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
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)
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)
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
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
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)
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)
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
- Dehydration, blood loss, GI loss (diarrhea, vomiting), diuretics, extensive burns
- Advanced liver disease
- CHF (decreased CO)
- Hypotension (antihypertensives)
- Sepsis (systemic vasodilation)
3. Decreased pressure in glomerulus (functional)
- Sepsis (systemic vasodilation)
- Afferent arteriole vasoconstriction (cyclosporine, tacrolimus, NSAIDs, COX 2 inhibitors, hepatorenal syndrome)
- Efferent arteriole vasodilation (ACE inhibitors, ARBs)
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
10
Q
Causes of intrinsic AKI
A
- Tubular (most common)
- Vascular
- Interstitial (2nd most common)
- Glomerular
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)
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
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
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)
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)
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
- 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 - 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
