microscopic findings on urinalysis

A
  • 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
22
Q

Urinalysis pattern: prerenal azotemia

A

Relatively high specific gravity, no heme pigment, normal sediment (i.e. any casts are waxy or finely granular).

23
Q

Urinalysis pattern: glomerulonephritis

A

Variable tonicity, + heme pigment, sediment exam reveals RBC and RBC casts.

24
Q

Urinalysis pattern: AIN

A

Isotonic urine, +/- heme pigment, white blood cell casts, eosinophils (with allergic interstitial nephritis)

25
Q

Urinalysis findings: vascular disease

A

Variable tonicity, ± hematuria

26
Q

Urinalysis findings: ATN

A

Typically isotonic, variable heme pigment (+ if from hemolysis or rhabdomyolysis). Sediment exam **will show pigmented coarsely granular casts and renal tubular epithelial cells (RTEs). **

27
Q

Urinalysis findings: Obstruction

A

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).

28
Q

UA patterns of SG, blood (dip), protein (dip), microscopic in various disease

A
29
Q

Biochemical differences: Prerenal vs. ATN

A

Test

Prerenal

ATN

Urine Na

< 20

> 20

Ucr/Pcr

> 20

< 10

Uosm

increased

isosmotic

FENa

< 1

> 2

30
Q

Complications of AKI

A
  • volume overload (pulmonary edema)
  • electrolyte abnormalities (hyperkalemia, acidosis)
  • ==> uremia
  • mortality is very high
    • infections
    • GI bleeding
31
Q

Therapy of AKI

A
  • 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)

CVPR: Renal (25 decks)

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