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CDM exam 2 > Renal Material > Flashcards

Renal Material Flashcards

1
Q

Things to look for to determine Prerenal

A 
20:1 BUN/Scr ratio
increase of BUN rapidly
no evidence of cell death
no RBC
no WBC
Urine Na < 20mEq/L
FeNA % <1 (conserving)
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2
Q

Things to look for to determine Intrarenal

A 
16:1 BUN/Scr ratio
Scr doubles, BUN increases (not as rapidly as prerenal)
muddy brown casts 
RBC, WBC
Urine Na >40 mEq/L
FeNA% >2 (wasting)
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3
Q

Things to look for to determine Postrenal

A 
16:1 ratio BUN/Scr
cellular debris
RBC -variable
WBC -1+
>40 mEq/L
FeNA% >2 (wasting) 
blockage/ obstruction
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4
Q

Prerenal AKI also known as

A

Prerenal Azotemia

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5
Q

Prerenal involves changes in

A

Volume and tone

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6
Q

Prerenal occurs in

A

afferent and efferent arterioles (Glomerulus)

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7
Q

Risk factors for prerenal

A 
Age
Diuretic use 
Poor oral intake 
GI fluid loss
CHF
Renal Artery Stenosis
ACEi/ARBs
NSAIDs
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8
Q

Prerenal Treatment

A

Fluid replacement with NaCl

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9
Q

Intrinsic kidney injury also known as

A

Intrarenal AKI

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10
Q

What is intrinsic kidney injury

A

structural damage to glomerulus, tubules or interstitium which often occur due to prolonged prerenal causes

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11
Q

Intrinsic kidney injury leads to

A

renal cell necrosis by mechanisms of ischemia, infection or immune response that result in inflammation

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12
Q

3 types of intrinsic kidney injury

A

Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN)
Glomerulonephritis

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13
Q

Diagnosing with ATN

A

muddy brown casts
epithelial cells
no crystals
mild proteinuria (

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14
Q

Diagnosing with AIN

A

WBC casts, eosinophilic casts
WBCs 2-4+, eosinophils
No crystals
mild proteinuria (

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15
Q

Diagnosing with Glomerulonephritis

A 
RBC casts 
RBCs
Crystals may be present
moderate-large proteinuria (.5-3g/day or >3g/day)
slower development over 7-10 days
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16
Q

Drug induced postrenal AKI

A

Common drug causes include acyclovir, indinavir, sulfadiazine, chemotherapy causing high cell turnover (e.g., uric acid nephropathy)

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17
Q

kidney calculi (kidney stones)

A

Nephrolithiasis: the process of forming kidney stones
May or may not lead to postrenal obstruction
Who develops?
Family history of calcium oxalate stones or urate stones
Diabetes, gout, obesity
Leads to flank pain and hematuria; may lead to renal obstruction
Prevention is key through hydration and dietary modifications (low oxalate and low urate containing foods)

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18
Q

AKI clues:

Tenting of skin

A

prerenal

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19
Q

AKI clues:

Dark urine

A

prerenal

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20
Q

AKI clues:

Fever/high WBC

A

AIN or Glomerulonephritis

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21
Q

AKI clues:

Fever/Rash

A

AIN or Glomerulonephritis

22
Q

AKI clues:

Blood in urine

A

Glomerulonephritis or postrenal obstruction (kidney stones)

23
Q

Kidney regulatory function

A

Control composition and volume of blood volume

Maintain stable concentrations of cations such as sodium (Na), potassium (K), and calcium (Ca)

Maintain acid-base balance

24
Q

Kidney Excretory function

A

Produce urine

Remove metabolic waste (e.g., urea and other waste products)

25
Q

Kidney Hormone function

A

Produce renin for BP control

Produce erythropoietin which stimulates marrow production of red blood cells

Activate 25(OH)-D (inactive vitamin D)  1,25(OH)2D (active vitamin D)

26
Q

Kidney Metabolic function

A

Gluconeogenesis

Metabolize drugs and endogenous substances (e.g., insulin)

27
Q

Normal kidney sodium reabsoprtion

A

Normal kidney = 99% of sodium is reabsorbed with a net loss of 1% or less into urine

28
Q

Afferent Arteriole

A

Looking at volume and tone

29
Q

Efferent Arteriole

A

looking at tone

30
Q

What is AKI?

A

200% increase of the serum creatinine over 24 hours

Acute ↑ in creatinine with or without↓ in urine output over a short period of time

31
Q

Nonoliguria

A

urine output > 500 mL in 24-hours (per day)

32
Q

oliguria

A

Urine output 100-500 mL in 24-hours (per day)

33
Q

Anuria

A

urine output < 100 mL in 24-hours (per day)

34
Q

Non-modifiable risk factors for AKI

A 
Chronic kidney disease
Diabetes
Older age
Chronic liver disease (e.g., cirrhosis)
Congestive heart failure (CHF)
Renal artery stenosis
Peripheral vascular disease
35
Q

Modifiable risk factors for AKI

A 
Volume depletion (e.g., poor oral intake/dehydration, diarrhea, vomiting)
Hypertension/Hypotension
Hypoalbuminemia
Sepsis/shock
Nephrotoxic medications 
Major surgery/anesthesia
36
Q

Drugs associated with prerenal AKI

A 
ACEi/ARBs *
NASAIDs *
Cyclosporine
Tacrolimus
SGLT-2 inhibitors
37
Q

impaired regulation with NSAIDs in prerenal

A

NSAIDs inhibit prostaglandins –> constriction of afferent arteriole -> reduced flow and pressure –> decreased perfusion pressure and filtration

38
Q

impaired regulation with ACEi/ARBs

A

ACEi/ARBs block angiotensin 2 –> dilation of efferent arterioles –> reduction in back pressure –> decrease perfusion pressure and filtration

39
Q

Drugs associated with ATN

A

Radiocontrast media

Aminoglycosides (AG)

40
Q

Contrast induced nephropathy (CIN)

A

↑ in SCr by ≥0.5 mg/dL or 25% from baseline

Usually begins 24-48 hrs post-procedure; Peaks in 3-5 days and begins downtrending; Returns to baseline in 7-10 days

41
Q

CIN risk factors

A 
Age 
anemia
HF
hypotension
volume depletion
42
Q

drug induced ATN

A

Major cause of drug-induced ATN
Variable incidence of nephrotoxicity, 1.7-58%
Onset: 5-10 days after initiation of therapy; serious; largely preventable
Proposed pathogenic mechanism
Cationic charge (heavily filtered into tubule)  binding and uptake by PCT cells  disrupt normal cell function  tubular cell death
Stimulate Ca sensing receptor in the apical membrane  induction of cellular signaling and cell death
Presentation: ATN (oliguric or non-oliguric), magnesium wasting, FeNa >2%, presence of muddy brown casts

43
Q

ATN MOA

A

rupture proximal tubular epithelial cell

44
Q

ATN patient related risk factors

A 
CKD
Advanced age 
Liver disease 
Dehydration 	
Hypotension 
Magnesium or potassium deficiencies
45
Q

ATN drug related risk factors

A 
Prolonged course 
Cumulative dose
Trough concentration >2 mcg/mL
Repeated courses (14-day wash out)
Concomitant nephrotoxic agents
46
Q

Drugs associated with AIN

A

Allergenic medication

penicillins, cephalosporins, fluoroquinolones, sulfamides, NSAIDs, PPIs

47
Q

Drug induced AIN onset

A

7-20 days due to sensitizing

48
Q

drug induced AIN treatment

A

Stop drug and start prednisone 1 mg/kg/day

49
Q

Drugs associated with Postrenal

A

Acyclovir
Sulfonamides
Indinavir

50
Q

Management of DIKD

A

stop offending agent
avoid nephrotoxins
maintain hydration

CDM exam 2 (12 decks)

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