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Clin Med II Unit III > 5 Acute Kidney Injury > Flashcards

5 Acute Kidney Injury Flashcards

1
Q

Why has Acute Kidney Injury replaced Acute Renal Failure as the term of choice?

A

Recognition that smaller decrements in kidney function that do not result in overt organ failure are of substantial clinical relevance and are associated with increased morbidity and mortality

The term ARF is now reserved for severe AKI, typically implying the need for dialysis

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2
Q

How do we define AKI?

A

Abrupt loss of kidney function resulting in RETENTION OF UREA and other nitrogenous waste products and DYSREGULATION of volume status and electrolytes

Criteria for Dx is usually based on SERUM CREATININE LEVELS used to calculate GFR or by a DECREASE IN URINE OUTPUT

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3
Q

What are the problems associated with using Serum Creatinine for diagnosing AKI?

A

Serum Cr may be low in early stages of AKI, even though the actual GFR is markedly reduced (may not have been sufficient time for the creatinine to accumulate)

Creatinine is removed by dialysis, so hard to assess kidney function once dialysis is started

Lack of consensus definition of AKI between experts

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4
Q

What is the main criteria used to diagnose AKI?

A

RIFLE criteria

AKIN (Acute Kidney Injury Network)

Most recent - Kidney Disease: Improving Global Outcomes (KDIGO) criteria to harmonize differences between RIFLE and AKIN

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5
Q

Summary of the KDIGO diagnostic criteria for AKI

A

Increase in serum creatinine by ≥ 0.3mg/dL within 48 hours

or

Increase in serum creatinine to ≥ 1.5x baseline (known or presumed to have occurred within the prior 7 days)

or

Urine volume < 0.5 mL/kg/hour for six hours

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6
Q

What are the KDIGO stagings?

A

Stage 1: Increase in serum Cr to 1.5 to 1.9 times baseline or by ≥ 0.3 mg/dL or reduction in urine output to <0.5 mL/kg/hour for 6 to 12 hours

Stage 2: Increase in serum Cr to 2.0 to 2.9 times baseline or reduction in urine output to < 0.5 mL/kg/hour for ≥ 12 hours

Stage 3: Increase in serum Cr to 3 times baseline or increase in serum Cr ≥ 4.0 mg/dL or reduction in urine output to < 0.3 mL/kg/hour for ≥ 24 hours OR anuria for ≥ 12 hours OR initiation of renal replacement therapy

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7
Q

The KDIGO criteria will likely be revised and possibly replaced as ___________ are developed

A

Biomarkers of kidney (tubular) injury

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8
Q

In the US, approx _____% of patients admitted to hospitals have AKI at the time of admission but the estimated incidence rate of AKI during hospitalization is _____%

A

1% —> 25%

AKI develops in up to 60% of ICU patients!!!

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9
Q

Etiology of AKI can be classified into …

A

Prerenal AKI (decreased renal perfusion)

Intrinsic renal AKI (pathology of the vessels, glomeruli, or tubules)

Postrenal AKI (obstructive)

Many times these etiologies overlap

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10
Q

AKI in the hospital is most often from ________

A

Prerenal disease or ATN (acute tubular necrosis - intrinsic renal pathology)

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11
Q

Examples of causes of prerenal disease

A

True volume depletion (GI loses, renal loses, burns, third spacing)

Hypotension (shock, or aggressive treatment of HTN)

Edematous states (HF, cirrhosis)

Selective renal ischemia (BL renal artery stenosis)

Drugs affecting GFR (NSAIDs and ACE-Is)

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12
Q

Acute Tubular Necrosis can be caused by …

A

Renal ischemia (from all causes of severe prerenal disease - lots of overlap)

Sepsis - may cause hypotension or release of cytokines and activation of neutrophils

Nephrotoxic - aminoglycosides, IV CONTRAST, heme pigments (rhabdo), cisplatin, HIV meds, IVIG, mannitol

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13
Q

________ causes renal tubular epithelial cell toxicity and renal medullary ischemia from vasoconstriction

A

IV contrast

Generally reversible

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14
Q

Risk factors for IV contrast induced AKI

A

Preexisting renal disease (rare in those with normal renal function)

Volume depletion

Repeated doses of contrast

Comorbid conditions (DM, CHF)

Age (less of a risk than above causes)

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15
Q

What is the key to preventing IV contrast AKI

A

HYDRATION, either PO or IV

Use of low-osmolal agents at low doses

Avoid repetitive doses

Avoidance of nephrotoxic drugs for at least 48 hours after exposure (ie Metformin, NSAIDs)

Sodium bicarbonate and acetylcysteine controversial and not used anymore

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16
Q

Postrenal AKI are due to …

A

Obstruction of the flow of urine

Can occur anywhere in the urinary tract, from the renal pelvis to the urethra

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17
Q

A reduction in GFR in patients without intrinsic renal disease requires…

A

BILATERAL OBSTRUCTION (or unilateral obstruction in a single functioning kidney)

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18
Q

Postrenal AKI is most commonly due to …

A

Prostatic Disease (hyperplasia or cancer) or metastatic cancer

Neurological disease can also cause neurogenic bladder and urinary retention

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19
Q

> 400 ml urine output in 24 hours

A

Nonoliguric

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20
Q

<400mL urine output in 24 hours

A

Oliguric

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21
Q

<100mL urine output in 24 hours

A

Anuric

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22
Q

Evaluation and diagnostic workup of AKI requires…

A

UA - gross eval, dipstick, and microscopy

Serum metabolic panel
• Cr to calculate GFR
• Calculation of fractional excretion of sodium (FENa)

Renal U/S, possibly CT or MRI

Renal biopsy

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23
Q

Urine collected for UA should be examined at _______ temperature within ______ of collection

A

Room temp, within 2 hours of collection

If not possible it should be refrigerated and re-warmed prior to assessment

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24
Q

Most common color for urine other than clear is …

A

RED (from blood) or BROWN (from myoglobin)

Certain meds and foods can also alter the color but have little clinical significance)

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25
Q

Muddy brown casts or degenerated cells are pathognomonic for …

A

Acute tubular necrosis

26
Q

What are the two most commonly used equations for calculating GFR

A

Cockcroft-Gault
[(140-Age) x Mass(kg) x 0.85 if female] / 72 x serum Cr

Modification of Diet in Renal Disease (MDRD) calculation
186 x Serum Cr^-1.154 x Age^-0.203 x (1.210 if black) x (0.742 if female)
Dr. Mitzel says this one is more accurate

27
Q

Any equation for calculating GFR that uses creatinine may…

A

Lead to errors among patients who are not in a steady state

28
Q

Dr. Mitzel’s preferred way to estimate GFR…

A

Cr 2x normal —> GFR 1/2 normal

Cr 3x normal —> GFR 1/3 normal

Cr 4x normal —> GFR 1/4 normal

Cr 5x normal —> GFR 1/5 normal

29
Q

Equation that measures the percent of filtered sodium that is excreted in the urine

A

Fractional excretion of sodium (FENa)

In an oliguric patient, the FENa may help to distinguish prerenal AKI from intrinsic renal pathology

FENa = (Urine Na/Serum Na) / (Urine Cr/Serum Cr) x 100

30
Q

A FENa <1% suggests…

A

A prerenal etiology of AKI

31
Q

A FENa >2% suggests …

A

Intrarenal etiology of AKI (ie ATN)

32
Q

A FENa value between 1-2% may be seen with

A

Either Prerenal OR Intrarenal AKI

33
Q

Downside of using FENa

A

Unreliable in patients on diuretics

Only useful in acute renal failure, not chronic renal failure

34
Q

Radiographic imaging is generally performed in patients with AKI when…

A

The underlying cause is not immediately apparent

The major reason for performing imaging is to ASSESS FOR URINARY TRACT OBSTRUCTION

35
Q

The most common Radiographic technique used in AKI is …

A

Renal ultrasound

Safe (no contrast or radiation)
Easy to perform (can do it bedside)
Sensitive for obstruction

36
Q

Urinary tract obstruction may predispose patient for …

A

UTI —> urosepsis and eventually cause kidney failure

37
Q

Relief of renal obstruction is dependent upon…

A

The cause of the obstruction

Kidney stone —> remove stone

BPH —> place foley cath

Mass (malignancy/polyp) —> remove mass

38
Q

Renal function after relief of the obstruction is dependent upon…

A

The SEVERITY and DURATION of the obstruction

39
Q

When is a renal biopsy performed

A

For patients who have no clear explanation for AKI, further evaluation is determined by the severity of disease and rate of further decline

If Cr is markedly elevated or if it significantly worsens over the course of days then a kidney biopsy should be performed

A biopsy usually provides a more definitive tissue diagnosis and may allow a therapeutic intervention to prevent ESRD

40
Q

Contraindications for renal biopsy

A

Bleeding diathesis

Pyelonephritis

Renal tumor

Solitary native kidney (maybe)

Biopsy rarely needed to diagnose AKI

41
Q

Possible life-threatening complications of AKI

A 
Volume imbalance
Metabolic acidosis (pH <7.4)
Hyperkalemia (serum K >5.5 or rapidly increasing)
Hypocalcemia
Hyperphosphatemia
Uremia
42
Q

Life threatening complications of AKI generally require…

A

The initiation of hemodialysis

Requires:
• Consult with nephrology
• Placement of a dialysis catheter
• Machinery and staff to perform dialysis

Must provide medical management of complications until it can be set up

43
Q

Correction of ___________ may improve or even reverse AKI

A

Volume imbalance (depletion or overload)

44
Q

When should you administer IV fluids?

A

Clinical Hx consistent with fluid loss (V/D)

Physical exam consistent with hypovolemia (hypotension/tachycardia)

Oliguria

45
Q

How should you administer IV fluids to a volume depleted AKI patient?

A

Fluid challenge attempts to identify prerenal failure

Crystalloid isotonic fluids (0.9 NS) are generally preferred

Total amount depends on degree of depletion, with desired endpoints to include the restoration of adequate urine flow and improvement of renal function

Begin with 1-3 liters of fluid, with careful and repeated clinical assess MTN

46
Q

Patients who do not respond to fluids are …

A

Unlikely to have prerenal disease and more likely to have ATN or other forms of intrinsic AKI

47
Q

What should you do for a patient who presents with volume overload or develops fluid retention from IV fluid therapy coupled with decreased ability to secrete sodium and water?

A

Daily fluid balance should be closely monitored (“ins and outs”)

Diuretics (typically furosemide) may be used to relieve hypervolemia BUT

  1. Should not be prolonged therapy as dialysis offers the most efficient method of fluid removal
  2. Urine output should be monitored closely and if UOP does not increase after diuretics are given they should be stopped
48
Q

In patients with AKI, the excretion of acid and regeneration of bicarbonate is impaired due to the low GFR, resulting in …

A

Metabolic acidosis

Daily metabolism creates acid but many of the causes of AKI such as sepsis, trauma, organ failure produce increased amounts of acid as well

Diarrhea causes a net loss of bicarbonate which can worsen the metabolic acidosis too

49
Q

Treatment for metabolic acidosis consists of what two possibilities?

A

Dialysis
Bicarbonate administration

Choice of therapy depends upon absence or presence of volume overload, and underlying cause/severity of the acidosis

50
Q

You should dialyze patients with severe oligo-anuric AKI who are …

A

VOLUME OVERLOADED and have severe METABOLIC ACIDOSIS

Dialysis is preferred to the administration of bicarbonate for patients who are VOLUME OVERLOADED b/c bicarbonate administration results in a large sodium load that may cause or contribute to further volume overload

51
Q

Patients with AKI who are NOT volume overloaded and have NO other indication for acute dialysis can receive bicarbonate instead of dialysis if …

A

Acidosis is related to diarrhea

pH <7.1 and awaiting dialysis

AKI DUE TO RHABDOMYOLYSIS in order to prevent further renal injury (though this is falling out of favor - expensive and no proof it works any better than saline)

52
Q

Why is hyperkalemia so dangerous?

A

It can cause impaired neuromuscular transmission and cardiac conduction abnormalities (arrhythmias)

Very few symptoms, until you DIE

53
Q

How do you treat hyperkalemia?

A

Both medical therapy and dialysis

Antagonize the membrane effects of potassium by driving extracellular potassium into the cells and removing excess potassium from the body

54
Q

___________ is common among AKI patients and is primarily related to increases in serum phosphorus levels caused by reduced GFR

A

Hypocalcemia

Serum ionized calcium should be measured

If the patient is asymptomatic and hyperphosphatemia is present, initial therapy is the correction of the hyperphosphatemia

55
Q

Symptomatic patients with hypocalcemia should be treated with….

A

IV calcium

BUT the admin of calcium who are severely hyperphosphatemia may result in the deposition of calcium phosphate into vasculature and organs —> DIALYSIS!!!

56
Q

Patients with moderately to severely elevated serum phosphate concentrations (>6 mg/dL) should be treated with…

A

Dietary phosphate binders

Selection depends on the level of serum ionized calcium concentration

If Ca is low, use a calcium-containing phosphate binder such as CALCIUM ACETATE or CALCIUM CARBONATE

If Ca is high, non-calcium phosphate binders such as ALUMINUM HYDROXIDE or LANTHANUM CARBONATE

57
Q

Generally, you’ll dialyze patients with severe hyperphosphatemia (>12mg/dL) because…

A

Dialysis works more rapidly than phosphate binders

Dialysis may be more effective in preventing injury due to the precipitation of calcium and phosphate

DIALYSIS SHOULD BE PERFORMED IN ANY PATIENT WHO CANNOT TOLERATE ORAL INTAKE

58
Q

Clinical syndrome associated wit fluid, electrolyte, hormone imbalances, and metabolic abnormalities, which develop in parallel with deterioration of renal function

A

Uremia

Literally “urine in the blood” - more common in chronic kidney disease

Dialysis should be initiated in patients with severe uremia because
• Pericarditis
• Neuropathy
• Unexplained decline in mental status

59
Q

AKI prognosis depends on…

A

Cause of AKI and presence/absence of pre-existing renal disease

Most patients with AKI recover renal function once UOP normalizes and creatinine normalizes

60
Q

Studies have shown that patients who recover from AKI are at significantly greater risk of…

A

Developing CKD and ESRD

AKI during a hospitalization is associated with high in-hospital and long-term mortality

Clin Med II Unit III (6 decks)

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