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Year 3 - Clinical (Winter) > 13 - Acute Kidney Injury > Flashcards

13 - Acute Kidney Injury Flashcards

1
Q

AKI definition

A
  • Abrupt (w/in 48 h) reduction in kidney function (GFR)
  • Loss of excretory function in kidneys
  • Accumulation of metabolic waste products – rapid rise in sCr and urea (azotemia)
  • Decreased urine output may occur (may or may not occur, depends on cause)
  • Reduced ability to maintain fluid, electrolyte, and acid-base balance
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2
Q

Classification of AKI

A
  • Classified in 3 stages based on change in serum creatinine level, change in urine output, and need for renal replacement therapy
  • Urine output:
    • Anuric = < 50 mL/day (usually only in post-renal cause)
    • Oliguric = 50-500 mL/day (more common w/ pre-renal or functional cause)
    • Nonoliguric = > 500 mL/day
  • Determination of stage based on worse parameter (ex: stage 3 for sCr but stage 1 for urine output => pt considered stage 3)
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3
Q

Limitations of classifications of AKI

A
  • Baseline sCr
  • sCr varies w/ age, gender, muscle mass, diet, and hydration (sCr increases w/ volume depletion)
  • Lag in increase of sCr w/ decreased GFR (can be 1-2 days b/c t1/2 of creatinine increases dramatically w/ decreased renal function)
  • Urine output may not be reduced (varies w/ volume status, diuretic administration, and presence of obstruction)
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4
Q

How to estimate kidney function (GFR) in AKI

A
  • Formulas to estimate GFR in px w/ AKI shouldn’t be used to adjust medication dosages
  • sCr levels isn’t in a steady state and continues to fluctuate (change in sCr of less than 10-15% w/in 24 h considered “constant”)
  • Consider changes over time
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5
Q

How common is AKI?

A
  • Uncommon in community
  • More often in hospital; especially in ICU (b/c px can be in shock or septic)
  • AKI associated w/ increased risk of mortality and morbidity
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6
Q

Types of AKI

A
  • Pseudo – no actual decline in renal function; increased sCr due to other causes
    1. Pre-renal – decreased blood flow to kidney = decreased GFR
    2. Intrinsic – structural damage to kidney
    3. Post-renal – obstruction to urine flow (if obstruction above bladder, must involve both kidneys to cause AKI) (ex: tumour, enlarged prostate)
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7
Q

Pseudo kidney injury

A
  • Elevated creatinine w/o change in GFR or renal damage
  • Inhibition of renal tubular secretion of sCr (trimethoprim, cimetidine) will appear to decrease CrCl (measured or estimated) but no change in urea
  • Cross-reactivity w/ serum assay (cefoxitin)
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8
Q

Pre-renal/ functional causes **most important to understand

A
  • Glomerular hydrostatic pressure = driving force for glomerular filtration
  • Not a result of kidney damage
  • Most common cause of AKI (50-60%)
  • Impaired renal blood flow due to:
    1. Intravascular volume depletion
    • Dehydration, blood loss, GI loss (diarrhea, vomiting), diuretics, extensive burns
      2. Reduced effective blood volume/ arterial pressure
    • Advanced liver disease
    • CHF (decreased CO)
    • Hypotension (antihypertensives)
    • Sepsis (systemic vasodilation)
      3. Decreased pressure in glomerulus (functional)
    • Afferent arteriole vasoconstriction (cyclosporine, tacrolimus, NSAIDs, COX 2 inhibitors, hepatorenal syndrome)
    • Efferent arteriole vasodilation (ACE inhibitors, ARBs)
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9
Q

Afferent/ efferent effects **very important

A
  • Want the afferent vessel to be dilated & the efferent vessel to be constricted to increase pressure in the glomerulus
  • Constriction of efferent arteriole mediated by angiotensin 2, so taking an ACE inhibitor or ARB causes dilation of efferent arteriole
  • Prostaglandins cause vasodilation of afferent arterioles, so taking an NSAID or COX 2 inhibitor inhibits prostaglandin production and causes vasoconstriction of afferent arteriole
  • Called a triple whammy when taking ACE/ARB & NSAID/COX 2 inhibitor
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10
Q

Causes of intrinsic AKI

A
  • Tubular (most common)
  • Vascular
  • Interstitial (2nd most common)
  • Glomerular
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11
Q

ATN aminoglycosides

A
  • Occurs in 10 – 20% of px
  • Defined as 50% increase from baseline sCr
  • Gent > tobra > amikacin
  • Mechanism – primarily a direct toxic effect to tubular epithelial cell; accumulation of drug in proximal tubule cells produces necrosis => decreased GFR
  • Reversible if d/c drug (ototoxicity from AGs is not reversible)
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12
Q

Risk factors for ATN from AGs

A
  • Pt specific = elderly, hypotension, volume depletion, shock, liver failure, chronic renal insufficiency
  • Drug-regimen = large total cumulative dose, frequent dosing interval, high trough levels (> 2 mg/L), duration > 5-7 days, other nephrotoxic agents
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13
Q

ATN presentation

A
  • Nonoliguric (> 500 mL/day) b/c tubules that should be controlling reabsorption aren’t working, so get a dilute urine
  • Granular casts in urine
  • Increased urea and sCr around day 5-10
    • Increased sCr may occur earlier in presence of dehydration, sepsis, hypotension, CHF, or concurrent use w/ other nephrotoxins
  • Usually mild and reversible
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14
Q

ATN prevention

A
  • Avoid use in high-risk px
  • Maintain adequate hydration (to prevent pre-renal injury)
  • Monitor sCr q2-4days
  • Monitor AG levels and adjust dose for renal function
  • Extended-interval (once daily) dosing
  • Limit duration of tx (< 7 days)
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15
Q

Post-renal causes

A
  • Kidney stones
  • Prostate enlargement or cancer
  • Bladder tumour or obstruction
  • Urethral stricture/ tumor
  • Crystal deposition in renal tubules (acyclovir, methotrexate, foscarnet, indinavir, sulfadiazine)
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16
Q

History assessment of AKI

A
  • Acute vs. chronic (baseline sCr, urea)
  • Past medical hx, family hx (diabetes, poorly controlled HTN)
  • Med hx (functional and intrinsic AKI often drug-induced; d/c any meds w/ potential to cause AKI, especially NSAIDs, COX 2, ACE/ARB)
  • Did they recently receive a contrast agent?
17
Q

Non-specific clinical presentation of AKI

A
  • Elevated sCr and urea
  • Decreased urine output
  • Uremic sx (weakness, fatigue, N/V, loss of appetite, mental confusion, asterixis, seizures)
18
Q

Hx findings of pre-renal AKI

A
  • Volume loss (vomiting, diarrhea, diuresis, hemorrhage, burns)
  • Thirst and reduced fluid intake
19
Q

Physical exam findings of pre-renal AKI

A
  • Weight loss, orthostatic hypotension, tachycardia
  • Poor skin turgor, dry mucous membranes
  • W/ CHF – edema, weight gain, SOB, ascites
20
Q

Hx findings of ATN

A
  • Nephrotoxin exposure
  • Prolonged hypotension
  • Trauma
  • Myalgia, rhabdo
21
Q

Physical exam findings of ATN and AIN

A
  • Fluid overload (HTN, edema, SOB, weight gain)
  • Urine coloured or foamy
  • Fever (AIN)
  • Rash (AIN)
22
Q

Hx findings of AIN

A
  • Meds (antibiotics, PPI)
  • Arthralgia
  • Infectious illness
23
Q

Diagnosis – lab parameters for AKI

A
  • Urea/ creatinine ratio (when calculating, make sure they are in same units; urea = mmol/L, sCr = umol/L)
  • Urinary Na
  • Fractional excretion of sodium (FENa) = (U/P Na / U/P Cr) * 100 **won’t need to calculate on exam; will give result & must know what it means
    • U Na = urinary Na; P Na = plasma Na
    • U Cr = urinary creatinine; P Cr = plasma creatinine
  • Include these along w/ hx & clinical presentation when giving justification for which type of AKI a pt is experiencing
24
Q

Pre-renal investigations

A
  • Renal response to decreased perfusion is to increase resorption of salt and water
    • Kidneys recognize decreased perfusion as a low BP state and work towards improving BP
  • Passively, urea resorption is also increased in the proximal tubule
    • Creatinine resorption is not affected by renal perfusion
  • This results in increased serum urea/creatinine (> 0.07), lower urinary Na (< 20) & lower FENa (< 1%)
25
Q

Lab data for diagnosis of pre-renal vs. intrinsic

A
  • Urea/Cr ratio > 70 = pre-renal; < 70 = intrinsic
  • Urine Na < 20 mmol/L = pre-renal; > 40 mmol/L = intrinsic
  • FENa < 1% = pre-renal; > 2% = intrinsic
  • Px receiving diuretics may have pre-renal AKI but increased sodium excretion induced by diuretic
26
Q

Urinalysis findings

A
  • Protein => intrinsic renal disease w/ glomerular damage; may investigate further using 24 h urine collection
  • Hematuria => acute intrinsic injury; glomerulonephritis
  • Casts => intrinsic renal damage
    • RBC casts = glomerulonephritis
    • WBC casts = acute interstitial nephritis, pyelonephritis
    • Coarse, granular “muddy brown” casts = ATN
  • Crystals => may suggest kidney stone/ post-renal obstruction
  • Eosinophils => acute interstitial nephritis
  • Osmolarity
    • Pre-renal = high osmolarity, concentrated urine (> 500 mOsm/L)
    • Intrinsic damage = low osmolarity (< 350 mOsm/L), structural damage unable to concentrate
27
Q

What to do if hx, physical exam, and lab findings are unclear for diagnosis of AKI?

A
  • Renal ultrasound
    • Detects obstruction (> 90% sensitivity)
    • Look for hydronephrosis (water on the kidneys; obstruction causes water to back flow into kidneys)
    • Size of kidneys also determined (small kidney < 10 cm = chronic disease)
28
Q

Goals of therapy for AKI

A
  • Minimize kidney injury (remove cause; d/c nephrotoxic agents)
  • Supportive therapy
    • Fluid, electrolyte, nutritional support
    • Possible renal replacement therapy (RRT)
    • Treat non-renal complications (sepsis, GI bleed)
    • Check for changes in drug dosing
  • Restore renal function to baseline (usually takes 10-14 days from resolution of last insult)
29
Q

Pre-renal/functional tx

A
  • Hydrate (ex: IV NS) to increase blood pressure and GFR, OR
  • Treat underlying disorder (ex: blood loss, sepsis, CHF, diarrhea, vomiting), OR
  • D/c common med causes (NSAIDs, COX 2, ACE/ARB) until cause of AKI determined
  • D/c diuretics in CHF and cirrhosis
  • D/c antihypertensives if hypotensive
30
Q

Intrinsic tx

A
  • ATN – no specific tx, manage complications
  • AIN (drug-induced) – withdraw precipitating drug, consider steroid therapy
  • Glomerulonephritis – depends on cause
31
Q

Post-renal tx

A
  • Urology consult – catheter if obstruction at bladder or below; nephrostomy tubes if obstruction above bladder
  • For drug-induced crystal nephropathy:
    • D/c medication, if possible
    • IV fluids to ensure adequate hydration
    • Methotrexate –> alkalinize urine (pH > 7) w/ IV or oral sodium bicarbonate
32
Q

AKI complications

A
  1. Fluid overload (may lead to pulmonary edema)
    - Tx – fluid restriction, oxygen, sitting position, diuretics
    - Monitoring – ins/outs, skin turgor/edema, lungs (rales/crackles, CXR), daily weights
  2. Hyperkalemia (if not managed w/ diuretics, must move to dialysis)
33
Q

Diuretic resistance reasons **probably an exam question

A
  • Excessive sodium intake
  • Decreased GFR and functioning nephrons (ATN)
  • Failure to reach site of action
    • Competes w/ organic acids for secretion (both loops & thiazides (metolazone) actively secreted into tubule)
    • Decreased PO bioavailability due to edematous GI tract
  • Distal tubule cells hypertrophy to reabsorb more Na+
    • Loop + thiazide –> large diuresis (thiazide blocks Na+ reabsorption in distal tubule)
    • Thiazide diuretics have longer t1/2 than loop diuretics
34
Q

Indications for renal replacement therapy

A

AEIOU

  • Acid-base abnormalities (metabolic acidosis from accumulation of organic/ inorganic acids)
  • Electrolyte imbalance (hyperkalemia, hypermagnesemia)
  • Intoxications (ex: salicylates, lithium, methanol, ethylene glycol, theophylline, phenobarbital)
  • Fluid overload (resistant to diuretics)
  • Uremia (severe and symptomatic) – mental confusion, asterixis, seizures
35
Q

Describe acute tubular necrosis (ATN)

A
  • Ischemia in kidney (ex: extended pre-renal state) producing cell damage or direct tubule toxins
  • Medication induced causes – aminoglycosides**, amphotericin B
  • Other – rhabdomyolysis (myoglobins released into bloodstream are toxic to kidneys), ethylene glycol (calcium oxalate crystals)
36
Q

Describe acute interstitial nephritis (AIN)

A
  • Inflammatory disorder of the renal interstitium (“allergic reaction”)
  • 2 most common causes:
    • Drugs – penicillins, cephalosporins, quinolones, thiazide diuretics, loop diuretics, sulfonamides, NSAIDs, allopurinol, phenytoin, etc.
    • Infections – streptococcal, HIV
  • Presentation = fever, rash, eosinophilia
37
Q

Describe glomerulonephritis

A
  • Uncommon
  • Results from stimulation of the immune system leading to inflammation of the glomerulus
  • Causes = DNA, proteins, viruses, bacteria stimulate immune activation

Year 3 - Clinical (Winter) (30 decks)

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