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Flashcards in Renal Failure Deck (66):
1

In a nutshell definition of AKI

rapid decline in renal function with increase in creatinine (0.5 - 1.0 increase)

2

acute renal failure vs AKI

Acute renal failure is the early stage of AKI when creatinine may be normal despite reduced GFR due to time it takes for creatinine to accumulate in body

3

3 types of AKI

prerenal - due to decreased renal blood flow (MCC)
intrinsic - due to damage to renal parenchyma
postrenal - urinary tract obstruction (least common)

4

What 3 aspects of kidney function does RIFLE criteria look at?

Creatinine increase, GFR decrease, urine output

5

What does RIFLE stand for?

Risk
Injury
Failure
Loss
ESRD

used to define AKI

6

Risk

1.5x increase creatinine
25% decrease GFR
<0.5 ml/kg/hr UO for 6 hours

7

Injury

2.0x increase in creatinine
50% decrease GFR
<0.5 ml/kg/hr UO for 12 hours

8

Failure

3.0x increase in creatinine
75% decrease GFR
<0.5 ml/kg/hr UO for 24 hours or anuria 12 hours

9

Loss

complete loss of kidney function (requiring HD) for more than 4 weeks

10

ESRD

complete loss of kidney function (requiring HD) for more than 3 months

11

T/F: AKI always results in oliguria or anuria

FALSE. can present with no oliguria (nonoliguric AKI)

12

Most common findings in AKI patient

Weight gain and edema due to positive water and sodium balance

13

What is azotemia?

Elevated BUN and Cr; characterizes AKI

14

What else causes elevated BUN besides AKI?

catabolic drugs like stereoids
GI/soft tissue bleeding
dietary protein intake

15

What else causes elevated Cr besides kidney problems?

baseline Cr depends on muscle mass
so any muscle breakdown can increase Cr...drugs can also increase Cr

16

Prognosis for AKI

80% of patients completely recover...but depends on age of patient and severity of renal failure

17

Most common causes of death in AKI patients

infection followed by cardiorespiratory problems

18

What mechanisms cause prerenal failure

ANYTHING THAT DECREASES BLOOD FLOW TO KIDNEYS

- decreased CO
- volume loss / sequestration
- hypotension

ie hypovolemia, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, diarrhea, CHF, renal arterial obstruction, cirrhosis/hepatorenal syndrome, patient on NSAIDs, ACE inhibitors, cyclosporin

19

What do NSAIDs do to kidneys? and ACE inhibitors?

NSAIDs - constrict afferent arterioles
Ace inhibitors - dilate efferent arterioles

20

Pathophysiology of prerenal AKI

DECREASED RENAL BLOOD FLOW leads to LOWER GFR which leads to decreased clearance of metabolites...

however renal parenchyma isn't damaged so tubular function and CONCENTRATING ABILITY IS PRESERVED.

21

What clinical features are typically seen in patient with prerenal AKI?

SIGNS OF VOLUME LOSS

dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)

22

What lab findings are seen in AKI

OLIGURIA ALWAYS (to preserve volume)
urine with HIGH OSMOLALITY (since kidney retains water) (>500)
urine with LOW Na, (FENa <1%)
Increased urine-plasma Cr ration (>40:1) (filtrate is reabsorbed, but not creatinine)
bland urine sediment

23

intrinsic renal failure

glomerular filtration and tubular function are imparied therefore kidneys CANNOT CONCENTRATE URINE

24

Causes of intrinsic renal failure

- ATN (Most common - due to ischemia, nephrotoxins
- glomerular disease (i.e. acute glomerulonephritis)
- vascular disesase
-interstitial disease

25

What kinds of glomerular diseases can cause intrinsic renal failure

poststrep glomerulonephritis
Wegner granulomatsosis
goodpasture syndrome
lupus

26

What kinds of vascular disease can cause intrinsic renal failure

TTP
HUS
renal artery occlusion

27

How does rhabdomyolysis damage kidneys

When skeletal muscle breaksdown (either from trauma, crush injuries, or snake bites), skeletal muscles release myoglobin which are toxic to kidneys. In addition, you get hyperkalemia, hyperuricemia, hypocalcemia, and elevated CPK. Treat with IV fluids, mannitol (to drain that bad shit out), and bicarb (to get K back into cells)

28

What causes ischemic AKI

ANYTHING THAT LEADS TO SEVERE DECLINE IN RENAL BLOOD FLOW

heart failure, DIC, shock, hemorrhage, sepsis

29

What can cause nephrotoxic AKI

any substance that damages renal parenchyma

NSAIDS, antibiotics (aminoglycosides, vanc), radiocontrast agents, NSAIDS (esp in CHF), poisons, myoglobin, hemoglobinuria, chemo (cisplatin), kappa gamma light chains seen in multiple myeloma

30

What recovery usually takes longer, prerenal or intrinsic renal failure?

intrinsic

31

Lab findings in intrinsic renal failure

DECREASED urine osmolality (kidney cannot concentrate urine)
Increased urine Na (kidney cannot retain Na)
DECREASED urine plasma Cr ratio (kidney cannot reabsorb filtrate)
Decreased BUN/Cr ratio (although both still elevated, kidney cannot reabsorb urea as well as in prerenal)

32

post renal failure

least common cause of AKI
obstruction in the urinary tract with intact renal blood supply and parenchyma intact.
Leads to increased GFR (both kidneys must be obstructed for Cr to rise)

33

causes of post renal

urethral obstruction secondary to BPH (most common cause)
kidney stones
obstructing neoplasm (i.e. bladder, cervical cancer)

34

How to monitor patient with AKI

- daily weight, Is and Os
- BP
- Serum electrolytes
- Hgb/Hct to check for anemia
- monitor for infection

35

What lab values will usually indicate AKI?

elevated BUN and Cr

36

What two types of AKI can cause ATN?

ischemic AKI and nephrotoxic AKI (anything that destroys tubular cells)

37

What 3 tests can you do to rule out postrenal failure?

- physical exam (palpate bladder)
- insert catheter (look for large volume of urine)
- bladder and kidney U/S to check for obstruction and hydronephrosis

38

What to always obtain in patient with AKI?

U/A
urine chem
serum electrolytes
bladder catheterization to rule out obstruction
renal u/s

39

What do muddy brown cast, RBC casts, fatty casts, and WBC casts indicate on U/A

muddy brown casts/renal tubular cells - ATN
RBC casts/ RBCs - glomerular disease
WBC casts/WBCs - pyelonephritis, acute interstitial nephritis
fatty casts - nephrotic syndrome

40

Where would you see increased protein and blood?

Acute glomerfulonephritis and acute interstitial nephritis

41

What are some complications of AKI?

ECF volume expansion -> pulmonary edema (treat with furosemide)
metabolic/electrolyte disturbances
uremia
infection

42

What electrolyte disturbances can be seen in AKI?

hyperkalemia
metabolic acidosis (increased anion gap) - correct with sodium bicarb
hyperphosphatemia -> hypocalcemia
hyponatremia
hyperuricemia

43

What is a common feared complication of AKI?

infection! (ex: pneumonia, UTI, wound infection, and sepsis)

uremia itself is thought to impair immune function; infxn likely multifactorial

44

General measures for AKI treatment

- avoid nephrotoxic meds (i.e. NSAIDS, aminoglycosides, radiocontrasts)
- adjust medication doses for renal function
- correct fluid imbalances/electrolyte disturbances
- optimize cardiac output
- dialysis if indicated

45

Indications for dialysis

symptomatic uremia
intractable metabolic acidosis
hyperkalemia
urgent symptoms of volume overload

46

Definition of chronic kidney disease (CKD)

decreased kidney function (GFR<60)

OR

kidney damage (structural/functional abnormalities) for at least 3 months regardless of cause

47

Causes of CKD

-DM (most common)
- HTN (25% of cases)
- chronic GN
- interstitial nephritis, polycystic kidney disease, obstructive uropathy (any AKI left untreated or prolonged)

48

CV features of CKD

- HTN
- CHF (due to volume overload, HTN, and anemia)
- pericarditis (from symptomatic uremia)

49

Mechanism behind HTN in CKD

decreased GFR stimulates RAAAS system -> BP increase

50

GI features of CKD

nausea/vomiting
anorexia

51

Neurologic features of CKD

lethargy, somnolence, confusion, confusion, peripheral neuropathy, uremic seizures, weakness, asterexis, hyperreflexia, "restless legs"

these come from hypocalcemia

52

Hematologic features of CKD

normocytic normochromic anemia (secondary to EPO deficiency)
bleeding (secondary to platelet dysfunction due to uremia (platelets can't degranulate in uremic environment)

53

Endocrine/metabolic features of CKD

- hyperphosphatemia -> hypocalcemia
- can also sometimes have secondary hyperparathyroidism causing hypercalcemia and (calciphylaxis from ppt) and renal osteodystrophy
- low testosterone in men and amenorrhea/infertility/hyperprolacinemia in women
- pruitis

54

What tests to run to dx CKD

- urinalysis (sediment)
- Cr and GFR
- CBC
- electrolytes
- Renal u/s to rule out obstruction

55

What diet to recommend in patient with CKD

LOW SALT, LOW PROTEIN
restrict potassium, phosphorus, and magnesium

56

What BP med recommended for CKD patient

ACE inhibitors (dilate efferent arteriole) shown to reduce risk of progression to ESRD (BUT WATCH OUT FOR HYPERKALEMIA)

57

How to treat hyperphosphatemia

calcium citrate (phosphate binder)

58

What supplements to give to prevent secondary hyperparathyroidism

calcium and vit D

59

What intoxications are indications for dialysis?

ethylene glycol, lithium, aspirin (salicyclic acid), magnesium containing laxatives

60

Options for HD access?

- central catheter in subclavian or jugular vein
- tunneled catheter (lowers rate of infxn, can use for up to 6 months)
- AV fistula (best form; needs surgery, audible bruit)

61

Pros and cons to HD

Pro: efficient than PD, can be initiated quickly
Con: less similar to true physiology of kidney, can lead to hypotension during rapid removal and fluid shifts, hypo-osmolality

62

How does peritoneal dialysis work?

peritoneum is the dialysis membrane, HYPEROSMOLAR HIGH GLUCOSE solution is used as dialysate fluid and infused into peritoneal cavity which draws up water from blood via osmosis...fluid has to be drained and replaced several times a day

63

Advantages of peritoneal dialysis

patient can perform dialysis on their own, mimics true physiology of kidney

64

What are dialysis still prone to despite having the filtration function of the kidney

since dialysis only can simulate FILTRATION and NOT SYNTHESIS...patients are still prone to vit D and EPO deficiency

65

Complications of HD

hypotension, hypo-osmolality (n/v, headache, seizures), anticoag complications, infection of access site, HD associated amyloidosis of b2 microglobulin in bones and joints

66

Complications of PD

peritonitis (accompanied by fever and pain some times, abdominal inguinal hernia, hyperglycemia, protein malnutrition