Acute kidney injury Flashcards

1
Q

Dx of AKI

A

increase in SCr by >26.5umol/L within 48 h
increase in SCr by 1.5x above baseline in 1 wk
urine volume < 0.5 ml/kg/hr for 6 hours
creatinine also secreted by tubules, slightly overestimates GFR

creatinine major marker for GFR, but slow to respond to AKI

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2
Q

Relationship btw SCr and GFR

A

not linear
high GFR: large changes in GFR only show small change in SCr
low GFR: small changes in GFR will show large changes in SCr

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3
Q

AKI classification

A

Prerenal
intrinsic renal
Postrenal

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4
Q

Prerenal AKI causes

A
response to systemic hypoperfusion
intrarenal v/c
impairment of autoregulation
can lead to renal ischemia
afferent arteriole v/d able to compensate for hypoperfusion up to MAP of 80mmHg
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5
Q

Intrinsic renal AKI causes

A

Large vessel disease
Microvascular, glomerular
Ischemic/nephrotoxic acute tubular necrosis
Tubulointerstitial disease (acute interstitial nephritis, intratubular obstruction)

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6
Q

Postrenal AKI causes

A

calculi

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7
Q

Pathophysiology of acute tubular necrosis

A

Ischemic/toxic damage to tubules –> sloughing of cells
occlusion of tubules with casts
loss of tubular integrity = backleak into interstitium
impaired renal autoregulation
inappropriate stimulation of tubuloglomerular feedback due to increased tubular Cl delivery
macula densa stimulated, afferent arteriole v/c
alterations in other vasoactive agents –> further impairment of renal autoregulation
Inflammation

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8
Q

Incidence of AKI

A

complicates 1-5% hospital admissions, 30% ICU

high morbidity & mortality

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9
Q

Risk factors for AKI

A
Pre-existing renal disease (GFR 75)
Volume depleted
Myeloma (light chain disease)
High osmolar ionic contrast
Nephrotoxin use
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10
Q

Approach to AKI

A

Hx
PE:
- dry - reduced skin turgor, JVP low, postural hypotension (drop in SBP > 20, DBP > 10), shock
- wet - pitting edema, JVP high, hypertension, pulmonary crackles/S3
CV, peripheral vascular, MSK
Urinanalysis - prerenal: hyaline casts
intrinsic renal: pigment, “muddy brown” granular casts (dysmorphic RBCs with glomerulonephritis, RBC, WBC)

Lab: SCr, phos, Ca, electrolytes, CBC-D,
Imaging: CXR, US, CT KUB

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11
Q

Fractional excretion of sodium

A

(Una/Pna) / (Ucr/Pcr)

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12
Q

Tx of AKI

A

prerenal : deal with shock
Intrinsic renal:

Large vessel disease: stenting/angioplasty, thrombolysis/anticoag, immunosuppression
Microvascular: immunosuppression if inflammatory
Glomerular: primary GN: immunosuppression
Ischemic/nephrotoxic ATN: improve perfusion, Drugs, - detox/decontaminate
Tubulointerstitial disease: deal with infection, stop offending agent, give vol, tumor lysis syndrome

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13
Q

Complications of acute renal failure

A
CV
Neurologic
GI
Metabolic - hyperkalemia, acidosis, hypocalcemia, hyperphosphatemia
hematologic
infection
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