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Acute Kidney Injury Flashcards

1
Q

acute kidney injury (AKI) - overview

A

*comprised of a wide spectrum of clinical syndromes characterized by an abrupt decrease in GFR
*resulting in the accumulation of nitrogenous waste products, including urea and creatinine, as well as other uremic middle molecules and inflammatory components
*decline in urine output can be variable
*no precise correlation exists between changes in sCr levels & GFR

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2
Q

relationship of GFR to steady-state serum creatinine & BUN

A

*elevation in serum creatinine is apparent only when GFR falls to about 70 mL/min

*early renal disease: slight elevations in sCr → substantial decline in GFR
*late renal disease: large elevations in sCR → small declines in GFR

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3
Q

most used indicators of renal function

A

*BUN and creatinine
*insensitive and late markers of renal dysfunction
*can also be affected by other confounding factors:
-elevated BUN: GI bleeding, steroids, etc
-elevated sCr: trimethoprim, rhabdomyolysis, etc

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4
Q

other conditions/medications that may increase serum creatinine

A

*rhabdomyolysis
*cimetidine
*trimethoprim
*probenacid

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5
Q

other conditions/medications that may increase BUN

A

*GI bleeding
*catabolic states
*high protein diet
*amino acid infusion/TPN
*tetracycline
*steroids

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6
Q

acute kidney injury (AKI) - definitions

A

*an acute or sustained increase in sCr by 0.5 (if baseline Cr < 2.5) OR an increase in sCr by 20% (if baseline Cr > 2.5)

*an abrupt (within 48 hrs) reduction of kidney function defined by an absolute increase sCr > 0.3 OR other

*RIFLE/AKIN criteria primarily used in research arena

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7
Q

RIFLE criteria for AKI

A
  1. renal risk
  2. renal injury
  3. renal failure
  4. renal LOSS
  5. ESRD (end-stage renal disease)
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8
Q

diagnostic approach to AKI

A
  1. review old records (establish a baseline Cr, previous urinalysis/imaging; plot Cr/urine output trend)
  2. thorough HPI & physical
  3. examination of URINALYSIS and urine studies
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9
Q

pre-renal acute kidney injury - defined

A

*clinical syndrome characterized by:
1. reduced renal perfusion
2. preserved renal parenchyma function
3. kidneys respond appropriately to reduced perfusion → Na+ and H2O retention, concentrated urine, LOW urine Na+

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10
Q

pre-renal AKI - pathophysiological mechanisms

A

*true intravascular hypovolemia
*decreased effective circulatory volume
*intrarenal vasoconstriction
*renal artery disease

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11
Q

autoregulation of GFR: what happens when there is decreased renal perfusion?

A

*2 mechanisms by which the kidney is able to adapt in order to maintain normal GFR, despite decreased renal perfusion:

  1. decreased renal perfusion → release of NO and prostaglandins → VASODILATION of AFFERENT arteriole → increased renal blood flow → increased Pgc to maintain GFR
  2. decreased renal perfusion → release of Ang II → VASOCONSTRICTION of EFFERENT arteriole → maintained GFR
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12
Q

effect of NSAIDs on autoregulation of GFR

A

*NSAIDs block prostaglandins → not able to vasodilate afferent arteriole → inability to increase renal blood flow to maintain GFR → DECREASE IN GFR

note - this is in patients with decreased renal perfusions on NSAIDs

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13
Q

effects of ACEi/ARBs on autoregulation of GFR

A

*ACEi/ARBs → inhibit the effect of Ang II on the efferent arteriole → inability to vasoconstrict the efferent arteriole → DECREASE IN GFR

note - this is in patients with decreased renal perfusions on ACEi or ARB

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14
Q

causes of pre-renal AKI: true volume depletion

A

*renal: diuretic use, diabetes insipidus, osmotic diuresis
*extra-renal: diarrhea, vomiting, pancreatitis, GI bleeding, surgery/trauma, blood loss, burns, third spacing, surgical drains

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15
Q

causes of pre-renal AKI: low effective circulation

A

*CHF
*cirrhosis
*shock/sepsis

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16
Q

causes of pre-renal AKI: intrarenal vasoconstriction

A

*hypercalcemia
*contrast dye
*cyclosporine
*tacrolimus

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17
Q

causes of pre-renal AKI: pharmacological

A

*NSAIDs
*ACEi / ARBs

recall:
1. NSAIDs block prostaglands, preventing vasodilation of the afferent arteriole; effectively, constrict the afferent arteriole → decreased GFR
2. ACEi/ARBs block angiotensin II’s effects, preventing vasoconstriction of efferent arteriole; effectively, dilate the efferent arteriole → decreased GFR

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18
Q

causes of pre-renal AKI: renal artery disease

A

*renal artery stenosis → decreased renal perfusion → decreased GFR

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19
Q

pre-renal AKI due to true volume depletion - clinical presentation

A

*history: extracellular fluid loss from skin, GI or renal source
-inquire about recent infections, fever, diarrhea, diuretic use, decreased hydration, orthostatic lightheadedness, thirst
*PE: signs of hypovolemia such as:
-orthostatic hypotension
-tachycardia
-dry mucous membranes
-decreased skin turgor
-no axillary moisture
-oliguria or concentrated urine

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20
Q

pre-renal AKI due to low effective circulation - clinical presentation

A

*history: heart failure, low cardiac output, cirrhosis
-inquire about SOB, PND, orthopnea, change in weight, edema
*PE: edema, third heart sound (S3 or S4), JVD, pulmonary crackles/effusion

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21
Q

pre-renal AKI diagnosis: serum chemistry findings

A

*elevated BUN and Cr
*BUN/Cr ratio > 20:1 (low urinary flow allows for increased urea absorption)
*monitor for complications of AKI (hyperkalemia, acidosis)

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22
Q

pre-renal AKI diagnosis: urinalysis

A

*normal/bland sediment (little to no protein, no blood, no WBCs, no other cellular elements)

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23
Q

pre-renal AKI diagnosis: fractional excretion of sodium (FEna)

A

*amount of filtered sodium that is actually excreted
*expected to be VERY LOW: FEna < 1%
*note - not helpful if pt is on a diuretic (use FEurea; should be < 35%)

recall: FEna = (Una x Pcr) / (Ucr x Pna) x 100

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24
Q

pre-renal AKI diagnosis: urine studies

A

*urine sodium: LOW (<20) due to increased proximal reabsorption of Na in response to hypovolemia

*urine Osm: HIGH (>500) due to increased concentration (reabsorption of water in effort to volume expand)

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25
pre-renal AKI - treatment
*key = **normalize the effective renal blood flow** *expedient treatment will help minimize the risk of progression of intrinsic renal failure *if true volume depletion, give fluids *if CHF, diurese
26
intrinsic (renal) AKI - defined
*primary lesion is **in the kidney** *renal parenchyma is NOT intact; can be: -vascular/microvascular -glomerular -interstitial -tubular *unlike pre-renal and post-renal causes, recovery is not expected to be as dramatic with removal of the culprit
27
acute tubular necrosis (ATN) - overview
*most common cause of **intrinsic acute kidney injury** in hospitalized patients *a form of AKI described as **acute damage to the renal tubules,** usually due to ischemia associated with shock, IV contrast, or excess myoglobin
28
acute tubular necrosis (ATN) - clinical presentation
*nonspecific signs and symptoms of renal failure *similar to prerenal symptoms (true volume depletion or low effective circulation) *also look at: -episodes of hypertension and recent surgeries -recent contrast administration -review meds for nephrotoxins
29
pre-renal AKI and ATN spectrum
*pre-renal AKI and ATN are two extremes of the same clinical spectrum *3 causes that can lead to **progression from pre-renal AKI to ATN**: 1. **ischemia**: prolonged hypoperfusion, crush injury & trauma, septic shock, pancreatitis 2. **endotoxins**: uric acid, hemoglobin & myoglobin, immunoglobulin light chains 3. **exotoxins**: heavy metals (lead), ethylene glycol, contrast dye, antibiotics (ex. ampho)
30
pathophysiology of ischemic acute tubular necrosis (ATN)
*ischemic ATN is a progression of the prerenal state to a point at which **compensatory mechanisms decompensate** 1. overwhelming levels of AngII and endothelin-1 causes intense vasoconstriction → further reduction of perfusion 2. increase in inflammatory cytokines potentiates endothelial injury 3. congestion & obstruction of capillaries 4. disruption of actin cytoskeleton → loss of brush border 5. loss of polarity of epithelial cells → failure of tight junctions → backleak of tubular fluid, detached BM 6. **apoptosis and necrosis of tubular epithelium**
31
acute tubular necrosis (ATN) - phases
1. initiation (OLIGURIC phase): -inciting event damages tubular epithelial necrosis → blockage of tubular lumen by necrotic debris → reduction in GFR, vasoconstriction, resulting in prolonged ischemia 2. maintenance: -ongoing renal failure -creatinine usually increases slightly per day *conversion from oliguria → nonoliguria does not improve mortality 3. recovery (POLYURIC PHASE): -regeneration of tubular epithelium, but unable to reabsorb H2O and electrolytes -gradual return of BUN/Cr to baseline or near-normal levels
32
ATN diagnosis: serum chemistries
*elevated BUN and creatinine ***BUN/Cr ratio < 20:1** (contrast to pre-renal, where ratio is greater than 20)
33
ATN diagnosis: urine studies
***FEna > 2%** ***urine sodium > 40** ***urine osmolarity < 350**
34
ATN diagnosis: urine sediment
*classic "muddy brown cast" (GRANULAR CASTS)
35
ATN diagnosis: renal biopsy
*tubular injury *flattened tubular epithelium *sloughed cells note - we typically do NOT biopsy these patients
36
acute tubular necrosis (ATN) - treatment
*largely supportive: -attempt to improve renal perfusion, maintain SBP > 100, avoid nephrotoxic agents, remember to adjust doses of meds for Cr clearance < 10-15 *medical therapy: -correct volume status, treat electrolyte disturbances, treat acidosis, consider dialysis
37
contrast urine and serum studies in pre-renal AKI vs. acute tubular necrosis (ATN)
*urine osmolarity (mOsm/kg) **-prerenal AKI: > 500 -ATN: < 350** *urine Na+ (mEq/L): **-prerenal AKI: < 20 -ATN: > 40** *FENa: **-prerenal AKI: < 1% -ATN: > 2%** *serum BUN/Cr ratio: **-prerenal AKI: > 20:1 -ATN: < 20:1**
38
contrast-induced nephropathy - overview
***subset of ATN injury** frequently seen in hospital settings *pathogenesis: **IV contrast → vasoconstriction of renal arteries & direct tubular injury** *risk factors: -underlying renal insufficiency -diabetic nephropathy with renal insufficiency -advanced heart failure -states of hypoperfusion -percutaneous coronary interventrions -high total dose of contrast agent
39
contrast-induced nephropathy - clinical presentation
*AKI apparent **within the first 24-48 hours after contrast study** *non-oliguric with mild decline in renal function *patients occasionally require dialysis
40
differentiating contrast-induced nephropathy from atheroembolic disease
ATHEROEMBOLIC DISEASE has the following: *presence of other **embolic lesions (as on the toes) or livedo reticularis** *transient eosinophilia and hypocomplementemia *onset of renal failure that may be **delayed for days to weeks after the procedure** *protracted course with frequently little or no recovery of renal function
41
contrast-induced nephropathy - diagnosis
*similar to ATN (FENa > 2%, urine Osm < 350, urine Na+ > 40, serum BUN/Cr ratio < 20:1) *history of **recent contrast administration and characteristic rise in creatinine 24-48 hrs later**
42
contrast-induced nephropathy - prevention
*avoid contrast, if possible, in high-risk individuals *use of nonionic, low osmolal agents *use lower doses of contrast *avoid repetitive, closely spaced studies *avoid volume depletion and NSAIDs
43
contrast-induced nephropathy - treatment
*VOLUME EXPAND: -fluids prior to/during/after contrast administration -ANY type of fluid suffices (saline) -if volume expansion contraindicated (i.e. CHF), just hold diuretic
44
atheroembolic disease - overview
*cholesterol crystal embolization occurs when **portions of an atherosclerotic plaque break off and embolize distally** *resulting in partial or total occlusion of multiple small arteries (or glomerular arterioles) *leading to tissue or organ ischemia *seen **after manipulation of the aorta or other large arteries**
45
atheroembolic disease - clinical presentation
***blue toe syndrome *livedo reticularis** *GI manifestations *renal failure *CVA
46
atheroembolic disease - renal manifestations
*occurs primarily in older patients *marked AKI with an **acute onset, seen within 1-2 weeks of event** *sub-acute presentation: renal dysfunction occurs in **staggered steps** separated by periods of stable kidney function
47
atheroembolic disease - diagnosis
*urine: bland urine sediment -eosinophiluria during active phase -proteinuria is usually not a prominent feature *eosinophilia & hypocomplementemia *definitive dx: biopsy -skin lesion (if present) -kidney
48
pigment-induced ATN - overview
*subset of ATN injury *seen with rhabdomyolysis: -associated with marked elevations in CPK -seen with trauma or statin therapy
49
pigment-induced ATN - clinical findings
*rapid rise in creatinine, often > 2 mg/L/day *hyperkalemia *hyperphosphatemia *hyperuricemia ***urine dipstick positive for blood BUT NO RBC on urinalysis (picks up myoglobin)**
50
causes of nephrotoxin drug-induced ATN
1. aminoglycosides (gentamicin, tobramycin, amikacin) 2. amphotericin B 3. vancomycin
51
nephrotoxin drug-induced ATN due to aminoglycosides
*NON-OLIGURIC AKI [5-10 days post-exposure to drug] *hypomagnesemia *mechanism of injury: non-protein bound drug filters into glomerulus & cationic properties allow it to be taken into PT → **accumulate in lysosomes and interfere with normal cells functions → cell death** *risk factors: high peak serum levels, cumulative dose
52
nephrotoxin drug-induced ATN due to amphotericin B
*mechanism of injury: -direct binding to tubular epithelial cells creates PORES → Na+, K+, Mag wasting (directly) -indirect mech: afferent arteriolar vasoconstriction
53
nephrotoxin drug-induced ATN due to vancomycin
*synergistic nephrotoxicity (worse when in conjunction with other nephrotoxic meds) *independent risk factors for nephrotoxicity: -use of concomitant nephrotoxic agents, age, duration of therapy, etc
54
acute interstitial nephritis (AIN) - overview
*defines a pattern of renal injury characterized histopathologically by **inflammation and edema of the renal interstitium** *a type of **intrinsic (renal) AKI** *most commonly caused by: -drugs (antibiotics, NSAIDs, etc) -infections (bacterial & viral) -autoimmune disorders (sarcoid, TINU syndrome) -idiopathic
55
acute interstitial nephritis (AIN) - clinical presentations
*nonspecific symptoms (except for drug-induced): -malaise, anorexia, N/V -acute or subacute onset -s/s of AKI *drug-induced AKI: -onset within 3 weeks of first exposure or 3-5 days after second exposure -**classic symptoms: RASH, FEVER, EOSINOPHILIA**
56
acute interstitial nephritis (AIN) - diagnosis
*clinical symptoms *AKI improves with removal of offending agent *peripheral eosinophilia *urine is VARIABLE: -**white cells, white cells casts** -urine eosinophils -sterile pyuria *definitive = biopsy
57
acute interstitial nephritis (AIN) - treatment
1. drug-induced: *discontinue offending agent (expect improvement in 3-7 days) *trial of corticosteroids 2. non-drug induced: -treat underlying disease
58
acute glomerulonephritis & vasculitis - overview
*another cause of intrinsic AKI (rare) *look at URINE: -active sediment? RBC casts? proteinuria, hematuria? -nephrotic vs. nephritic
59
3 causes of intrinsic (renal) AKI
1. acute tubular necrosis (ATN) 2. acute interstitial nephritis (AIN) 3. acute glomerulonephritis & vasculitis
60
post-renal AKI - overview
*an **impediment of urine flow due to structural or functional obstruction** *resulting in an increase in pressure proximal to obstruction *obstruction can occur anywhere from the renal pelvis to the tip of the urethra
61
post-renal AKI - obstructive nephropathy
*when the kidney parenchyma itself if damaged *functional or pathological changes in the kidney that results from urinary tract obstruction *obstruction classified based on: -duration (acute vs. chronic) -level of obstruction (upper vs. lower tract) -degree of obstruction (complete vs. partial) -unilateral vs. bilateral
62
ureteral causes of post-renal AKI
*intrinsic: crystals, light chain casts, stones, blood clots, papillary necrosis, fungus balls, edema *extrinsic: gravida uterus, uterine prolapse, uterine tumors, RP fibrosis, RP tumor, radiation therapy
63
bladder causes of post-renal AKI
*diabetes mellitus *multiple sclerosis *spinal cord injury *anticholinergic agents
64
urethral causes of post-renal AKI
*posterior urethral valves *BPH *diverticula *strictures *tumors ***obstructed foley catheters**
65
post-renal AKI - clinical presentation
*VARIABLE, depending on site, duration, and severity *common symptoms: -pain -change in urine output -palpable mass -bladder symptoms
66
diagnosis of post-renal AKI - serum chemistries
*elevated BUN/Cr > 15:1 *FEna > 2-4% *hyponatremia *hyperkalemia note - VARIABLE!!
67
diagnosis of post-renal AKI - urine studies
*bland sediment *hematuria (stones, tumors) *crystals
68
post-renal AKI - treatment
*relieve obstruction *depends on level of obstruction & cause
69
post obstructive diuresis
*commonly seen after **relief of severe bilateral obstruction** *polyuria: -osmotic diuresis caused by retained urea -volume overload -tubular concentration defect
70
compare serum chemistries of pre-renal, intrinsic, and post-renal AKI
*BUN/Cr > 20:1 = prerenal *BUN/Cr < 20:1 = intrinsic *BUN/Cr > 25:1 and variable in post-renal
71
compare urinalysis of pre-renal, intrinsic, and post-renal AKI
*bland sediment: prerenal or post-renal *epithelial cells & muddy brown casts: ATN *RBC casts: glomerulonephritis *WBCs, WBC casts, sterile pyuria: AIN

Renal Exam (44 decks)

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