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Flashcards in Acute Kidney Injury Deck (31)
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1

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

2

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

3

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

4

Symptoms of uremia

  • nausea, vomiting
  • abdominal pain, diarrhea
  • weakness, fatigue

5

Azotemia definition

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

6

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

7

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

8

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 

9

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  

10

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

11

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)

12

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/Pcr ratio < 10)
  • FENa > 2% 
  • renal ultrasound shows hydronephrosis = expasion of the collecting system
  • catheter test = bladder catheter following void ==> volume is "post-void residual"

13

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)

14

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 

15

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

16

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

17

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)

18

Hx/PE: evidence of postrenal AKI

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

19

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

20

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

21

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

22

Urinalysis pattern: prerenal azotemia

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

23

Urinalysis pattern: glomerulonephritis

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

24

Urinalysis pattern: AIN

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

25

Urinalysis findings: vascular disease

Variable tonicity, ± hematuria

26

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). 

27

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).

28

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

29

Biochemical differences: Prerenal vs. ATN

Test

Prerenal

ATN

Urine Na

< 20

> 20

Ucr/Pcr

> 20

< 10

Uosm

increased

isosmotic

FENa

< 1

> 2

30

Complications of AKI

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