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PHAR 255 > Kidney > Flashcards

Kidney Flashcards

1
Q

What are the three functions of the kidney?

A

Excretory
Endocrine
Metabolic

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2
Q

Blood enters the glomerulus through the:

A

Afferent arteriole

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3
Q

Blood leaves the kidney through the:

A

Efferent arteriole

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4
Q

What is the filtrate composed of? (The urine)

A

Glucose
Electrolytes
Amino acids
Water
Urea
Uric acid
Creatinine
Protein

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5
Q

What does the kidney secrete to maintain acid-base balance?

A

Acids (H+)

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6
Q

What do the kidneys do in acidosis?

A

In response to excess acid, kidneys reabsorb all filtered bicarbonate and produces new bicarbonate

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7
Q

What do the kidneys do in alkalosis?

A

In response to too little acid, kidneys excrete bicarbonate to restore H+ concentration to normal

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8
Q

What are the key renal blood pressure mechanisms?

A

Renin-angiotensin-aldosterone system (RAAS)
Antidiuretic hormone (ADH)
Atrial natriuretic peptide (ANP)

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9
Q

The filtrate should not contain a significant amount of:

A

Protein

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10
Q

Why do we check renal function?

A

Monitoring and early recognition of CKD
To adjust doses of medications excreted by the kidneys
Monitoring nephrotoxic medications

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11
Q

What is creatinine?

A

A by-product of muscle metabolism that is primarily eliminated by glomerular filtration

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12
Q

What happens to SCr when GFR is low?

A

It is increased

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13
Q

What is the equation used for classifying the severity of kidney disease?

A

CKD-EPI (measures GFR)

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14
Q

What is the equation used for making renal dose adjustments to medications?

A

Cockcroft-Gault

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15
Q

T or F: the CKD-EPI equation is used to estimate kidney function in a patient receiving dialysis.

A

False. Don’t report a GFR in dialysis, wouldn’t be relevant or accurate.

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16
Q

When will our estimate of GFR be in accurate if we are using creatinine?

A

AKI
Extremes of muscle mass/body size
High protein diet
Dialysis
Muscle wasting diseases

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17
Q

What is the impact of eliminating race as a factor when using the CKD-EPI equation?

A

Lower eGFR in black patients
Higher eGFR in non-black patients

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18
Q

When do we use indexed or normalized eGFR?

A

For CKD staging/progression

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19
Q

When do we used non-indexed or without normalization eGFR?

A

For drug dosing (but caution in obese patients)

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20
Q

What happens to urea (blood urea nitrogen-BUN) in renal impairment?

A

Urea levels are increased

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21
Q

What can affect urea concentrations?

A

Dietary protein
GI bleeding
Hydration status (could be high when dehydrated)

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22
Q

Is urea a renal function test?

A

No. Urea can be high without having renal impairment.

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23
Q

What is proteinuria and what does it tall us about kidney function?

A

Presence of increased amounts of protein in the urine.
Persistent increase in urine protein is a marker of kidney damage.

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24
Q

What is albuminuria and what can it tell us about kidney function?

A

Albumin in the urine(a small amount is normal)
Increased levels are an early predictor of glomerular dysfunction (may even see this before we see a decrease in GFR)

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25
Q

What are the categories of albuminuria in CKD?

A

A1: ACR<3mg/mmol - normoalbuminuria
A2: ACR=3-30mg/mmol - microalbuminuria
A3: ACR>30mg/mmol - macroalbuminuria

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26
Q

T or F: the term microalbuminuria means that the protein in the urine are small.

A

False. This means that there is a small amount in the urine which could either be normal or mildly increased.

27
Q

What can cause albuminuria without causing a concern for CKD?

A

Recent major exercise
UTI
Febrile illness
Decompensated congestive HF
Acute severe elevation in BP or BG

28
Q

What characteristics does a urinalysis look at?

A

Colour, turbidity
Presence of cells, micro-organisms, “casts”, crystals
Urinary eosinophils = interstitial nephritis
pH analysis, specific gravity
Glucose, ketones = indicative of diabetes/DKA
Leukocyte esterase and nitrite = positive in UTIs

29
Q

What are the urinary sediment abnormalities that are markers of kidney damage?

A

RBC casts
WBC casts
Fatty casts in diseases with proteinuria
Granular casts - second most common cast
Isolated microscopic hematuria with abnormal RBC morphology
(Casts are protein structures formed within the tubule of the kidney)
Cells in the urine are indicative of a problem!!

30
Q

What is an AKI?

A

A sudden decline in renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)

31
Q

How is an AKI defined by KDIGO?

A

Any of the following:
- increase in SCr by >/= 0.3mg/dl within 48 hours
- increase in SCr to >/= 1.5 times baseline, which is known or presumed to have occurred within the past 7 days
- urine volume < 0.5mL/kg/hr for 6 hours (need to rule out other causes first) (also a non-specific marker)

32
Q

How can AKI’s be classified?

A

Anuric - less then 50mL/day urine output
Oliguric - less then 500mL/day urine output
Non-oliguric - greater then 500mL/day urine output (normal urine)

33
Q

How is CKD staged?

A

RIFLE category or AKIN criteria(stage 1-3)
Stage would be based on the worst criteria met

34
Q

What does RIFLE category stand for?

A

Risk
Injury
Failure
Loss
ESRD

35
Q

What do the staging systems depend on?

A

SCr and urine output

36
Q

What do we need to know about the patient when using the staging systems for an AKI?

A

Need to know there baseline as the criteria are based on change in SCr

37
Q

What are the symptoms of an AKI?

A

Most people are asymptomatic
~50% are oliguric
Symptoms of dehydration
Uremia - malaise, nausea, vomiting
Severe abdominal or flank pain
Decreased force of urine stream
Cola-coloured urine
Excessive foaming of urine
Sudden weight gain, edema

38
Q

Can an AKI be due to dehydration or fluid overload?

A

It can be due to either one!

39
Q

Susceptibilities for AKI

A

CKD
Dehydration
Advanced age
Female
Black race
Chronic disease
Diabetes
Cancer
Anemia

40
Q

Exposures that increase risk of AKI

A

Sepsis
Critical illness
Circulatory shock
Burns
Trauma
Cardiac surgery
Nephrotoxic drugs

41
Q

What % of AKI’s are caused by drugs?

A

~20%

42
Q

What are the three ways to classify the cause of an AKI?

A

Pre-renal (blood supply)
Intra-renal or intrinsic (within kidney)
Post-renal (after urine is produced: collecting tubule, ureter, bladder, urethra)

43
Q

What is the most common cause of an AKI?

A

Pre-renal (~60%)

44
Q

What is a pre-renal AKI?

A

The kidneys are not getting adequate blood supply but the kidneys themselves are healthy.
Kidney perfusion is decreased, from:
- intravascular volume depletion(hemorrhage, dehydration, burns, diuretic therapy)
- decreased effective circulating volume (HF, cirrhosis)
- hypotension (vasodilation medications, septic shock)
- decreased glomerular filtration pressure (ACEi/ARB + NSAIDs)

45
Q

How would filtration be increased for a pre-renal AKI?

A

Dilate the Afferent arteriole and constrict the efferent arteriole to increase filtration.

46
Q

What is the second most common cause of an AKI?

A

Intrinsic AKI (25-35%)

47
Q

What is an intrinsic AKI?

A

Results from direct damage to the kidneys and there are 4 main types.

48
Q

What are the 4 types of intrinsic AKI’s?

A

Acute tubular necrosismost common (endogenous(myoglobin) or exogenous(aminoglycosides) toxins, ischemia)
Acute interstitial nephritis (idiopathic hypersensitivity immune reaction to drugs(NSAIDs, penicillin), infection)
Acute glomerulonephritis (post-strep antigen-antibody complexes)
Vascular kidney injury (renal artery stenosis, HTN)

49
Q

What is a post-renal AKI?

A

Obstruction to urinary flow anywhere in the urinary tract:
- urethral obstruction
- ureter obstruction
- bladder neck obstruction

50
Q

What are the cause of a post-renal AKI?

A

Nephrolithiasis (kidney stones)
Prostate enlargement most common
Cervical cancer tumors
Drugs that crystallize (sulfonamides, acyclovir, MTX)

51
Q

How are AKIs diagnosed?

A
  1. Get a full history
  2. Labratory data (increased SCr, increased BUN, acidosis, hyperkalemia)
  3. Urinary sodium concentration
  4. Fractional excretion of sodium (decreased with pre-renal AKI, increased with tubular damage)
    - also note this is not specific - sodium excretion may be increased with diuretic use
  5. Urinalysis
    If necessary: renal ultrasound or kidney biopsy
52
Q

What are casts(cellular debris) on urinalysis seen with?

A

Acute tubular necrosis

53
Q

What do hematuria or proteinuria in urinalysis indicate?

A

Glomerular injury

54
Q

What do increased WBC in urinalysis mean?

A

UTI or pyelonephritis (kidney infection)

55
Q

What does pyuria, urinary eosinophils on urinalysis mean?

A

Acute interstitial nephritis

56
Q

What do crystals on urinalysis mean?

A

Post renal AKI

57
Q

What would a pre-renal AKI look like on urinalysis?

A

Few WBCs, casts, and decreased fractional excretion of sodium

58
Q

What is the treatment for pre-renal AKI?

A

Hydration with IV fluids - stop diuretics if hypovolemic
BP support with vasopressors
Diuretics for fluid removal in state of volume overload
Stop/hold drugs that impair kidney function/urine flow (NSAIDs)

59
Q

What is the treatment for intrinsic AKI?

A

Discontinue offending agents
Manage underlying autoimmune disease

60
Q

What is the treatment for post-renal AKI?

A

(Remove obstruction)
Catheter to restore urine flow
Identify and remove obstruction
Adequate hydration when giving drugs with potential to crystallize

61
Q

What is our main concern with AKI and treatment?

A

Hyperkalemia
Moderate (K+ 5.1-7mmol/L)
Severe (K+ >7mmol/L)

62
Q

How do we treat hyperkalemia caused by AKI?

A

Mild: may not require therapy or can use kayexalate (sodium polystyrene sulfonate) or furosemide IV to increase urinary excretion
Severe(medical emergency): calcium gluconate to stabilize myocardium, drive K+ into cells with insulin +/- glucose, kayexylate to eliminate excess K+ from body, dialysis if refractory

63
Q

How is metabolic acidosis with AKI treated?

A

Sodium bicarbonate IV

64
Q

When to dialyze in AKI?

A

(AEIOU)
Acidosis
Electrolyte abnormalities (hyperkalemia)
Ingestion of toxins
Overload of fluid
Uremia

PHAR 255 (8 decks)

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