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Flashcards in Week 3: acute kidney injury Deck (14):

Define Acute Kidney Injury (AKI)

-syndrome characterized by rapid deterioration of renal function tha treads to accumulation of nitrogenous wastes in the body (azotemia).
-plasma Cr and BUN used as surrogate markers of azotemia
-bilateral process
-may or may not be associated with uremic symptoms
-may or may not be associated with drop in urine output


what is the criteria for diagnosing acute kidney injury?

One of the following occurring within 48 hrs (based on 2 creatinine elevations within 48 hrs)
1. absolute increase in serum Cr concentration of greater than 0.3 mg/dL from baseline
2. relative increase in serum Cr concentration of greater than 50%
3. urine output < 0.5mL/kg/hr for more than 6 hours


How is acute kidney injury staged?

I. increase of Cr 1.5 x baseline, or > 0.3 mg/dL
II: increased Cr 2x baseline
III: increase Cr 3x baseline or >4 mg/dl or on dialysis
There's also urine output criteria


What are circumstances that Cr is elevated but GRF is normal?

1. medications that block tubular secretion of cr
2. substances that interfere with Cr assay
-1st gen cephalosporins
-ketotic states by acetoacetate


What are circumstances that Bun is elevated without changes in GFR?

-GI bleeding (endogenous protein load)
-high protein diet (protein metabolized to urea)
-catabolic steroids such as glucocorticoids (results in increase protein catabolism)


What are manifestations of AKI?

Main: azotemia- increase in BUN and creatinine
-metabolic acidosis -problem with ammoniagenesis
-volume overload


Distinguish between AKI and chronic kidney disease.

-chronic: kidney damage> 3 mos.
-hx: duration of symptoms of pruritus, nausea, loss of appetite, etc, usually means chronic
-renal size: small in CKD, except in DM, amyloid, polycystic kidney disease, and HIV nephropathy
-CDK: hyperparathyroidism, bone disease, anemia, half and half nails


What are causes of pre-renal AKI?

syndrome of renal hypo perfusion
1. intravascular volume depletion
-diarrhea, vomiting, diuretics, hemorrhage, dehydration
2. Decrease effective intravascular volume
-Heart failure, cirrhosis, sepsis
3. renal hypoperfusion
-renovascular disease, NSAIDS, ACEI, hepatorenal syndrome


Clinical presentation of pre renal AKI.

-orthostatic symptoms
-volume loss
-intraoperative hypotension
-heart failure
-liver disease
-hypotension, orthostatic changes in bp, tachycardia, dry mucous membranes, poor skin turgor, flat neck veins
-signs of CHF or liver disease: edema, JVD, acites


laboratory findings in pre-renal AKI

1. BUN: Cr ratio> 20:1
-due to depleted intravascular volume and response. BUN is first thing that goes up because kidney reabsorbs urea.
2. Urine indices
-oliguria: 1.020, Uosm>500mmol/L
-high renal sodium avidity: Una<20 mmol/L, Fractional excretion of Na is less than 1%
-inactive urine sediment


What are causes of post-renal AKI?

1. upper tract obstruction(ureteric)
-Intrinsic: kidney stone, transitional cell CA
-Extrinsic: Retroperitoneal adenopathy, abdominal aortic aneurysm
2. lower tract obstruction (bladder neck)
-prostate CA
-urethral stricture
-neurogenic bladder


Clinical presentation of post-renal AKI

-flank pain, hematuria, pelvic malignancy
-symptoms of bladder outlet obstruction: nocturne, urinary frequency, urgency, decrease urinary stream, incomplete voiding
-PE: distended bladder, enlarged prostate, abdominal/pelvic mass


What are intra-renal causes of AKI?

1. vascular: atheroemboli, malignant HTN, HUS-TTP
2. glomerular: glomerulonephritis
3. tubular: acute tubular injury
4. interstitial: acute interstitial nephritis


Distinguish between pre-renal AKI from ATN

-bland, hyaline casts
-BUN:Cr ratio >20:1
-improvement in renal function to volume challenge
-muddy brown or granular casts
BUN to Cr 10:1
-may or may not be oliguric
-no improvement in renal fxn to volume challenge
-Uosm about 300