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Renal Disease > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

Ettinger Ch. 300 (62 cards)

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1
Q

What are the 4 phases of intrinsic AKI?

(I Eat Many Recess)

A

Induction
Extension
Maintenance
Recovery

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2
Q

-An insult (ischemic, nephrotoxic) occurs and continues until there is a reduction in UOP or GFR.

-Duration is variable and depends on the insult

-Early intervention during this phase may prevent progression

-CS are not yet apparent during this phase, making recognition of AKI extremely difficult.

What phase of AKI is being described?

A

induction

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3
Q

-Further injury to the kidney via alterations in perfusion, continued hypoxia, secondary inflammation and ongoing epithelial endothelial injury

What phase of AKI is being described?

A

extension

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4
Q

-Occurs after insult and a critical amount of damage has been established.

-Results in decreased GFR and renal hypoperfusion

-Detectable azotemia

-May experience signs of uremia

-Elimination of inciting factors during this phase will not decrease existing damage or expedite rate of recovery

What phase of AKI is being described?

A

maintenance

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5
Q

-Period where renal tissue undergoes regeneration and repair

-The amount of restoration of renal function is variable

-May take days to months

What phase of AKI is being described?

A

recovery

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6
Q

Based on the following information, what is the grade of AKI:

-Crea <1.6 mg/dL (<140 mcmol/L), non-azotemic

-Hx, CS, laboratory, imaging evidence of an AKI

-Progressive non-azotemic increase in serum Crea >0.3 mg/dL within 48 hours

->6h duration of oligoanuria

A

IRIS - Grade 1 AKI

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7
Q

Based on the following information, what is the grade of AKI:

-Crea 1.7-2.5 mg/dL, mild azotemia

-documented static or progressive azotemia

-progressive increase in Crea >0.3 within 48 hours

->6h duration of oligoanuria

A

IRIS - Grade II AKI

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8
Q

Based on the following information, what is the grade of AKI:

-Crea 2.6-5.0, moderate to severe

A

IRIS - Grade III AKI

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9
Q

Based on the following information, what is the grade of AKI:

-Crea 5.1-10, severe AKI

A

IRIS - Grade IV AKI

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10
Q

Based on the following information, what is the grade of AKI:

-Crea >10 mg/dL (>880 mcmol/L), severe

A

IRIS - Grade V

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11
Q

How are AKI’s graded?

A

-serum creatinine

-subgraded by UOP (non-oligoanuric vs oligoanuric)

-need for renal replacement therapy

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12
Q

T/F: Patient’s with an AKI are azotemic.

A

F - The trend of increasing Crea in a hospitalized dog or cat should increase concern for an AKI, even if the patient is non-azotemic. Dogs with IRIS Grade I AKI have a higher in-hsopital mortality (58%) than those without an AKI (16%).

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13
Q

What are the 3 categories of AKI based on the underlying etiology?

A

Pre-renal (hemodynamic) - hypoperfusion, parenchyma is not damaged

Intrinsic Renal - ischemia/ nephrotoxin, parenchyma damaged

Post-renal or obstructive

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14
Q

Biomarkers can help you to localize the site of injury. Which biomarker(s) are used to help estimate GFR?

A

Crea
BUN
symmetric dimethylarginine (SDMA)
cystatin C (CC)

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15
Q

Biomarkers can help you to localize the site of injury. Which biomarker(s) suggest that there is an increase in glomerular permeability?

A

Urine protein
Urine albumin
Urine immunoglobulin (Ig - A, G, M)
Urine C-reactive protein (CRP)

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16
Q

Biomarkers can help you to localize the site of injury. Which biomarker(s) suggest injury of the PCT?

(Rose mGowan Nags Girls (like) Kim C)

A

Retinol-binding protein (RBP)
Microglobulins (alpha1, beta2)
N-acetyl-beta-D-glucosaminidase (NAG)
Gamma-glutamyl transpeptidase (GGT)
kidney injury molecules-1 (KIM-1)
Urine cystatin C
serum inosine

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17
Q

Biomarkers can help you to localize the site of injury. Which biomarker(s) suggest injury to the DCT?

A

IL-8

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18
Q

Biomarkers can help you to localize the site of injury. Which biomarker(s) suggest generalized nephron injury?

A

Neutrophil gelatinase-associated lipocalin (NGAL)

Clusterin

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19
Q

What is the normal fractional excretion of sodium (FeNa)?

What variables influence this calculation?

A

<1%

FeNa is calculated using the concentrations of sodium and creatinine in the blood and urine

The formula is: FENa (%) = (U Na × V) / (GFR × P Na)

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20
Q

a persistent decrease in kidney function that persists >7 days

A

acute kidney disease (AKD)

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21
Q

What 2 clinical syndromes are sequelae to AKI? What is their timeline?

A

Acute kidney disease (AKD) - 7-90d

Chronic kidney disease (CKD) - >90d

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22
Q

AKD are substaged and can be suggestive of whether or not a patient is likely to experience renal recovery. Based on the description, what is the substage of AKI?

Serum Crea remains above baseline 7 days after diagnosing AKI.

A

AKD 1C - patient does NOT demonstrate recovery and renal function to be monitored closely for evidence of further loss

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23
Q

AKD are substaged and can be suggestive of whether or not a patient is likely to experience renal recovery. Based on the description, what is the substage of AK?

The patient’s creatinine normalizes, but biomarkers suggest renal injury is persistent (proteinuria, hypertension, etc.).

A

AKD 1C/B

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24
Q

AKD are substaged and can be suggestive of whether or not a patient is likely to experience renal recovery. Based on the description, what is the substage of AKD?

Patient’s serum creatinine completely recovers/returns to baseline. Biomarkers show no evidence of active renal injury.

A

AKD 1A

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25
T/F - Normalizing GFR biomarkers is indicative of complete kidney recovery.
F - "recovery" may only indicate 25-50% improvement in GFR; these tests are NOT sensitive for identifying mild decreases in GFR
26
Differentials for pre-renal AKI.
Hypovolemia (hemorrhage, GI loss, renal loss, increased insensible fluid loss, third spacing, drugs in the face of dehydration) Decreased CO (myocardial/valvular disease, pericardial effusion, sepsis anaphylaxis) Systemic vasodilation (sepsis, drugs) Renal vasoconstriction (NE, sepsis, hypercalcemia, liver dz, drugs)
27
MOA of carprofen contributing to AKI
inhibit production of PGs and kinins preventing vasodilation and decreasing RBF -> vasoconstriction and reduced renal perfusion -> ischemic injury
28
MOA of ACEi's (benazepril, enalapril) contributing to AKI.
block conversion of AngI to Ang II -> vasodilation of efferent arteriole decreases tubuloglomerular feedback -> decrease glomerular filtration pressure -> decreases GFR
29
etiologies of intrarenal vasoconstriction
hypercalcemia (constriction of afferent arteriole, contain CaSRs) bacterial endotoxin (immune system activation and release of TNF -> renal vasoconstriction) radiocontrast agents (i.e., iohexol - release of adenosine or endothelin) cyclosporine (increases production of endothelin-1, potent vasoconstrictor)
30
What are the 4 different processes that can contribute to damaging the renal parenchyma?
Large renal vessels (thrombosis, vasculitis, compression) Renal microvasculature and glomeruli (glomerulonephritis, vasculitis, hypertension) ischemic/ nephrotoxic acute tubular necrosis (hypoperfusion, endogenous and exogenous toxins) Diseases of the tubulointerstitium (neoplasia, oxidative injury, infectious)
31
T/F: Occlusion of large renal vessels is a common cause of AKI in dogs and cats.
F - Most thromboembolic disease involves the lung and distal aorta.
32
What are common toxins that can contribute to AKI?
ethylene glycol lily grapes, raisins
33
MOA - sepsis and intrinsic AKI (broad)
arterial vasodilation - systemic wide dilation -> decrease in circulating blood volume -> decreased renal perfusion increased SVR production of ROS -> tubular injury DIC -> hypercoagulable -> thrombosis inflammation/ immune response activation -> renal damage 12.3% of dogs with sepsis and MODS had renal dysfunction
34
MOA - heatstroke and intrinsic AKI (broad)
hypoperfusion, direct thermal injury, pigment nephropathy (myoglobinemmia), SIRS 63% of dogs with heatstroke have developed AKI at presentation/ during hospitalization; associated with both tubular/ globmerular damage; biomarkers not predictive of outcome
35
Why is the kidney vulnerable to toxic injury?
kidney receives 25% of CO making it inherently vulnerable to toxins most nephrotoxins cause injury with one of or a combination of intrarenal vasoconstriction, tubular cell toxic injury and intratubular obstruction
36
MOA - myoglobulin, hemmoglobin toxicosis - renal ischemia
nephrotoxic injury via NO scavenging -> vasoconstriction -> renal ischemia
37
Examples of nephrotoxic drugs
aminoglycosides amphotericn B cyclosporine tacolimus albumin
38
What is thought to be the agent that causes nephrotoxicity in grapes?
tartaric acid, MOA unknown
39
MOA - Lepto kidney injury
Leptospiremia -> replicates/ persists in renal tubular epithelial cells -> interstitial nephritis, intracellular Ca accumulatoin, cell death // active sediment/ granular casts (sloughing into tubular lumen)
40
Isothenuria and azotemia typically do not occur until ____% and ____% of nephron function is lost, respectively.
isothenuria - 66% azotemia - 75%
41
T/F: Patients with unilateral nephroureteral obstruction are typically azotemic.
F - may not have biochemical abnormalities if the remaining kidney is normal
42
generally develops from disruption of the distal ureters, bladder or proximal urethra
uropreitoneum
43
results from injury to a kidney or proximal ureter with the peritoneum remaining intact
uroretroperitoneum
44
What are findings found on aFAST/ultrasound supportive of ureteral obstruction?
renal pelvis dilation blunting of diverticuli proximal ureteral dilation
45
What measurement (mm) is typically supportive of renal pelvis dilation due to a ureteral obstruction?
>7-13 mm
46
If you are unable to confirm a ureteral obstruction via AUS and radiographs, what diagnostic modality could be beneficial?
Percutaneous antegrade pyelopgraphy - 94% diagnostic rate, 2% major complication rate
47
Which organ systems are most commonly affected by uremia?
GI CNS CVS
48
What are signs of overhydration?
serous ocular and nasal discharge SC edema cavitary effusions pulmonary edema
49
What is the normal UOP in healthy dogs and cats?
1-2 mL/kg/h
50
Oliguria is a medical term used to describe low urine output. What UOP indicates *relative* oliguria?
<2 ml/kg/h
51
Oliguria is a medical term used to describe low urine output. What UOP indicates *absolute* oliguria?
<1 mL/kg/h
52
Anuria is a medical emergency in which the kidneys are producing no or too little urine. What is the UOP for anuric patients?
0-0.5 ml/kg/h
53
What is the mortality rate in patients with oligoanuric AKIs?
20-fold increased risk of death compared with PU pets
54
MOA - mannitol
6-carbon, linear, simple sugar that is only mildly metabolized that draws water out of cells and into the intravascular space, increasing plasma tonicity (IV); freely filtered by the glomerulus and excreted in urine.
55
How does mannitol help to convert oligoanuria to polyuria?
It is an osmotic diuretic that decreases cellular swelling. It may help wash out obstructive casts and debris from tubules and may work as a free radical scavenger. Should only be given to euhydrated patients, contraindicated in dehydrated patients. IV, 0.25-1 g/kg over 15-20 min
56
MOA - furosemmide
Loop diuretic that inhibits the Na-K-2Cl transporter in the thick ascending loop of Henle.
57
T/F - Furosemide is an effective diuretic used to increase UOP.
F - Furosemide enters tubular filtrate in the PCT and filtered as non-protein bound across the glomerular filtrastion barrier. Since anuric patients have minima ln anuric patients there is no tubular flow, it is **unlikely** that this drug will reach the site of activity.
58
What are indications for renal support therapy (extracorporeal therapy)?
symptomatic uremia acidosis hyperkalemia volume overload refractory to medical management
59
What is peritoneal dialysis? What are pros/cons of this technique.
A type of extracorporeal renal support therapy that utilizes abdominal lining to filter blood. Pro - low tech Cons - requires intense and continuous monitoring; contraindicated in patients with abdominal wall trauma, peritoneal infections, severe hypoalbuminemia/ catabolic states
60
Complications of peritoneal dialysis
Perotinitis - 22% catheter occlusion excessive protein loss pleural effusion dialysis disequilibrium syndrome (DDS)
61
What is the survival rate for dogs and cats with AKI that receive hemodialysis?
30-day survival for dogs was 42% and for cats 48% 1-year survival in 38% of cats and 33% in dogs
62
What is the prognosis for patients with AKI?
Limited studies, in humans the mortality rate is ~50%, even with dialysis. Meta-analysis of AKI survival showed a pooled mortality rate of 45% in dogs and 53% for cats Mortality is highly dependent on underlying cause (infectious etiologies having a superior survival rate to non-infectious causes).

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