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Renal 3 > Acute Kidney Injury- Dr. Alex > Flashcards

Acute Kidney Injury- Dr. Alex Flashcards

1
Q

What is acute kidney injury?

A
  • Rapid deterioration in renal function resulting in the accumulation of nitrogenous waste (BUN-Azotemia)
  • Inability of the kidney to regulate electrolyte, acid-base, and/or water homeostasis
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2
Q

What is the timeline for acute kidney injury?

A

Days to weeks in development (under 3 months)

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3
Q

What factors are not included in the definition of acute kidney injury?

A
  • No specific level of BUN or K

- Clinical signs or symptoms

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4
Q

What is diagnosed by a change in serum creatinine of greater than 0.3mg/dL in days to weeks (under 3 months)?

A

Acute Kidney Injury (AKI)

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5
Q

What is diagnosed by a decrease in GFR (over 3 months duration)?

A

Chronic Kidney Disease (CKD)

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6
Q

What is an irreverisble loss of renal function that may or may not lead to End Stage Renal Disease (ESRD)?

A

Chronic Kidney Disease (CKD)

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7
Q

What is an irreversible renal failure of a magnitude that requires renal replacement therapy to survive (dialysis or kidney transplant)?

A

End Stage Renal Disease (ESRD)

-Creatinine clearance is under 10cc/min

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8
Q

What is azotemia?

A

Elevation of the BUN (blood urea nitrogen) level

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9
Q

What is BUN?

A

One of many nitrogen based molecules that accumulates in AKI and CKD and may lead to the development of uremia

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10
Q

What is uremia?

A

The clinical SE of excess accumulation of nitrogenous compounds (nausea, vomiting, confusion, anorexia)

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11
Q

Oliguria?

A

Under 500 cc of urine output in 24 hours

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12
Q

Non-Oliguric?

A

Greater than 500 cc of urine output in 24 hours

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13
Q

Anuric?

A

Under 100 cc of urine output in 24 hours

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14
Q

What is oliguric, non-oliguric, and anuric used to describe?

A

Types of AKI

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15
Q

What is used to assess renal function?

A

GFR

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16
Q

What is an indirect predictor of GFR?

A

Serum creatinine

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17
Q

What is used for measured GFR?

A

24 hour creatinine clearance

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18
Q

What 2 mathematical formulas are used for estimated GFR?

A
  1. Cockroft and Gault

2. MDRD

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19
Q

What is serum creatinine (2 things)?

A
  1. End product of muscle metabolism

2. Cyclic anhydride of creatine (nonenzymatic)

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20
Q

Where is creatine made and stored?

A
  • Synthesized in the liver and stored in muscle (CPK)

- Also ingested orally and localized to muscle

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21
Q

What 2 ways is creatinine excreted renally?

A
  1. GFR- Filtration

2. Proximal tubular secretion

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22
Q

So, are creatine and creatinine the same thing?

A

NOPE…creatine is converted to creatinine (end product of muscle metabolism)

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23
Q

What is CPK?

A 
Creatine phosphokinase (energy source for muscles)
*Can raise serum creatinine level slightly
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24
Q

What pathway is used in the secretion of creatinine in the proximal tubule?

A

Organic cation secretory pathway

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25
Q

What % of urinary creatinine in healthy patients is from secretion?

A

15%

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26
Q

In patients with renal disease what is the % of urinary creatinine that is secreted and what is the relevance of this?

A

30-35% –> Overestimates true function since the blood level of creratinine will be lower than it really should be at any given GFR

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27
Q

What is a normal creatinine level relate to?

A

Muscle mass

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28
Q

What is normal creatinine for women?

A

Under 1.2 mg/dL (average is 0.95)

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29
Q

What is normal creatinine for men?

A

Under 1.5 mg/dL (average is 1.15)

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30
Q

What change in seru creatinine is needed to be confident that a real change in renal function has occurred?

A

0.3mg/dL

This is because the accuracy of the serum creatinine measurement is variable

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31
Q

What are the 3 cases where baseline creatinine is unusually very low (under 0.6mg/dL) and a rise of 0.3mg/DL will not increase the creatinine above the critical upper limit levels? (1.2 in woman and 1.5 in man)

A
  1. Cirrhosis: Minimal protein intake with severe malnutririon and liver failure with impaired creatine production
  2. Pregnancy: Volume expansion and an increase in GFR
  3. Extrenes of age/nutrition: Pediatric or elderly
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32
Q

In patients with cirrhosis, pregnancy, or extremes of age/nutrition, what is the serum creatinine where they can be in AKI?

A

1.1mg/dL

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33
Q

Is creatinine level an effective indicator of the degree of renal function?

A

NO, creatinine is a poor predictor of GFR

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34
Q

Is the change in serum creatinine with kidney failure linear?

A

No, it’s exponential

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35
Q

What must you use the range of normal values for serum creatinine as?

A

A relative guide

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36
Q

What must you use for each patient to determine what the normal range of creatinine for that patient should be?

A
  1. Clinical characteristics

2. Underlying medical disease state (not cause of kidney disease

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37
Q

4 tools for assessment of renal function?

A
  1. Serum creatinine
  2. Creatinine clearance
  3. Cockroft and Gault
  4. Iothalamate clearance
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38
Q

What assessment overestimates true kidney function by 15% in normal patients and by over 30% in patients with kidney failure?

A

24 hour creatinine clearance

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39
Q

Why does 24 hour creatinine clearance overestimate true kidney function?

A
  • Creatinine is filtered but also secreted by tubules

- Accuracy of 24 hour urine collection isn’t proven (retained urine in bladder and timing errors of collection)

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40
Q

What is required for 24 hour creatinine clearance?

A
  1. Complete 24 hour urine collection

2. Simultaneous measurement of urine creatinine and serum creatinine

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41
Q

What is the clearance formula?

A

[(Urine concentration)*(Urine volume)]/Plasma concentraion

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42
Q

What is creatinine clearance always expressed in?

A

mL/min

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43
Q

How many minutes are in a day?

A

1440

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44
Q

What is normal creatinine clearance?

A

90-120mL/min

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45
Q

What is the most common mistake with calculating creatinine clearance?

A

Forgetting to include the minutes per day

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46
Q

What is the Cockroft and Gault Formula?

A

(140-age)weight (kg) / (72cr)

Multiply by 0.85 for women

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47
Q

Does the Cockroft and Gault formula require urine collection?

A

NO

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48
Q

What factors does the Cockroft and Gault formula take into consideration?

A
  1. Age
  2. Weight (muscle mass)
  3. Sex (muscle mass)
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49
Q

What is the MDRD formula?

A

186 * cr^-1.154 * age^-0.203

  • 1.212 if black
  • 0.742 if female
  • More accurately predicts GFR
  • Standard used by most laboratories
  • From study…modification of diet in renal disease
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50
Q

Are all creatinine values the same?

A

NO…same creatinine level will mean different degrees of renal function based on

  • Age
  • Sex
  • Weight
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51
Q

With the same creatinine value will renal function be better (higher GFR/creatinine clearance) in

  • Men or women
  • Young or old
A

Better in men v. women and young v. old

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52
Q

Quick and dirty of the urea cycle?

A

Amino Acids –> Ammonia (NH3) –> Liver –> Urea Cycle –> Urea –> Kidneys –> Excretion

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53
Q

What is blood urea nitrogen (BUN) directly related to?

A

Protein intake (AA)…byproduct of metabolism

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54
Q

What is the constant ratio of BUN to creatinine?

A

BUN/Cr = 10-15:1 * KNOW THIS*

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55
Q

Is BUN directly toxic to the body?

A

No…it reflects the simultaneous accumulation of other nitrogenous compounds that may result in the clinical sequaela of uremia

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56
Q

Is uremic syndrome due to the accumulation of urea?

A

Not directly

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57
Q

What is uremic syndrome?

A

A constellation of clinical findings resulting from the retention of toxic nitrogenous molecules in the setting of kidney injury (acute or chronic)

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58
Q

What are symptoms of uremic syndrome?

A
  1. Confusion/disorientation
  2. Nausea/vomiting
  3. Pericarditis (pericardial friction rub)
  4. Asterizes/Myoclonus (neurologic irritability)
  5. Seizures
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59
Q

When can you see an elevation of BUN (azotemia) with normal renal function?

A
  1. Corticosteroids
  2. GI Bleeding
  3. Catabolism
  4. Increased protein intake
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60
Q

Can the BUN be used independently as a marker for kidney function?

A

NO

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61
Q

What 3 questions must be asked with approach to the patient with renal injury?

A
  1. Is it real?
  2. Is it acute or chronic?
  3. If acute- Where is the lesion?
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62
Q

What 3 situations can give spurious elevations of serum creatinine with normal renal function?

A
  1. Interference with the creatinine assay
  2. Impaired tubular secretion of creatinine
  3. Increased creatinine production
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63
Q

What 2 circumstance (where other chromogens cause a false reading) can cause interference with the creatinine assay (Jaffe reaction- Calorimetric)

A
  1. Jaunidce: Bilirubin leads to a falsely lower level of creatinine measurement
  2. Diabetic Ketoacidosis: Ketones lead to a falsely higher level of creatinine
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64
Q

What 2 drugs result in impaired proximal tubular secretion?

A
  1. Trimethoprim- Bactrim (trimethoprim and sulfamethoxazole)

2. Cimetidine (Tagement)- H2 antagonist

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65
Q

What % increase in serum creatinine does trimethoprim cause?

A

15-35%

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66
Q

What % increase in serum creatinine does cimetidine cause?

A

20%

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67
Q

Is an increase in serum creatinine seen with proton pump inhibitors?

A

No

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68
Q

What can cause increased production of creatinine?

A
  1. Rhabdomyolysis

2. Increased intake (cooked meat/AA supplements)

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69
Q

What is rhabdomyolysis?

A

-Release of creatinine from damaged muscle membrane–> Conversion of creatine peripherally to creatinine

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70
Q

What are the etiologies for rhabdomyolysis?

A
  1. Trauma
  2. Statins (HMG CoA reductase inhibitors
  3. Seizures
    * Check CPK levels in these patients
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71
Q

What are clinical clues for spurious elevations of serum creatinine with normal renal function?

A
  1. Normal level of BUN
  2. BUN/Cr ratio decrease under 10:1 (remember, normal was 10-15:1
  3. Normal urine output
  4. No obvious hemodynamic or toxic insult
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72
Q

What are 4 features of AKI?

A
  1. Renal size over 10cm *
  2. Normal echogenicity *
  3. Normal PTH level (absent osteodystrophy)
  4. Granular casts or bland sediment on urinalysis
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73
Q

What are 4 features of CKD?

A
  1. Renal size under 9cm
  2. Increased echnogenicity
  3. Elevated PTH level (renal osteodystropy)
  4. Waxy casts
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74
Q

What are 4 factors that don’t correlate with ARF or CRF?

A
  1. Calcium
  2. Phosphorous
  3. Anemia
  4. Acidosis
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75
Q

What is the purpose of a renal US?

A

Compare the echo texture of the kidneys to the liver

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76
Q

Are kidneys normally more or less echogenic than liver?

A

Kidneys are normall less echogenic than the liver due to the presence of glomeruli and tubules (the liver if more homogenous)

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77
Q

What is seen in a normal kidney US?

A

A clear differentiation is usually seen due to the difference in density of the tubules between the cortex and medulla of the kidneys (corticmedullary differentiation)
-10-12cm in length

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78
Q

What is seen on US in AKI?

A
  • No change in echogenicity

- No loss of the corticomedullary differentiation

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79
Q

What is seen on US in CKD?

A
  • Increased echogenicity of the kidneys (increased fibrosis of the cortex)
  • Decreased size
  • Loss of the corticomedullary differentiation
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80
Q

What is the first step in AKI workup?

A

Determine the site of the lesion

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81
Q

What are the 3 categories of AKI?

A
  1. Pre-renal: Inadequate perfusion of the kidney
  2. Renal: Specific damage to the kidney
  3. Post-renal: Obstruction to urinary flow with preserved perfusion
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82
Q

What are 4 potential causes of renal AKI?

A
  1. ATN
  2. Interstitial nephritis
  3. Glomerulonephritis
  4. Vascular
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83
Q

What are the etiologies of AKI in the hospital?

A
  1. ATN (48%)*
  2. Pre-renal azotemia (22%)
  3. Obstruction (11%)
  4. Acute on chronic (9%)
  5. Interstitial nephritis (5%)
  6. Glomerulonephritis (5%)
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84
Q

What are the etiologies of outpatient AKI?

A
  1. Pre-renal azotemia (66%)*
  2. Acute GN (14%)
  3. Obstructive uropathy (10%)
  4. Acute interstitial nephritis (10%)
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85
Q

What are the 3 categories of AKI?

A
  1. Pre-renal: Inadequate perfusion of the kidney
  2. Renal: Specific damage to the kidney
  3. Post-renal: Obstruction to urinary flow with preserved perfusion and lack of direct nephrotoxic damage
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86
Q

What is pre-renal azotemia?

A

A state of underperfusion of the kidneys

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87
Q

What is the normal response of the kidney to underperfusion?

A
  • Expand intravascular volume

- Initiate renal autoregulation

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88
Q

How do the kidneys expand intravascular volume?

A
  1. They reabsorb sodium: 80% in proximal tubule, 20% in TALH, under 5% in DCT
  2. The reabsorb water: Collecting duct via ADH
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89
Q

What is MAP?

A

(Systolic-diastolic) * 1/3 + Diastolic

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90
Q

If BP is 120/80, what is MAP?

A

93

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91
Q

If BP drops to 80/50, what is MAP?

A

60

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92
Q

What is renal autoregulation?

A

The ability of the kidney to maintain adequate blood flow and GFR through a wide range of systemic blood pressures…a complex interaction of multiple enzyme and cytokine systems

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93
Q

What systems are involved in renal autoregulation?

A
  1. Renin-angiotensin
  2. Prostaglandin
  3. Neurohumoral
  4. Endothelial
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94
Q

What 2 things does hypovolemia induce?

A
  1. Activation of local myogenic response

2. Activation of carotid and cardiac baroreceptors

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95
Q

What does activation of carotid and cardiac baroreceptors lead to?

A
  1. Increased neurohumoral responses
  2. Norepinephrine
  3. Angiotensin II
  4. ADH
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96
Q

Where are filatration pores located?

A

In the basement membrane of the endothelial cell (In the glomerular capillary)

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97
Q

What is a podocyte?

A

Visceral epithelial cell (these contain foot processes)

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98
Q

In hypoperfusion does the intraglomerular pressure increase or decrease?

A

Decrease

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99
Q

In hypoperfusion, the kidneys will renal autoregulate to bring the intraglomerular pressure close to normal via what 2 mechanisms?

A
  1. Afferent arteriolar vasodilation

2. Efferent arteriolar constriction

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100
Q

What 3 substances cause afferent arteriolar vasodilation?

A
  1. PGE2/PGI2
  2. NO
  3. Dopamine
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101
Q

What substance causes efferent arteriolar constriction?

A

Angiotensin II

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102
Q

What is filtration fraction (FF)?

A

GFR/RBF

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103
Q

What is FF in normal perfusion?

104
Q

What is RBF, GFR, and FF in hypoperfusion?

A

RBF and GFR are decreased equally, so FF is still 0.20

105
Q

What is RBF, GFR, and FF in autoregulation?

A

RBF is increased, GFR is super increased, and FF is greater than 0.20

106
Q

What is a big player in renal autoregulation?

A

The juxtaglomerular apparatus

107
Q

What are the 3 components of the JGA?

A
  1. DCT: Macula densa
  2. Afferent arteriole: Juxtaglomerular cells
  3. Lacis cells: Extraglomerular mesangial cells
108
Q

What is the cascade from prostaglandins released by the macula densa cells in the DCT?

A

Prostaglandins –> Renin (from the juxtaglomerular cells in the afferent arteriole) –> Angiotensin I –> Angiotensin II –> Aldosterone (adrenal gland)

109
Q

What are 4 causes of pre-renal azotemia decreased effective circulating volume

A
  1. Absolute volume depletion
  2. Relative volume depletion
  3. Impaired cardiac output
  4. Impaired renal autoregulation
110
Q

What are 5 categories of pre-renal azotemia absolute volume depletion?

A
  1. GI: Diarrhea and vomiting
  2. Hemorrhage
  3. Sweating
  4. Renal: Diuresis (osmotic or diuretics) and salt-wasting
  5. Burns
111
Q

What is pre-renal azotemia relative volume depletion?

A 
3rd spacing (interstitial space)
-1st space is intravascular and 2nd space is intracellular
112
Q

What 3 conditions lead to 3rd spacing (interstitial space) in pre-renal azotemia?

A
  1. Hypoalbuminemia: Nephrotic syndrome, liver disease, malnutrition
  2. Pancreatitis
  3. Sepsis
113
Q

What are the cardiac/pulmonary dysfunctions leading to relative volume depletion in pre-renal azotemia?

A
  1. Cardiomyopathy
  2. Valvular disease
  3. Myocardial infarction
  4. Tamponade
  5. Pulmonary HTN
  6. Renal artery stenosis
114
Q

What conditions cause low CO states or cardio-renal syndrome?

A

Cardiomyopathy, valvular disease,MI, and tamponade

115
Q

What 2 causes of abnormal autoregulation can lead 2 pre-renal azotemia?

A
  1. Blockade of angiotensin activity (ACEi or ARBs)

2. Prostaglanin inhibitos (NSAIDS which inhibit the enzyme cyclooxygenase)

116
Q

What are psotaglandins?

A

A group of lipid compounds derived from essential fatty acids
-Originally isolated from the prostate (seminal fluid) in 1935

117
Q

Where are prostaglandins found?

A

In all tissues and organs

  • Autocrine (self-stimulatory)
  • Paracrine (locally active)
118
Q

What converts cell membrane phospholipids into arachidonic acid?

A

Phospholipase A

119
Q

What converts arachidonic acid into prostaglandins?

A

Cyclooxygenase (COX)

120
Q

What are the 3 drug categories that disrupt renal autoregulation?

A
  1. NSAID
  2. ACEi
  3. ARB
121
Q

What are some examples of NSAIDs?

A
  1. Ibuprofen (motrin or alleve)
  2. Naprosyn
  3. Toradol
  4. Vioxx
  5. Celebrex
122
Q

What are some examples of ACEi?

A
  1. Catopril
  2. Ramipril
  3. Zestril
  4. Lisinopril
  5. Enalapril
123
Q

What are some examples of ARBs?

A
  1. Losartan
  2. Irbesartan
  3. Candesartan
  4. Olmesartan
124
Q

What do NSAIDs block?

A

Cyclooxygenase (prevents arachidonic acid from converting to PGG2 and PGH2)
-Ultimately prevent formation of prostacyclins which cause vasodilation and renin production

125
Q

What way do NSAIDs shift the range for MAP?

A

To the right

126
Q

What is the effect in the renal vasculature of an ACEi or ARB?

A

Dilated efferent arteriole with reduced intraglomerular pressure due to absent or blocked angiotensin II

127
Q

What way to ACEi/ARB shift the range for MAP?

A

To the right

128
Q

Overall effect of NSAIDs?

A

-Affterent arteriolar constrictionand efferent arteriolar vasodilation leading to decreased intraglomerular pressure

129
Q

Overall effect of ACEi/ARB?

A

Efferent arteriolar vasodilation leading to decreased intraglomerular pressure

130
Q

How do NSAIDs affect RBF/GFR/FF?

A

They decrease RBF and GFR proportionately so filtration fraction is still 0.20

131
Q

How do ACEi and ARB affect RBF/GFR/FF?

A

They decrease RBF and super decrease GFR so filatraion fraction is less than 0.20 (because FF = GFR/RBF)

132
Q

Who are the patients at highest risk for AKI due to impaired renal autoregulation?

A
  1. CHF
  2. Cirrhosis
  3. Nephrotic
  4. Renovascular disease- renal artery stenosis (bilateral)
    * Use of ACEi or ARB in these patients requires very careful and frequent monitoring
133
Q

What is COMPLETELY PROHIBITED in patients at highest risk for AKI due to impaired renal autoregulation?

134
Q

Is a normal individual with euvolemia at risk from NSAID or ACEi/ARB?

135
Q

Why are ACEi/ARB high recommended for patients with CKD?

A

The benefit of these agents in preserving renal function exceeds any potential risk of AKI… ACEi/ARB are reno-protective!
(Renal artery stenosis is excluded by clinical and radiologic studies)

136
Q

What can intrinsic AKI lead to?

A

Acute tubular necrosis (ATN)

137
Q

What are the 2 types of ATN and their %?

A
  1. Ischemic (60%)

2. Toxic (40%)

138
Q

Which part of the kidney has a higher oxygen delivery and oxygen content?

A

Cortex (v. medulla)

139
Q

What is the O2 comsumption/O2 delivery ratio in the outer medulla?

A

79% –> The outer medulla operates in a delivate balance as it consumes almost all of the oxygen delivered

140
Q

What structures are in the cortex?

A
  1. Proximal Tubules: Pars Recta (further from the glomerulus) and Pars Convoluta (closer to the glomerulus)
  2. Outer Medulla: Proximal tubules (pars recta) and TALH (thick ascending limb of henle)
141
Q

What structures are in the outer medulla?

A
  1. Proximal tubules: Pars Recta

2. TALH: Thick Ascending Limb of Henle

142
Q

What structures are in the inner medulla?

A
  1. Thin Descending Limb of the Loop of Henle
  2. Thin Ascending Limb of the Loop of Henle
  3. Collecting Duct
143
Q

Where do you see ischemic injury in AKI?

A

Outer Medulla:

  • Proximal Tubule: Pars recta
  • TALH (major site)
144
Q

Where do you see toxic injury in AKI?

A

Proximal tubule (pars convoluta) over the distal tubule

145
Q

What can prolonged pre-renal azotemia lead to?

146
Q

How does prolonged pre-renal azotemia lead to ATN?

A

Due to the high O2 requirements for sodium absorption, cellular ischemia will result if impaired delivery of blood remains prolonged

  • Breakdown of cell membrane
  • Entry of Ca and efflux of intracellular contents leading to cell death and sloughing of the renal tubular cell in the urine
147
Q

What is progression of prolonged hypotension/shock/hypoperfusion os the kidneys (intrinsic AKI)?

A

This leads to pre-renal azotemia which can lead to ATN

148
Q

Why is there an increased risk of ATN from toxins?

A

Increased risk secondary to:

  1. High delivery of blood flow: 25% of CO
  2. Concentration of toxins in the medulla and interstitium through the countercurrent mechanism
  3. Organic transporters: Proximal tubule
  4. Local metabolism to toxic compounds
149
Q

What is a common clinical cause of ATN?

A

Radiology material:
-IV contrast is an iodinated compound that is directly toxic to the proximal tubule and extreme care must be taken when using these agens in patients with CKD

150
Q

What are 2 drugs that can cause ATN?

A
  1. Aminoglycosides: Antibiotics for gram - infections (gentamycin, tobramycin, amikacin)
  2. Amphotericin: Antifungal agent
151
Q

Where are aminglycosides toxic?

A

Proximal tubule

152
Q

Where is amphotericin toxic?

A

Distal tubule (still considered a form of ATN

153
Q

What are 2 intrinsic structures that can cause ATN?

A
  1. Heme pigments: Released from damaged muscle cells (rhabdomyolysis) or damaged red cells (hemolysis) leading to toxicity in the proximal tubule
    2, Light chains: More Kappa than Lambda from overflow proteinuria as a result of hemtopoeitic malignancy (myeloma) that cause proximal tubule damage
154
Q

Can rhabdomyolysis cause both a false elevation of the creatinine and cause actual ATN?

155
Q

Is pre-renal azotemia rapidly reversible?

156
Q

Can you recover from ATN?

A

It will require 2-3 weeks for recovery and possible temporary or permanent dialysis

157
Q

What does the diagnostic workup for AKI include?

A
  1. Check volume status of the patient
  2. Rule out obstruction
  3. Urinary electrolytes
  4. Urinalysis
158
Q

What are signs of volume overload?

A
  1. DOE (Dyspnea on exertion)
  2. Orthopnea
  3. PND (paroxysmal nocturnal dyspnea)
  4. JVD (jugular venous distension)
  5. Rales
  6. LE (lower extremity) edema
  7. Ascites
  8. Peri-orbital edema
  9. HTN (Systolic > 140 mmHg))
  10. S4 gallop
159
Q

What are signs of volume depletion?

A
  1. Poor skin turgor
  2. Dry mucosa : Axillae / oral cavity / vaginal- groin
  3. Orthostatic hypotension: Decreased systolic (>20 mmHg) and diastolic BP (>10 mmHg) with upright position, Increased heart rate (> 100 bpm)
  4. Absent edema
  5. Absent JVD
160
Q

Why is radiology used in the diagnosis of AKI?

A

Because obstruction can account for 10% of cases of AKI

161
Q

What imaging techniques are used for diagnosis of AKI?

A
  1. US: Preferred modality
  2. MRI: No Gaolinium (In renal failure may lead to an irreversible systemic inflammatory condition with diffuse organ fibrosis- Nephrogenic systemic fibrosis)
  3. CT Scan: No IV contrast (nephrotoxic)
162
Q

What is done for laboratory evaluation of AKI?

A
  1. Urine Na
  2. FENA (Fractional Excretion of Sodium)
  3. FEUREA (Fractional Excretion of Urea)
  4. BUN/Cr ratio
  5. Urine Specific Gravity
  6. Urinary Sediment
163
Q

What happens in pre-renal azotemia?

A

The kidney is underperfused so it will make every effort to restore the intravascular volume

164
Q

How does the kidney try to restore the intravascular volume?

A
  1. Sodium and water reabsorption (sympathetic nervous system): Proximal tubule, TALH, and distal tubule
  2. Water reabsorption (ADH production): Collecting duct
165
Q

What is the urine sodium concentration in pre-renal azotemia?

A

Markedly reduced… a random urine sodium will be under 20mEq/L (intense sodium avidity)

166
Q

What is the urine sodium concentration in ATN?

A

Over 40mEq/L- No attempt at sodium retnention

-In ATN, the tubules are physically damaged so sodium cannot be retained adequately

167
Q

What is the fractional excretion of sodium (FENA)?

A

It compares the clearance of sodium to the clearance of creatinine and is expressed as a %

168
Q

What is FENA is a sodium avid state (the proximal tubule is absorbing as much sodium as possible)?

A
  • Creatinine will continue to be secreted (also by the proximal tubule)
  • Clearance of sodium will decrease while the clearance of creatinine does not decrease to the same degree
  • As a ratio, the clearance of sodium / clearance of creatinine will decrease*
169
Q

What does the calculation of FENA require?

A

Simultaneous:

  • Urine sodium
  • Urine creatinine
  • Serum sodium
  • Serum creatinine
170
Q

What is the formula for FENA?

A

(Una/Pna)/(Ucr/Pcr) * 100

171
Q

If FENA is under 1%?

A

Sodium retention (pre-renal azotemia)

172
Q

If FENA os over 2%?

A

Sodium diuresis (ATN)

173
Q

Is volume used in the calculation for FENA?

A

No, because it is the same in numerator and denominator and cancels itself out

174
Q

What is a big problem with interpretation of FENA?

175
Q

If a patient has effective diuresis therapy, what does this do to FENA?

A

I causes and increase in FENA…so

  • Elevated FENA is not meaningful during diuretic therapy
  • Need to stop diuretics 48 hours or more for the effect to wear off
176
Q

What does a low FENA indicate in diuretic therapy?

A

Ineffective diuresis

177
Q

What lab value can suggest pre-renal azotemia and what lab value confirms pre-renal azotemia?

A

Urina Na: Suggests

FENA: Confirms

178
Q

Will a patient with pre-renal azotemia respond to fluid replacement?

A

YES… need to fill the intravascular compartment as quickly as possible

179
Q

What is the BUN/Creatinine ratio?

A

A clinical tool to provide an indirect marker for volume status in the setting of renal failure

180
Q

What is normal BUN/Cr ratio?

181
Q

What happens to the BUN/Cr ratio in volume depletion?

A
  • The BUN will increase to a greater extent than the creatinine secondary to obligate creatinine secretion in the proximal tubule and BUN reabsorption
  • BUN/Cr ratio will increase above 20:1
182
Q

What Happens to the BUN/Cr ratio in established renal injury (ATN or CKD)?

A

BUN and Creatinine will increase to the same proportion since the tubules are damaged to the same extent as the glomeruli preventing creatinine secretion
-Ratio stays the same

183
Q

BUN/Cr ratio > 20:1 in the presence of an elevated creatinine?

A

Volume depletion –> Pre-renal azotemia

184
Q

BUN/Cr ratio = 10-15:1 in the presence of an elevated creatinine?

A

Intrinsic renal failure (ATN or CKD)

185
Q

Can the BUN/Cr ratio confirm pre-renal azotemia?

186
Q

What is urea?

A

A nitrogenous compound derived from protein metabolism

187
Q

What is BUN?

A

Blood urea nitrogen: An indirect measurement of the amount of urea by detecting only the 2 nitrogens within the molecule

188
Q

Where is BUN absorbed?

A

In the proximal tubule with water passively

189
Q

What happens to the absorption of BUN (urea) in patients with volume depletion?

A

It increases

190
Q

What happens with regards to the handeling of creatinine?

A

It is absorbed also, but then i gets secreted in the tubule

191
Q

So what is the Fractional excretion of urea in patients with volume depletion?

A

The fractional excretion of BUN (urea) compared to creatinine will decrease

192
Q

What is the formula for fractional excretion of urea?

A

(U urea nitrogen/Pbun) / (Ucr/Pcr) * 100

193
Q

If the fractional excretion of urea is under 35% what does this indicate?

A

Pre-renal azotemia

194
Q

If the fractional excretion of urea is over 50% what does this indicate?

A

Intrinsic AKI (ATN or CKD)

195
Q

When if the fractional excretion of urea useful?

A

In patients on diuretics which will increase the FENA and mask pre-renal azotemia
-Diuretics don’t affect BUN absorption

196
Q

What is urine specific gravity used for?

A

A marker for urinary concentration…this reflects the removal of water from the urine by the action of ADH on the collecting tubules

197
Q

What is the definition of urine specific gravity?

A

The “weight” of urine compared to water

198
Q

What is the specific gravity value of water?

A

1 (nothing can be less than this)

199
Q

What does urine specific gravity correlate with?

A

The osmole concentration of urine (for every 30mosm/L increase in the urine, the specific gravity increases by 0.001)

200
Q

What isosthenuria?

A

Urine that is neither concentrated nor diluted (the same osmolality as plasma)

201
Q

What is the osmolality and specific gravity of isothenuria?

A

Osmolality: 300

Specific gravity: 1.010

202
Q

What is concentrated urine?

A

Due to increased ADH

-Urine osmolality is greater than 450-500 and specific gravity is greater than 1.015

203
Q

What kind of urine is seen with damaged tubules?

A

Isosthenuric (specific gravity of 1.010)

-Damaged tubules won’t respond to ADH

204
Q

Lab Values for Pre-renal Azotemia?

A
  1. Urine Sodium: Under 20
  2. Urine Osmolality: Greater than 500
  3. Specific Gravity: Greater than 1.015
  4. FENA: Under 1%
  5. BUN/Cr: Over 20:1
205
Q

Lab Values for ATN?

A
  1. Urine Sodium: Over 40
  2. Urine Osmolality: 280
  3. Specific Gravity: 1.010
  4. FENA: Over 2%
  5. BUN/Cr: 10-15:1
206
Q

What is seen on urinalysis in ATN?

A
  1. Renal tubular cells
  2. Granular casts
  3. Muddy brown casts
  4. Renal tubular cells casts
207
Q

What are casts made of and where are they derived from?

A

Tamm-Horsfall glycoprotein (derived from the ascending limb of the loop of henle)

208
Q

Are hyaline casts normal constituients?

A

YES… they are not indicative of renal disease**

209
Q

Are granular casts normal constituents?

A

NO…they are indicative of acute tubular damage…NOT A NORMAL CONSTITUENT

210
Q

Are granular casts present in pre-renal azotemia?

211
Q

What are waxy casts indicative of?

A

CKD… the injury has been present for more than 3 months

212
Q

Are RBCs, WBCs, RBC casts, waxy casts, or granular casts seen in evaluation of pre-renal azotemia?

213
Q

Are RBCs, WBCs, RBC casts, waxy casts, or granular casts seen in evaluation of ATN?

A

Just granular casts

214
Q

Are RBCs, WBCs, RBC casts, waxy casts, or granular casts seen in evaluation of CKD?

A

Just waxy casts

215
Q

Are RBCs, WBCs, RBC casts, waxy casts, or granular casts seen in evaluation of CKD and AKI?

A

Waxy casts and granular casts

216
Q

Can patients with CKD develop AKI?

217
Q

What is clue in urinalysis that a CKD patient developed AKI?

A

Granular and waxy casts

218
Q

What are the 6 features of management of AKI?

A
  1. HTN control
  2. Anemia control
  3. Dietary modification
  4. Calcium and Phosphorous balance
  5. Acid-Base Balance
  6. Potassium Control
219
Q

What is a natural accompaniment of all forms of AKI?

A

Impaired K secretion in the distal tubule

220
Q

What needs to be initiated early in AKI?

A

Potassium dietary restriction

221
Q

What factors predispose to increased K?

A
  1. Catabolism
  2. GI Bleed
  3. Constipation
  4. K sparing drugs (ACEi, All blockers, Bactrim, NSAIDS)
222
Q

How do NSAIDs lead to hyperkalemia?

A

NSAIDs block prostaglandins, so they never cause renin secretion, which never causes aldosterone secretion (No aldosterone, no Na reabsorption, and K secretion) which leads to hyperkalemia

223
Q

How do ACEi lead to hyperkalemia?

A

ACEi block conversion of angiotensin I to angiotensin II, which means that aldosterone is blocked, leading to hyperkalemia

224
Q

How to ARB cause hyperkalemia?

A

ARB block antiotensin II receptors, which cause blockage of secretion of aldosterone, leading to hyperkalemia

225
Q

How does trimpethoprim affect creatinine secretion?

A

It impairs creatinine secretion in the proximal tubule leading to false elevation of creatinine with normal GFR

226
Q

What does the chemical structure of trimethoprim resemble and what is the effect of this?

A

It resembles amiloride, which is a K-sparing diuretic in the distal tubule and leads to hyperkalemia

227
Q

What does hyperkalemia cause in terms of EKG?

A
  1. Peaked T-waves
  2. Loss of P wave (Sinus node failure)
  3. Widening of QRS (Slow conduction)
  4. Sine wave pattern (Cardiac arrest)
228
Q

With normal K levels, what is the resting membrane potential and threshold potential?

A

Resting: -90mV
Threshold: -60mV

229
Q

What is nerst equation for resting membrane potential (RMP)?

A

RMP = -61 log (K intracellular/K extracellular)

230
Q

What does hyperkalemia do to the RMP?

A

Becomes less negative

231
Q

What does hypokalemia do to the RMP?

A

Becomes more negative

232
Q

In hyperkalemia is the threshold potential for spontaneous depolarization increased or decreased?

A

Its decreased (because hyperkalemia causes the RMP to become less negative)

233
Q

Along with making the RMP less negative, what else does hyperkalemia do to the AP?

A

It can lead to an inability to repolarize since the RMP is above threshold potential

234
Q

What does increased Ca do to the AP?

A

In increases the threshold potential

235
Q

If Ca increases the threshold potential, what does this mean for treatment of hyperkalemia?

A

You can use Ca to treat hyperkalemia

236
Q

What does K affect in the AP?

A

The resting membrane potential (it makes the RMP less negative and results in spontaneous depolarization, but prevents repolarization)

237
Q

What does Ca affect in the AP?

A

If affects the threshold potential of the cell (Increase Ca will make the threshold potential less negative making it harder for the cell to depolarize)

238
Q

What 4 things can be done to treat symptomatic hyperkalemia (EKG changes)?

A
  1. Antagonize membrane effects (Calcium)
  2. Redistribute K from extracellular to intracellular environement (insulin and beta-2 receptor stimulation)
  3. Remove K from body (Exchange resin: Kayexalate, dialysis)
  4. Bicarbonate therapy (only if severe acidosis is present)
239
Q

What does exchange resin (Kayexalate) do?

A

Exchanges a K for a Na in the colon

240
Q

What do insulin and beta-2 receptor stimulation do to redistribute K from extracellular to intracellular?

A

Increase the Na/K ATPase pump stimulation

241
Q

What are 5 indications for dialysis in ARF?

A
  1. Uncontrolled hyperkalemia
  2. Intractable fluid overload
  3. Uremia
  4. Pericarditis
  5. Intractable metabolic acidosis
242
Q

Is there any proven benefit of any treatment in enhancing recovery of ATN?

A

No (Dopamine and diuretics- Lasix)

243
Q

What is the purpose of treatment in ATN?

A

Supportive to allow time for tubular regeneration

244
Q

What is dopamine?

A

A neurotransmitter that binds to peripheral receptors (D1/D2 receptors in the kidney)

245
Q

What does dopamine do in the kidney?

A
  1. Dilates the afferent and efferent arteriole (no change in GFR or FF)
  2. Inhibits proximal tubular Na re-absorption (increased urine output and natriuresis)
246
Q

Since ATN is a result of cell damage, what does this mean with regards to agents used?

A

No improvement can occur with agents that increase renal blood flow or cause a higher urine output

247
Q

What are the 4 phases of AKI?

A
  1. Initiating Phase
  2. Oliguric Phase
  3. Diuretic Phase
  4. Recovery Phase
248
Q

What is the initiating phase?

A

Time of exposure to hemodynamic or toxic insult

249
Q

What is the oliguric phase?

A

-Period of oliguria (67%)

Urine volume is under 400cc/day

250
Q

When do most patients die from AKI?

A

In the oliguric phase

251
Q

What is the duration of AKI during the oliguric phase?

A

10-14 days

252
Q

What is the diuretic phase?

A
  • Increasing urine output (non-oliguric)

- No change in renal function

253
Q

What is the recovery phase?

A

-May last 3-12 months before full functional recovery occurs (acid base/water homeostasis)

254
Q

What are 4 outcomes of ATN and their associated %?

A
  1. Death: 50%
  2. Complete recovery: 15%
  3. Partial recovery: 30%
  4. Dialysis dependent: 5%
255
Q

What are 5 causes of death in AKI and their associated %?

A
  1. Pneumonia: 35%
  2. Gram negative sepsis: 30%
  3. GI Bleed: 10%
  4. Cardiac: 20%
  5. Hyperkalemia: 5%
256
Q

What 5 things does the buildup of uremic toxins do in AKI that can lead to death?

A
  1. Impairs immune system (decreases antibody production)
  2. Reduces the function of PMNs (phagocytosis)
  3. Increase the permeability of the skin and GI barriers to bacterial translocation
  4. Decreases platelet function (GI BLEED)
  5. Na and water overload (CHF/MI)
    * The first 3 lead to infection
257
Q

What are the 9 things in the check-list approach to AKI?

A
  1. Document with repeat values for BUN and Cr
  2. Assess for spurious increases in BUN and Cr
  3. Look at BUN/Cr ratio
  4. Evaluate hemodynamic status
  5. Look for nephrotoxin exposure
  6. Examine the urinary sediment and urinary indices- FENA, Urine Na, Specific gravity
  7. Order radiologic evaluation of the kidneys
  8. Follow course of electrolytes / volume status / nutrition on a daily basis
  9. Watch the potassium level !

Renal 3 (17 decks)

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