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Clin Med III > AKI > Flashcards

AKI Flashcards

1
Q

AKI

A
  • abrupt decline in renal function -> increased BUN and Cr over hours to weeks
  • AKI DOES NOT equal ARF
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2
Q

what is the RIFLE criteria

A
  • assessment of AKI
  • risk
  • injury
  • failure
  • loss of function
  • end stage renal disease (dialysis)
  • based on Cr elevation or decreased urine output
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3
Q

azotemia

A
  • increase in BUN andd Cr without sx
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4
Q

uremia

A
  • increase in BUN and Cr with sx
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5
Q

function of kidneys

A
  • acid base balance
  • water regulation
  • electrolyte balance
  • toxin excretion
  • BP
  • EPO
  • vit D regulation
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6
Q

pts at risk for AKI

A
  • HTN pts
  • CHF- low flow
  • diabetes
  • multiple myeloma
  • chronic infections
  • myeloproliferative disorders
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7
Q

multiple myeloma

A
  • bone marrow cancer
  • produces huge amounts of IgM
  • IgM antibodies clog up tubules
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8
Q

classification of AKI

A
  • pre-renal
  • intrinsic
  • post-renal
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9
Q

pre-renal causes of AKI

A
  • generally low flow states
  • NSAIDs
  • ACEI/ARBs
  • MAP < 80
  • hypovolemia, decreased CO
  • CHF, liver failure
  • sepsis
  • pancreatitis
  • nephrotic syndrome
  • hepatorenal syndrome
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10
Q

renal causes of AKI

A
  • glomerular
  • interstitial- ischemia, sepsis, nephrotoxins
  • vascular
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11
Q

post-renal causes of AKI

A
  • anything blocking urine from exiting
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12
Q

key factors to consider in AKI history taking

A
  • volume depletion
  • cardiac failure
  • radiocontrast exposure- sx usually 2-5 days later
  • rhabdo
  • vasculitis/ proliferative glomerulonephritis
  • hypotension/ shock
  • nephrotoxin exposure or any new meds
  • vascular/ cardiac surgery, anesthesia
  • any hx of liver disease, kidney disease, SLE, AIDs, MM, maligancy
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13
Q

why do NSAIDs cause impaired renal autoregulation

A
  • impair afferent arteriol dilation
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14
Q

why do ACEI/ARBs impair renal autoregulation

A
  • impair efferent arteriole constriction
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15
Q

what is the most common cause of renal failure

A
  • pre-renal
  • due to poor renal perfusion
  • reversed with reperfusion/ glomerular pressure
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16
Q

what does BUN:Cr ratio of 20:1 suggest

A
  • pre-renal injury
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17
Q

what is FeNa

A
  • fractional excretion of Na
  • aka % Na excreted in urine
  • < 1%= pre-renal azotemia
  • > 1%= intrinsic renal failure
  • > 4%= post-renal failure
  • not accurate if pt is on diuretics*
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18
Q

what is an alternative to FeNa

A
  • FeUrea or FeUA
  • not influenced by diuretics
  • FeUrea < 35% or FeUA <9-19% suggests prerenal
  • FeUrea > 50% or FeUA > 10-12% suggests ATN
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19
Q

what labs should you monitor for pre-renal injury

A
  • det volume depletion: H&H, albumin, Ca, Na, BUN, Cr
  • urine output- only half of pts will have oliguria
  • high specific gravity of urine
  • low urine Na < 20 meq/L
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20
Q

pre-renal injury treatment

A
  • fluid resuscitation
  • want to optimize effective circulating volume/ CO
  • diuretics if pt is fluid overloaded
  • nitrates, dobutamine if cardiac issue
  • avoid or dose adjust meds that are renally excreted
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21
Q

acute interstitial nephritis (AIN)

A
  • renal cause of AKI
  • usually allergic rxn
  • most commonly due to abx
  • can be post-infectious or autoimmune
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22
Q

presentation of acute interstitial nephritis

A
  • after recent drug exposure
  • fever, rash
  • peripheral eosinophilia
  • oliguria
  • more commonly found incidentally due to increasing Cr after new med
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23
Q

meds assoc with AIN

A
  • beta lactams*
  • sulfonamides*
  • vanco
  • erythromycin
  • rifampin
  • acyclovir/ valacyclovir
  • NSAIDs
  • anticonvulsants
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24
Q

UA findings for AIN

A
  • pyuria- WBC casts
  • hematuria- less common
  • if see WBC casts must also r/o pyelonephritis
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25
Q

treatment for AIN

A
  • d/c offending agent
  • steroids X 6 weeks
  • damage may be permanent if long duration of drug exposure
26
Q

what is the most common cause of intrinsic renal failure

A
  • acute tubular necrosis
27
Q

acute tubular necrosis (ATN)

A
  • due to ischemia, sepsis, or toxins

- usually reversible

28
Q

exogenous toxins causing ATN

A
  • NSAIDs
  • chemo- esp cisplatin
  • aminoglycosides
  • amphotericin
  • vanco
  • radioconstrast dye
  • poison- ethylene glycol, heavy metals
29
Q

endogenous toxins causing ATN

A
  • rhabdo
  • uric acid
  • multiple myeloma
30
Q

lab findings for ATN

A
  • pigmented or granular casts- muddy brown*
  • Cr and BUN elevated
  • FeNa> 2%
  • serum hyperK
  • serum hyperP
  • serum hyperuricemia
31
Q

treatment for ATN

A
  • aggressive volume replacement
  • if oliguria and extracellular volume normalized consider lasix- very controversial
  • protein restriction
  • d/c offending agent if due to nephrotoxin
  • dialysis- last line
32
Q

acute glomerular diseases

A
  • post-strep glomerulonephritis
  • nephrotic syndrome
  • minimal change disease
  • membranous glomerulonephritis
  • IgA nephropathy
  • henoch-schonlein purpura
33
Q

post-strep glomerulonephritis (PSGN)

A
  • immune complex with strep antigen gets deposited into glomerulus
  • 7-12 d after strep/ impetigo
34
Q

sx of PSGN

A
  • oliguria
  • cola colored urine
  • edema
  • HTN
  • malaise, anorexia, flank pain
35
Q

treatment for PSGN

A
  • abx
  • symptomatic
  • anti- HTN drugs
  • salt restriction
  • diuretics
36
Q

prognosis for PSGN

A
  • kids usually recover with treatment

- can be permanent damage in adults

37
Q

UA findings for PSGN

A
  • proteinuria
  • hematuria
  • pyuria
  • +/- RBC casts
38
Q

diagnosis of PSGN

A
  • clinical manifestations
  • kidney injury- elevated Cr
  • UA findings
  • MUST prove there was recent GABHS infection
  • cultures only pos 25% of time- get ab titers, usually ASO titer
39
Q

IgA nephropathy

A
  • IgA deposition into glomerulus
  • following URI
  • urine red or cola colored 1-2 days after onset
  • more of a chronic illness, most pts don’t recover
  • usu require transplant
40
Q

treatment for IgA nephropathy

A
  • ACEI/ARB
  • steroids
  • renal transplant
41
Q

Henoch schonlein purpura

A
  • small vessel vasculitis PLUS IgA complex deposition

- usually in kids 6 y/o

42
Q

presentation of henoch schonlein purpura

A
  • rash- esp in LE and buttock
  • abd pain/ vomiting- severe
  • arthralgias
  • edema
  • elevated Cr and BUN
  • urine hematuria/ proteinuria
43
Q

treatment for henoch schonlein purpura

A
  • mostly supportive
  • excellent prognosis
  • steroids and/or plasmapheresis for worsening disease
  • skin biopsy can be considered for dx but not usually necessary
44
Q

nephrotic syndrome

A
  • heavy proteinuria 3.5 g/day
  • hypoalbuminemia > 3 g/dL
  • peripheral edema
45
Q

other findings for nephrotic syndrome

A
  • lipiduria- foamy urine
  • minimal hematuria
  • hypercholesterolemia
  • HTN
  • hypercoag states- DVT/PE may be first presentation
  • no cells or casts on UA
46
Q

etiology of nephrotic syndrome

A
  • membranous nephropathy
  • minimal change disease
  • amyloidosis
  • SLE
  • membranoproliferative glomerulonephritis
  • focal segmental glomerulosclerosis
  • IgA nephropathy
47
Q

minimal change disease

A
  • 70-90% of nephrotic syndrome in childhood
  • unknown cause
  • abrupt onset edema and nephrotic syndrome
48
Q

dx of minimal change disease

A
  • normal biopsy
  • urine protein 10 gm/day
  • hypoalbuminemia
  • HTN
49
Q

treatment for minimal change disease

A
  • some may spontaneously recover
  • all kids get treated with steroids
  • prednisone X 8 weeks, may need up to 16 weeks
  • ESRD is rare but may have relapses
50
Q

causes of vascular AKI

A
  • renal artery obstruction- rapid decline in fn
  • renal vein obstruction- more chronic presentation
  • microangiopathy- TTP, HUS, DIC
  • malignant HTN
  • scleroderma renal crisis
  • recent invasive vascular procedure or trauma
51
Q

treatment for vascular AKI

A
  • BP control and manage sx
52
Q

causes of post-renal failure

A
  • bladder outlet obstruction
  • neurogenic bladder
  • pregnancy
  • gyn surgery or abdominopelvic malignancy
53
Q

sx of post-renal failure

A
  • elevated BUN and Cr
  • flank pain
  • hematuria
  • possible renal calculi or papillary necrosis
54
Q

medication induced post-renal failure

A
  • acyclovir
  • mtx
  • triamterene
  • indinavir
  • sulfonamides
  • can cause collecting system/ ureteral obstruction by crystal formations
55
Q

treatment for post-renal failure

A
  • relieve obstruction
  • foley can or suprapubic cath
  • nephrostomy tube
56
Q

polycystic kidney disease

A
  • genetic disorder
  • cyst formation and enlargement of kidneys
  • affects multiple sys: pancreas, liver, spleen
57
Q

prognosis of polycystic kidney disease

A
  • 50% need transplant or dialysis by 60
  • must screen families
  • intracranial aneurysm is 2X more common than general population
58
Q

sx of polycystic kidney disease

A
  • VERY painful- abd/ flank/ back pain
  • hemorrhage into cysts
  • perinephric hematoma
  • infections common- esp pyelonephritis
  • HTN*
  • palpable flank mass
  • nodular hepatomegaly
  • very susceptible to trauma
59
Q

diagnosis of polycystic kidney disease

A
  • classic appearance on US
  • elevated H&H
  • UA shows hematuria, possible microalbuminuria
  • elevated Cr
60
Q

treatment for polycystic kidney disease

A
  • manage BP with ACEI/ARB
  • pain control - very challenging, avoid NSAIDs
  • surgical cyst decompression
  • nephrectomy
  • treat recurrent infections
  • hydrate

Clin Med III (26 decks)

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