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Renal :') > Renal Approach to AKI and CKD > Flashcards

Renal Approach to AKI and CKD Flashcards

1
Q

how is AKI defined?

A

one of the following: increase in serum creatinine by >.3 mg/dL within 48 hours; increase in serum creatinine to >1.5 times baseline within 7 days; urine volume

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2
Q

how is anuria defined?

A

urine output less than 50-100 mL/day

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3
Q

how is oliguria defined?

A

urine output <400-500 mL/day

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4
Q

what is pre-renal azotemia?

A

elevation in serum BUN out of proportion to elevation in serum creatinine, specifically due to poor renal perfusion

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5
Q

what are two physical exam findings seen in patients with uremia?

A

asterixis and uremic frost

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6
Q

what are the 4 broad causes of pre-renal AKI?

A

hypovolemia, hypervolemia, systemic vasodilation, or drugs causing impaired renal autoregulation

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7
Q

what could cause systemic vasodilation leading to pre-renal AKI?

A

sepsis, SIRS, cirrhosis

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8
Q

what drugs could cause impaired renal autoregulation leading to pre-renal AKI?

A

NSAIDs or ACEi

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9
Q

what is the most common cause of pre-renal AKI?

A

hypovolemia

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10
Q

what could cause hypovolemia leading to pre-renal AKI?

A

bleeding, vomiting/diarrhea, or overdiuresis

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11
Q

how do they kidneys respond to seeing a decreased blood flow?

A

they activate the RAAS, which then signals the adrenal glands to release aldosterone. The aldosterone then tells the kidneys to reabsorb Na+ and water follows

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12
Q

what are the three lab values to know for pre-renal AKI?

A

there is going to be a urine Na <20 mEq/L; the BUN/Cr ratio is going to be >20:1; the urine osmolality is going to be > 500 mosm/kg

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13
Q

why is the urine osmolality >500 mosm/kg in cases of pre-renal AKI?

A

the kidneys are holding onto water, so they are going to create a concentrated urine

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14
Q

when renal blood flow increases, what is another way the body responds besides the RAAS?

A

dilation of the afferent arterioles and constriction of the efferent arterioles

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15
Q

how is the dilation of the afferent arteriole seen in cases of pre-renal AKI blunted by medications?

A

NSAIDs inhibit prostaglandin production (so you don’t get that vasodilation)

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16
Q

how is the constriction of the efferent arteriole blunted by medications?

A

ACEi/ARBs inhibit angiotensin II production (angiotensin II preferentially constricts the efferent arteriole)

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17
Q

what are 4 broad things that could lead to intrarenal AKI?

A

acute tubular necrosis, acute interstitial nephritis, glomerular disease, or vascular issues

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18
Q

what could cause acute tubular necrosis (ATN) leading to intrarenal AKI?

A

prolonged prerenal AKI (sepsis is common cause) or toxins

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19
Q

what are some toxins that lead to ATN?

A

myoglobin, uric acid, myeloma light chains, IV contrast

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20
Q

what things could lead to acute interstitial nephritis?

A

PPIs, NSAIDs, certain antibiotics

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21
Q

what vascular issues could lead to intrarenal AKI?

A

vasculitis, malignant HTN, or TTP/HUS

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22
Q

what is the most common cause of intrarenal AKI?

A

acute tubular necrosis

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23
Q

what is the pathophysiology of ATN?

A

prolonged prerenal state or toxin leads to ischemia, which then leads to tubular necrosis; the tubular necrosis leads to debris obstructing the tubular flow, which ultimately leads to to decreased GFR

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24
Q

what happens if pre-renal AKI is present long enough?

A

acute tubular necrosis will develop

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25
Q

what is acute interstitial nephritis caused by?

A

type I and type IV hypersensitivity due to nonsteroidal anti-inflammatory drugs (NSAIDs)/penicillins, diuretics

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26
Q

what are the pain problems associated with intrinsic renal AKI?

A

1) problems with filtration 2) problems with reabsorption and secretion

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27
Q

what are the lab values you need to know for intrinsic renal AKI?

A

urine Na > 40, BUN/Cr ratio is going to be <15:1, urine osm< 350 mosm/kg

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28
Q

what are the two main causes of post-renal AKI?

A

bladder outlet obstruction and ureteral obstruction

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29
Q

what could cause bladder outlet obstruction?

A

BPH and blood clots

30
Q

what could cause ureteral obstruction?

A

stones or external compression from malignancy

31
Q

what is important to remember about post-renal AKI?

A

you need either bilateral ureteral obstruction or bladder outlet obstruction to cause post-renal AKI

32
Q

what is the most common cause of post-renal AKI?

A

BPH

33
Q

what should all patients with an AKI get for their workup?

A

at least a basic metabolic panel and a UA

34
Q

what things could be included in the initial workup for AKI?

A

BMP, UA with microscopy, urine electrolytes, urine microalbumin/Cr ratio or urine protein/Cr ratio

35
Q

if you see a urinary pattern of hylaine casts, which kidney disease is suggested?

A

non-specific; pre-renal azotemia

36
Q

if you see a urinary pattern of renal tubular epithelial cells, granular casts (“muddy brown”), which kidney disease is suggested?

A

acute tubular necrosis

37
Q

if you see WBCs, WBC casts, or urine eosinophils on urinary pattern, which kidney disease is suggested?

A

acute interstitial nephritis

38
Q

if the urinary pattern shows proteinuria (less than 3.5 g/day), hematuria, dysmorphic RBC, and RBC casts, what kidney disease is suggested?

A

nephritic syndrome

39
Q

if you see a urinary pattern of heavy proteinuria (>3.5 g/ day), fatty casts, oval fat bodies, and minimal hematuria?

A

nephrotic syndrome

40
Q

What is the FENa? and what is it used for?

A

the fractional excretion of sodium; often used to differentiate between pre-renal AKI and ATN

41
Q

what does the FENa tell you?

A

if it is less than 1% it suggests pre-renal; if it is greater than 2% is suggests ATN

42
Q

when can you not rely on FENa? and what should you use in these cases?

A

FENa is less accurate in patients on diuretics; use FEUrea instead

43
Q

what does the FEUrea tell you?

A

if it is less than 35% then it is prerenal; if it is greater than 50% then it suggests ATN

44
Q

what are 4 additional tests you can order for someone with AKI?

A

post-void residual, renal ultrasound, urine eosinophils, and renal biopsy

45
Q

when should you order a post-void residual if you suspect AKI?

A

if you have concerns for bladder outlet obstruction

46
Q

when should you order a renal ultrasound if you are diagnosing AKI?

A

if you have concerns for ureteral obstruction or other post-renal process

47
Q

when do you order a urine eosinophils when diagnosing AKI?

A

it has historically been used to assess for AIN, but sensitivity and specificity are poor

48
Q

when do you order a renal biopsy when diagnosing AKI?

A

it is reserved for severe AKI of unclear etiology

49
Q

in all patients with AKI, what should you consider when treating the patient?

A

avoid nephrotoxins, renally dose all meds, dialysis if needed

50
Q

how do you treat pre-renal AKI?

A

correct hemodynamics; if low preload–> fluids; if high preload–> diuretics

51
Q

how do you treat intrinsic renal AKI?

A

treat the underlying disease: ATN–> supportive care; AIN–> stop offending med, consider steroids; glomerular disease–> depends on cause

52
Q

how do you treat post-renal AKI?

A

relieve the obstruction; ureteral obstruction: nephrostomy tube or stent; BPH with obstruction–> foley catheter

53
Q

the likelihood of recovery depends on what two things?

A

severity of renal injury and baseline renal function

54
Q

What are the indications for dialysis?

A

AEIOU
A: acidosis (ph<7.1-7.2)
E: electrolytes (life threatening hyperkalemia)
I: Intoxication (methanol, ethylene glycol, lithium)
O: overload
U: Uremia (if encephalopathy or pericarditis)

55
Q

what is the text book difference between AKI and CKD?

A

if it is less than 3 months with GFR less than 60 ml/min and/or markers of kidney damage present, then the patient has AKI; after three months, then the patient can be labeled with CKD

56
Q

what are the stages of CKD?

A

1,2,3a,3b,4, and 5

57
Q

what also effects the severity of the CKD stages?

A

albuminuria

58
Q

what is the vast majority of CKD cases caused by?

A

diabetes and hypertension

59
Q

what is the pathophysiology of CKD?

A

there is damage to nephrons from underlying disease (eg DM or HTN)–> nephrons die–> hyperfiltration and hypertrophy of remaining nephrons–> glomerular damage from increased pressure and flow

60
Q

what are the symptoms specific to CKD if the patient is not asymptomatic?

A

anemia (the kidneys normally produce EPO); bone pain and fragility (secondary to secondary hyperparathyroidism)

61
Q

besides decreased EPO, how else can CKD lead to anemia?

A

CKD can lead to iron deficiency due to chronic blood loss from hemodialysis and from a decrease in GI iron absorption

62
Q

how does CKD lead to bone disease?

A

in cases of CKD, there is phosphate retention leading to increased serum phosphorus, which leads to hypocalcemia. The hypocalcemia leads to secondary hyperparathyroidism; also, in cases of CKD, there is decreased active vitamin D, leading to decreased gut Ca reabsorption, leading to hypocalcemia

63
Q

what is the pathophysiology of secondary hyperparathyroidism?

A

there is low serum calcium–> increased PTH production by the parathyroid gland–> leading to increased bony turnover

64
Q

what do the labs look like in cases of secondary hyperparathyroidism?

A

calcium is low, PTH is high, and phosphorus is high

65
Q

what is the pathophysiology of tertiary hyperparathyroidism?

A

prolonged secondary hyperparathyroidism–> parathyroid gland hyperplasia–> autonomously functioning parathyroid gland + loss of function of Ca2+ sensing receptors

66
Q

what do the labs look like for tertiary hyperparathyroidism?

A

calcium is high, PTH is high, and phosphorus is high

67
Q

which bone disease is associated with CKD?

A

osteitis fibrosis cystica

68
Q

what is osteitis fibrosis cystica?

A

theres excess PTH–> osteoclast activation–> bony breakdown

69
Q

what pathologic findings are associated with osteitis fibrosis cystica?

A

subperiosteal bony reabsorption, bone cyst formation, “brown tumors”

70
Q

why are pathologic fractures common in patients with advanced CKD?

A

due to renal osteodystrophy

71
Q

what can renal ultrasound be used for in cases of CKD?

A

you may be able to see small atrophic kidneys in CKD; to assess for hydronephrosis

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