Acute renal failure Flashcards

1
Q

Acute Renal Failure aka Acute Kidney Injury

A

● Defined as rapid decrease in kidney function, resulting in…
○ Inability to maintain acid-base balance
○ Inability to maintain electrolyte concentrations/water homeostasis
○ Inability to excrete nitrogenous waste products (urea and
creatinine)

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2
Q

Several causes of Acute renal failure

A

hypovolemia, glomerulonephritis, BPH, etc.
○ Pre-renal, intrinsic, post-renal

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3
Q

Approximately ____% of all ICU patients have AKI

A

65

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4
Q

What is the 2012 Kidney Disease Improving Global Outcomes (KDIGO) AKI Diagnostic Criteria?

A

Diagnose acute kidney injury in
patients with any one of the following criteria:
GU-ACUREN-1
○ Increase in serum creatinine by ≥ 0.3
mg/dL within 48 hours
○ Increase in serum creatinine to ≥ 1.5 times
baseline, within prior 7 days
○ Urine volume less than 400-500 ml/day
(oliguria) or output < 0.5 mL/kg/hour for six
hours

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5
Q

Staging the severity of Acute Kidney Injury

A

○ Stage 1-
■ Serum creatinine criteria - Increase by ≥ 0.3 mg/dL in 48 hours or
a 150-199% (1.5 to 1.9 times) increase from baseline OR
■ Urine output criteria - decline to < 0.5 mL/kg/hour for > 6-12
hours.
○ Stage 2-
■ Serum creatinine criteria - Increase to 200%-299% from baseline
OR
■ Urine output criteria - < 0.5 mL/kg/hour for > 12 hours.
○ Stage 3-
■ Serum creatinine criteria - Increase to > 300% from baseline, or
to ≥ 4 mg/dL OR
■ Urine output criteria - < 0.3 mL/kg/hour for 24 hours +, or
anuria for 12 hours + OR
■ Initiation of renal replacement therapy OR if <18 y/o and a
eGFR of 35

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6
Q

When the kidney is injured, _____ decreases, which results in accumulation of _____

A

glomerular filtration; nitrogenous waste (BUN and Creatinine)

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7
Q

______- The laboratory increase in
BUN and Creatinine (may be
asymptomatic)

A

Azotemia

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8
Q

______- Pathologic manifestation of
Azotemia (these patients are ill)

A

Uremia-

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9
Q

To sort out the causes of acute kidney injury, we break them into 3 main categories:

A

○ Pre-Renal Azotemia i.e. hypovolemia
○ Intra-renal (Intrinsic) Azotemia i.e. glomerulonephritis
○ Post-Renal Azotemia i.e. BPH

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10
Q

Look at slide ____

A

13

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11
Q

Pre-Renal AKI

A

● Most common of the 3 categories, causing 40-80% of AKI cases.
● When you think of Pre-Renal causes, think of Renal Hypoperfusion.
● Whatever the cause may be, the body is not able to maintain adequate blood flow to the kidneys, resulting in decreased GFR, azotemia, and possible oliguria. Hydrostatic pressure

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12
Q

Pre-Renal Causes of AKI

A

○ Hypovolemia (hemorrhage, dehydration, burns, third spacing, GI fluid loss).
○ Hypotension (due to low volume or due to decrease vascular resistance, such as from some medications)
○ Ineffective circulation or Low Cardiac Output (CHF, sepsis)
○ Abdominal Aortic Aneurysm/Dissection (AAA)
○ Renal Artery Stenosis with acute thrombosis
○ Nearby neoplasm (causing renal artery blood flow obstruction)

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13
Q

Pre-Renal Tx of AKI

A

dependent upon the cause.
● However, mainstay of therapy is based on…
○ Maintenance of intravascular volume level
(IVFs)
■ Need to restore renal perfusion
○ Attention to serum electrolyte imbalances
○ Avoidance of nephrotoxic drugs in order to
not add insult to injury

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14
Q

Intrinsic (Intra) AKI

A

● Intrinsic causes account for a range of 25-40% of AKI cases
● The sites of damage with Intrinsic
Kidney Injury include the glomeruli, the
interstitium, and/or the tubules
● When you think of Intrinsic (Intrarenal)
kidney injury, think of Direct Organ Insult
● First, r/o pre- and post-renal issues

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15
Q

Intrinsic (Intra) Renal Causes

A

○ Acute Tubular Necrosis (most common intrinsic cause)
■ Disease secondary to ischemia or nephrotoxins
■ Prolonged pre-renal AKI can become intrinsic AKI
○ Acute Interstitial Nephritis
○ Acute Glomerulonephritis (various types)
○ Others (infections like TB or pyelonephritis, vasculitis)

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16
Q

Post-Renal AKI

A

● The least common category of Acute Renal Failure (5-10%).
● These are important to detect because of their reversibility
● Azotemia only occurs if outflow obstruction affects BOTH kidneys
● If only one is obstructed, renal
function is usually maintained by the
other kidney
● With post-renal AKI, think of Urinary Outflow Obstruction that causes pressure to back up through the kidneys

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17
Q

Post-Renal Causes

A

○ Benign Prostatic Hyperplasia (BPH) (most common cause in men)
○ Urolithiasis - stones anywhere in the urinary tract
○ Bladder Outlet Obstruction (mass, pregnancy- rare)
○ Anticholinergic medications - inhibits smooth muscle contractions
○ Obstructive bladder, prostate, or cervical cancers

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18
Q

Post-void bladder scans or catheter placements may reveal more
than 300 mL residual urine with _____

A

post-renal causes

19
Q

Treatment of post-renal causes

A

○ Reverse the obstruction (often requires procedure of some sort)
○ Perhaps Foley catheter placement or ureteral stent placement
○ Most azotemia reverses fully with reversal of obstruction

20
Q

Clinical Presentation of AKI

A

May be asymptomatic
○ Abnormal urine output (anuria, oliguria, polyuria- due to loss
of sodium)
○ Confusion / Change in mental status
○ Lethargy / Fatigue
○ Anorexia
○ Nausea and Vomiting
○ Weight gain / Swelling

21
Q

History of nausea, vomiting, acute blood loss, or shock may indicate systemic volume depletion and may suggest what cause of AKI?

A

Pre-Renal AKI)

22
Q

Trauma or prolonged immobilization may indicate Rhabdomyolysis, which can cause Acute Tubular Necrosis ans suggest what cause of AKI?

A

Intrarenal AKI

23
Q

Increased urinary frequency and hesitancy may indicate BPH and suggest what cause of AKI?

A

Post-Renal AKI

24
Q

Signs/symptoms consistent with Pre-Renal AKI:

A

Thirst with reduced fluid intake, nausea/vomiting, diarrhea, acute hemorrhage

25
Q

Signs/symptoms consistent with Intrinsic AKI:

A

Fatigue, anorexia, fevers, foamy urine, blood in urine, myalgias, arthralgias, arthritis, maculopapular rash

26
Q

Signs/symptoms consistent with Post-Renal AKI:

A

Urinary urgency or hesitancy, abdominal pain, blood in
urine, enlarged prostate, abdominal mass

27
Q

Diagnostic evaluation steps for AKI

A

● Once you are suspecting Acute Kidney Injury, quickly narrow it down to Pre-Renal, Intrinsic, or Post-Renal causes
● Laboratory evaluation is the next step in the work-up:
○ Should include serum creatinine, serum BUN, serum
electrolytes, urinalysis with microscopy, and CBC
○ CBC, CMP, and a Urinalysis will give you all of this
● Depending on labs and the likely cause, other tests may include EKG, renal/bladder ultrasound, and possible renal biopsy

28
Q

Key labs for diagnosis of AKI:

A

Elevated BUN and Creatinine

29
Q

Normal range BUN:Creatinine Ratio

A

Normal range is 10:1 to 20:1

30
Q

During slower blood flow rates or during ADH-induced antidiuresis (such as with renal hypoperfusion and/or lower urinary obstruction), BUN reabsorption ____ while Creatinine reabsorption _____

A

increases; stays the same.

31
Q

Fractional Excretion of Sodium (FENa)-

A

This is the percentage of sodium filtered by the kidneys that is excreted in the urine.

32
Q

Urine Microscopy findings for AKI

A

○ May reveal abnormal “sediments” that suggest certain renal
conditions as the underlying cause, such as:
■ RBCs - glomerulonephritis
■ WBCs - UTI vs intrinsic disease
■ Tubular epithelial cells - nephrotic syndrome
■ Casts

33
Q

______ can occur from
impaired renal potassium
excretion.

A

Hyperkalemia

34
Q

AKI and hyperkalemia with EKG
changes is an indication for _____

A

dialysis

35
Q

EKG findings with hyperkalemia

A

EKG may reveal peaked T waves, PR
prolongation, complete AV block, and possible ventricular arrhythmias

36
Q

_____ occurs when phosphorus cannot be
excreted by damaged tubules as it normally should.

A

Hyperphosphatemia

37
Q

Hyperphosphatemia secondary to renal failure can result in
____ due to phosphate binding the calcium.

A

hypocalcemia

38
Q

Hypocalcemia finding on EKG

A

QT prolongation

39
Q

Most common acid-base imbalance with AKI

A

○ Reabsorption of H+ and Bicarb is thrown off.
■ Often results in a Metabolic Acidosis (most common acid-base disorder seen with acute kidney injury)

40
Q

Management of AKI

A

● Once an underlying cause of AKI is discovered, treatment
should be directed at the cause:
○ Discontinue nephrotoxic medications
○ Rehydration / Volume correction
○ Treat an identified infection
○ Relief of obstruction, etc
● Additionally, monitor and adjust fluid and electrolyte balance

41
Q

_____ in AKI should be reserved for patients with
significant and symptomatic volume overload (CHF and nephrotic syndrome)

A

Diuretic therapy

42
Q

Start Renal Replacement
Therapy (AKA: Dialysis)
emergently when
_____

A

life-threatening changes in volume status, electrolytes, and acid-base balance occur

43
Q

When should a patient with AKI be admitted?

A

● Your patient should be admitted if there is sudden loss of kidney function resulting in abnormalities that cannot be handled expeditiously in an outpatient setting.
○ This includes acute hyperkalemia (especially with EKG
changes), volume overload, or uremia.
○ May also include other requirements for acute
intervention, such as emergent urologic intervention or dialysis.