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Nephrology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Rapid (< 1 week) reduction in glomerular filtration rate (GFR)

A

Acute kidney injury

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2
Q

the inability of output to match the input (water, sodium, potassium, nitrogen, phosphorus, acid)

A

Failure of balance

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3
Q

increase 1.5-1.9 baseline Cr
Increase in Cr by 0.3 mg/dL in 48h
urine output < 0.5mL/kg/hr for 6 hours

A

AKI stage 1

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4
Q

increase of 2-2.9 baseline cr
urine output: < 0.5ml/kg for 12 hours

A

AKI stage 2

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5
Q

increase 3x baseline Cr
increase in Cr > 4.0mg/dl
intiated on renal replacement therapy
urine output < 0.3mL/Kg for 24 hours
anuric for 12 hours

A

AKI stage 3

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6
Q

accumulation of nitrogenous waste; increased BUN

A

Azotemia

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7
Q

Organ dysfunction caused by retention of uremic toxins
“symptomatic renal failure”

A

uremia

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8
Q

< 500mls in 24 hours

A

oliguria

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9
Q

< 100mls in 24 hours

A

anuria

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10
Q

decreased renal perfusion

A

prerenal

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11
Q

damage to particular parts of the kidney; ATN, AIN, GN

A

intrinsic

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12
Q

urinary obstruction

A

post-renal

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13
Q
  • 10% off all patients with acute renal failure
  • potentially and often easily reversible
  • many times will need involvement of urology and or interventional radiology
A

post-renal

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14
Q
  • Common
  • reversible if treated promptly
  • renal tubules are functional
  • concentrate urine avidly (azotemia/elevated BUN/Cr ratio)
A

pre-renal

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15
Q

what are some etiologies of pre-renal problems?

A
  • Hypovolemia: ex. diarrhea, vomiting, decreased po intake, diuretics, hemorrhage
  • impaired cardiac function: ex. CHF (cardiorenal)
  • peripheral vasodilation (ex. sepsis, liver failure (hepatorenal syndrome)
  • renal vasoconstriction (ex. NSAIDs, iodinated contrast, hypercalcemia, calcineurin inhibitors
  • renal vascular obstruction (ex: renal artery stenosis)
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16
Q

etiologies of intrinsic AKI

A

Glomerular nephritis

  • glomerular nephritis: lupus, igA, ANCA, anti, GBM

Tubules

  • ATN: Ischemic (prolonged/severe prerenal state); Toxic (exogenous meds, endogenous pigments)

Interstitium

  • AIN: medications, infections, autoimmune
17
Q

what are classic toxins and their clincial findings in ATN?

A
  • radiocontrast; oliguric
  • aminoglycosides: non-oliguric
  • pigments (rhabdo); hemoglobinuria without RBCs
  • amphotericin; hypokalemia, hypomagnesemia
18
Q
  • AKI in the setting of medication use
  • 5-14 days
  • rash
  • fever
  • eosinophilia
  • triad 10%
  • non medcation causes less common (malignancy, infectious, autoimmune, idiopathic)
A

Acute interstitial nephritis (AIN)

19
Q

drugs assocaited with acute intersitial nephritis?

A

ANTIBIOTICS

others: PPIs, NSAIDs, chemotherapy

20
Q
  • rare but very serious
  • urgernt renal referral and biopsy
  • therapy varies based on underlying etiology
A

glomerulonephritis

21
Q
  • fluid losses (diuretics, burns, hemorrhage)
  • symptoms of CHF and hypervolemia
  • decreased PO intake
  • symptoms of infections
A

diagnostic history of prerenal AKI

22
Q
  • shock
  • sepsis
  • surgery: anesthesia intraop reports, blood loss
  • review med list
  • joint pain, rashes , fever, constitutional symptoms
A

diagnostic history of renal AKI

23
Q
  • older male
  • neurologic disorder (neurogenic bladder)
  • hx of pelvic malignancies or radiation
  • single kidney
A

diagnostic history of postrenal

24
Q
  • cylindrical structures formed in tubular lumen- shape and size of renal tubule
  • matrix composed of Tamm-horsfall mucoproein (uromoduliln)- most abundant protein in normal urine
A

Urine sediment- casts

25
Q

what casts would you expect in AIN, GN?

A

AIN- WBC
GN- RBC cast

26
Q

Disgnosis of AKI- obstruction

A
  1. post void residual (bladder scan): false readins in obesity or ascities
  2. catheter insertion (straight or foley)
  3. renal ultrasound (most sensitive- provides structural information)
27
Q

Current therapies for managment

A
  • avoid nephrotoxins and maintain renal perfusion (NSAIDs, contrast, extremes of blood pressur)
  • maintanence of metabolic and volume balance (restriction of sodium, potassium, phosphorus; more fluids is Not always the answer, if oliguric, hypervolemic—> diuretics)
28
Q

when to dialyze?

A
  • acidosis; specifically metabolic acidosis
  • electrolytes: hyperkalemia, K > 6.0meq/L; rarely other electrolye abnormalities (Ca, Mg, phos)
  • intoxicants: toxic alcohols, lithium, metformin
  • fluid overload
  • uremia: pericarditis, progressive encephalopathy, not just elevated BUN (azotemia)
  • typically refractory to medical management
  • RTCs do not clearly support early or late initiation
29
Q

what would be seen on physical exam of prerenal AKI?

A
  • Hypotension/orthostatic hypotension
  • rales, S3, JVD, edema
  • ascities/jaundice
  • POCUS of lungs, heart, IVC
30
Q

what would be seen on physical exam of renal AKI?

A

rash
findings of other systemic illness

31
Q

what would be seen on physical exam of postrenal AKI?

A
  • distended bladder
  • POCUS with distended bladder or renal collecting system
32
Q

management of AKI?

A
  1. avoid nephrotoxins and maintain renal perfusion
  • NSAIDs, contrast, extremes of blood pressure

2 . maintanence of metabolic and volume balance

  • restriction of sodium, potassium, phosphorus
  • more fluids are not always the anwer
  • if oliguric, hypervolemic –> diuretics

Nephrology (12 decks)

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