9/16- Acute Kidney Injury (AKD) Flashcards

1
Q

Knowing a pt’s GFR is how we clinically estimate kidney fct. The serum creatinine is an easy marker to use since it is easy to measure in the blood. However, which of the following properties make the serum creatinine an imperfect marker?

A. Not free filtered by glomerulus

B. Secreted by tubules (overestimates GFR)

C.

A

Knowing a pt’s GFR is how we clinically estimate kidney fct. The serum creatinine is an easy marker to use since it is easy to measure in the blood. However, which of the following properties make the serum creatinine an imperfect marker?

A. Not free filtered by glomerulus

B. Secreted by tubules (overestimates GFR)

C.

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2
Q

What is acute kidney disease (AKD)?

A
  • Acute damage to kidney
  • Syndrome; can be caused by many things
  • Usually reversible, but residual kidney damage is possible
  • Chronic Kidney Damage (CKD) may result years after AKD
  • Diagnosis of AKD hampered by its relative asymptomatic nature in early stages
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3
Q

What are some possible causes of AKD?

A
  • Urinalysis
  • BUN
  • Creatinine

Damage may or may not be present (can have either damage or functional changes and then gain the other)

  • Damage without functional change = AKD
  • Damage with functional change = AKD or CKD
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4
Q

What are clinical indicators of kidney injury?

A
  • Urine output
  • Blood chemistry
  • Estimate of glomerular filtration
  • History comaptible with kidney injury
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5
Q

What is the specific definition of AKD?

A

ONE OF:

  • Rise in serum creatinine > 0.3 mg/dL within 48 hours
  • Rise in serum creatinine > 1.5x the baseline within previous 7 days
  • Urine volume < 0.5 mL/kg/hr for 6 hrs
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6
Q

Creatinine estimates ___

A

Creatinine estimates GFR

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7
Q

Damage to any part of the nephron results in what?

How does this affect GFR?

A

Decreased reabsorption

  • Tubulo-glomerular feedback ensures that GFR falls to match decreased reabosrption

(Thus decrease in GFR indicates alteration or damage of renal mechanisms)

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8
Q

Case)

  • 35 yo pregnant woman found to have placenta percreta
  • Emergency C-section and hysterectomy
  • 1 wk chronic abdominal pain worse than expected post op
  • Sudden drop BP 70/P, altered mental status, O2 desaturation, WBC increases to 17,000, urine output stops, Creat increases form 0.6 to 1.3 mg/dL (1.3 is in normal range!), intubated
A

Had ruptured colon, fluid challenge, emergent surgical repair, recovery in 24 hours

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9
Q

Diagnostic approach to analyzing AKD: what is the renal rule of 3 (broad overview)?

A

Acute kidney disease (AKD):

1. Prerenal- not the kidney’s fault

2. Intrinsic/Renal- parenchymal disease of any sort

  • Glomeruli
  • Tubules
  • Space in between glomeruli/tubules

3. Postrenal- urinary obstruction at any level

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10
Q

What is pre-renal AKD? Processes occurring?

A

In pre-renal states, kidneys are not initially damaged, but can progress to AKD

Pre-renal states without AKD:

  • Intense volume reabsorption
  • Fall in capillary pressure, decreased glomerular surface area
  • Increased reabsorption by tubules
  • RAS, Aldo, ADH, SNS activated
  • Kidney still anatomically normal (can reverse rapidly with correction)
  • If toxin in blood, kidney will inadvertently concentrate it in the tubules; possibly -> renal damage/injury

Pre-renal state, now AKD:

  • All of the above physiological changes
  • Kidney damage identifiable
  • Commonly acute tubular necrosis develops
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11
Q

What are some pre-renal etiologies?

A

Kidneys function as if pt is hypovolemic

Decreased vascular volume:

  • Bleeding
  • GI losses
  • Insensible losses
  • Diarrhea
  • Diuresis

Ineffective Circulating Volume

  • Sepsis
  • Heart Failure
  • Cardiogenic shock
  • Liver failure
  • Pre-eclampsia

COMMON CAUSES of PRE-RENAL STATE

  • Hepatorenal syndrome
  • Renal Artery stenosis
  • Congestive heart failure
  • NSAIDS

KEY:

  • A pre-renal cause of AKD does not mean volume contraction
  • You may or may not need to give the patient fluid
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12
Q

Pre-renal vs. intrinsic kidney damage compare/contrast in terms of:

  • BUN: creatinine ratio
  • Urinalysis
  • Urine sodium
  • FeNa
  • Urine Osmolality
A
  • Relatively more BUN in pre-renal than intrinsic damage states
  • Pre-renal urinalysis is normal while it contains cellular material, RBC, and WBC in intrinsic damage
  • Urine sodium high in intrinsic damage; low pre-renal
  • FeNa follows urine sodium trend (higher in intrinsic damage)
  • Urine osmolality is greater than serum in pre-renal states but ~ same as serum in intrinsic damage
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13
Q

What is hepatorenal syndrome?

A

Severe liver failure causing intense pre-renal state

  • Kidneys anatomically normal and renal function normalizes after liver transplant
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14
Q

What is renal artery stensosis?

A

Kidney not perfused; thinks pt is dry

-> pre-renal state

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15
Q

How does CHF -> pre-renal state?

A

Low cardiac output state and low renal perfusion trigger intense sodium and volume conservation

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16
Q

How do NSAIDs-> pre-renal state?

A

Prostaglandin inhibition prevents renal regulation when volume depletion, CHF, or hepatorenal syndrome present

17
Q

Pre-renal state increases the risk of what? How?

A

Tubule and interstitial damage

  • Pre renal state stresses kidney tissue by increasing osmolality of medulla, and increasing tubule transport and ATP utilization
  • Pre renal state increases cellular concentrations of renal toxins, when present, increasing risk of tubule damage
18
Q

What are some parenchymal causes of AKD?

A
  • Glomerulonephritis
  • Acute tubular necrosis
  • Cortical necrosis
  • Papillary necrosis
  • Renal vascular disease
  • Inflammatory processes of interstitial space (Infection, NSAIDS, many others)
  • Urinary tract obstruction (?)
19
Q

How is polyuria defined? What can cause it?

A

Polyuria is > 3 L/day

  • May be normal if large volume of water consumed

Abnormal causes:

  • Osmotic diuresis (e.g. glucosuria if out of control diabetes)
20
Q

How is oliguria defined?

A

< 500 mL/day

21
Q

How is anuria defined?

A

< 50 mL/day

  • Not common
  • Suggests specific differential diagnosis
22
Q

What could cause anuria?

A

Most likely:

  • Urinary tract obstruction (most common cause!)
  • Vascular disaster: no renal blood flow

Less likely:

  • Intense pre-renal states (severe heart or liver failure, fatal sepsis)
  • Acute glomerular nephritis (rare cause)
  • Acute tubular necrosis (rare cause)
23
Q

What can be seen on x-ray? Indications?

A

KUB (Kidney, Ureters, Bladder)

Indications:

  • Calcifiations
  • Stones

Simple and inexpensive, but lacks details

24
Q

What are advantages/disadvantages of renal ultrasound? Indications?

A

Indications:

  • Obstruction
  • Parenchymal disease
  • Doppler blood flow

Advantages

  • Safe, no contrast
  • Widely available
  • GFR independent

Disavantages

  • Doesn’t show ureteral anatomy well
  • Lower resolution than CT
25
Q

What is IVP? Advantages/disadvantages? Indications?

A

Intravenous pyelography

Indications:

  • Hematuria, stones
  • Malignancies
  • Congenital anomalies

Advantages:

  • Simple, inexpensive
  • Shows collecting system and bladder wall

Disadvantages:

  • Poor parenchymal resolution
  • Dye toxicity, renal insufficiency In picture: right side is blocked! (less dye in other side because it has already gone down)
26
Q

CT scan and MRI: Indications? Advantages/Disadvantages?

A

Indications:

  • Tumors, trauma
  • Vascular images

Advantages:

  • High resolution
  • Non-invasive

Disadvantages:

  • Expensive
  • Dye toxicity
  • Claustrophobia
27
Q

Renal angiography indications? Advantages/disadvantages?

A

Indications:

  • Renal vascular disease
  • Transplant donor

Advantages

  • Precise vascular imaging
  • Angioplasty

Disadvantages

  • Invasive
  • Dye nephropathy
  • Expensive
28
Q

Overview of tests used to look at kidneys:

  • KUB
  • IVP
  • CT/MRI
  • US
A

- KUB: Simple, but doesn’t tell you much

- IVP: Shows urinary system well. Requires good kidney function to excrete dye into urinary tract

- CT/MRI: Very informative but expensive, involves contrast, and a hassle

- US: Simple, non invasive, but doesn’t show urinary tract

29
Q

What is the natural history of AKD?

A
  • Multi-organ consequences (brain, lung, liver, GIT, bone marrow, heart)
  • AKD generally recovers (typ under 3 wks)
  • Severe renal damage may not heal, leading to chronic kidney disease
  • Overall outcome may depend on effects of AKD on other organs