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Clinical Pathology > Renal Physiology & Assessment > Flashcards

Renal Physiology & Assessment Flashcards

Dr. Helmer

1
Q

What causes increased EPO production? Which organ?

A

hypoxia

kidneys

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2
Q

What are the roles of the kidney?

A

hormone synthesis

excretion of nitrogenous waste - phos, K+, H+, lipase, amylase

conservation of Na+, Cl-, Ca2+, albumin, antithrombin III, H2O

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3
Q

Which hormones do the kidneys synthesize?

A

EPO
vitamin D
prostaglandins
renin

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4
Q

What is calcitriol?

A

formed in the liver and activated in the proximal tubule

promotes calcium reabsorption in kidney and GI tract

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5
Q

Which species do lack an enzyme regarding calcitriol? What happens and what is the enzyme?

A

horses - no 1alpha-hydroxylase so Ca2+ is diet-dependent

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6
Q

What is the role of prostaglandins?

A

there in order to maintain medullary blood flow; vasodilation

NSAIDs inhibit this

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7
Q

What stimulates renin?

A

low renal perfusion (hypoperfusion)

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8
Q

What is the end goal of releasing renin?

A

increases blood pressure by vasoconstriction

promotes Na+ and H2O retention

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9
Q

What is BUN?

A

blood urea nitrogen - a nitrogenous waste

product of protein catabolism either endogenous (fever, corticosteroids) or increased protein digestion (dietary intake or hemorrhage into GI tract)

filtered at the glomerulus then recycled

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10
Q

What is creatinine?

A

produced in muscle

freely filtered at the glomerulus but NOT reabsorbed

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11
Q

T/F: Creatinine is a nitrogenous waste

A

FALSE - a marker for kidney function

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12
Q

What substances are NOT filtered out of the blood?

A

albumin
white blood cels
red blood cells
platelets
urobilinogen

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13
Q

What can be freely filtered across to glomerulus?

A

water
glucose
amino acids
urea
creatinine
Na/Cl/K
phosphorus
magnesium
calcium

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14
Q

What substances are filtered but are completely reabsorbed (100%)?

A

glucose
amino acids

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15
Q

Where is water impermeable in the nephron?

A

thick ascending limb

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16
Q

T/F: Filtrate in the nephron becomes more and more concentrated

A

TRUE

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17
Q

When is water passively moving out of the nephron?

A

thin descending limb
distal collecting

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18
Q

When does urea have active transport?

A

urea
NaCl

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19
Q

What are the glucose renal thresholds for each species?

A

canine: 180-200 mg/dL
feline: 270-290
bovine: 100-140
equine: 160-180

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20
Q

A cat has a glucose concentration of 310 mg/dL, what will you expect to see?

A

glucose in the urine

polyuria, polydipsia because glucose has an osmotic effect and water can no longer leave the tubule

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21
Q

What type of kidney disease do you expect to see with problems with EPO?

A

non-regenerative normocytic, normochromic anemia

hallmark of kidney disease

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22
Q

What type of kidney disease do you expect to see with problems with vitamin D?

A

renal secondary hyperparathyroidism - NOT horses

loss of Ca2+

low calcitriol (means lower calcium reabsorption in GI and kidney) = low blood calcium = higher in the tubules

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23
Q

What happens with a defect in excretion of nitrogenous wastes - kidney disease?

A

they will increase

azotemia
hyperphosphatemia
hyperkalemia
metabolic acidosis
hyperamylasemia and hyperlipasemia

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24
Q

What happens in hyperkalemia?

A

kidneys are diseased, so you cannot get rid of potassium

can lead to bradyarrythmias and death - also urethral stones

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25
Q

What decreases with kidney disease?

A

conservation of Na+, Cl-, Ca2+, albumin, antithrombin III, H2O

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26
Q

What happens when Ca2+ is decreased with kidney disease?

A

Ca2+ loss exacerbates renal PTH

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27
Q

What happens when albumin is decreased with kidney disease?

A

edema - protein-losing nephropathy

(albumin has a role in keeping fluid in blood (oncotic pressure), so when this is gone, fluid can go into tissues easier)

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28
Q

What happens when antithrombin is decreased with kidney disease?

A

thrombotic disease

29
Q

What happens when H2O is decreased with kidney disease?

A

dehydration

30
Q

What is BUN?

A

synthesize in liver from ammonia with protein digestion

freely filtered at glomerulus and reabsorbed based on GFR and filtrate rate of flow

31
Q

What is the result of a BUN below reference range?

A

lack of production - dietary protein restriction
> liver disease - takes nitrogen and bundles it into urea, increase ammonia because it can’t get converted

increased excretion - any cause of polyuria

32
Q

What is the result of a BUN above reference range?

A

increased production - digest more protein - endogenous protein catabolism

decreased excretion - decreased glomerular filtration rate

33
Q

What is creatinine?

A

produced during muscle metabolism

filtered freely at glomerulus but NOT reabsorbed in the tubules (except in goats)

34
Q

What is the result of a creatinine below reference range?

A

decreased production - starvation, cachexia

increased excretion

35
Q

What is the result of a creatinine above reference range?

A

increased production - very heavily muscle animals

decreased excretion - decreased GFR (pre-renal, renal, or post-renal causes)
> insensitive

36
Q

What percentage of functional kidney mass needs to be lost in order for creatinine to go up?

A

75% (only 25% functioning)

37
Q

What is SDMA?

A

sensitive and early marker of declining GFR in dogs and cats

produced by all cells at a constant rate, excreted by kidneys with no reabsorption in renal tubules

38
Q

What is the result of a SDMA below reference range?

A

not clinically applicable

39
Q

What is the result of a SDMA above reference range?

A

decreased GFR - acute kidney injury, chronic kidney disease

40
Q

What is azotemia?

A

too much nitrogen in blood

an increase of urea nitrogen and/or creatinine in the blood due to decreased renal excretion

41
Q

How do you differentiate azotemia from uremia?

A

describes clinical picture that goes along with being azotemic

PUPD, vomiting, weight loss, depression, oral ulceration

42
Q

What is pre-renal azotemia?

A

kidneys have nothing to do with it
because of lack of blood flow to the kidneys

  • hypovolemia
  • cardiac disease / poor perfusion
  • renal vasoconstriction
43
Q

What are some causes of pre-renal azotemia?

A

hypovolemia

cardiac disease / poor perfusion

renal vasoconstriction

44
Q

What is renal azotemia?

A

caused by decreased GFR due to loss of >75% renal mass

stuff gets there, but kidneys are like peace out

45
Q

What are some causes of renal azotemia?

A

primary renal disease or injury (glomerulonephritis, toxicity)

secondary to renal ischemia or obstruction

46
Q

What is post-renal azotemia?

A

caused by obstruction or rupture of urinary outflow tracts

stuff never leave body - keeps getting reabsorbed and recycled

47
Q

What are some causes of post-renal azotemia?

A

urolithiasis (cats, small ruminants, ferrets) - stones that obstruct urethrea

uroabdomen (HBC trauma, other) - urine all in abdomen —> urea gets reabsorbed from abdomen in bloodstream and leads to high BUN and high K+

48
Q

What is specific gravity?

A

how much solute is in the blood

“how well are the kidneys concentrating urine?”

water has a SG of 1.00

49
Q

T/F: The higher the SG, the more concentrated the urine is

A

TRUE

50
Q

Lack of renal function, >_____% of renal mass, results in the inability to concentrate urine adequately

A

66% - patients will produce isothenuric urine

51
Q

Why use specific gravity?

A

can differentiate between pre-renal and renal azotemia

pre-renal: kidney is still functioning and should have normal, concentrated urine

52
Q

What does the kidney need to produce adequately concentrated urine?

A

a medullary gradient

ADH

nephrons that can respond to ADH - adequate number and receptors

53
Q

What are the urine specific gravities of each species?

A
54
Q

What is evidence of pre-renal azotemia?

A

decreased blood flow to kidneys
- dehydration
- shock
- acute hemorrhage

55
Q

The body responds to hypovolemia with ____, increased ______ and increased ________

A

ADH
increased H2O resorption
increased USG

renal function is adequate so UDG is above adequate cut off

56
Q

Where does ADH have control in the nephron?

A

collecting ducts

57
Q

What is evidence of renal azotemia?

A

any intrarenal disease

glomeruli, tubules, interstitial, vasculature

reflects at least 75% of renal functional mass

58
Q

Azotemia with _______ is diagnostic for renal azotemia

A

isosthenuria - USG 1.008-1.012

59
Q

What is the range for hyposthenuric? What does it mean?

A

1.00-1.008

can dilute the urine but CANNOT concentrate

60
Q

Describe post-renal azotemia

A

disease that is distal to the kidney so urine can’t leave body - either obstructed or leaking into the abdomen

azotemia with variable USG, often very high K+ which can be fatal

dysuria, anuria - straining to urinate, history of trauma, uroabdomen

61
Q

What are the types of renal disease?

A

duration of injury: acute kidney injury (AKI) vs chronic kidney injury (CKD)

location-tubular injury vs glomerular injury

62
Q

What is acute kidney injury?

A

rapid deterioration of renal function over hours to days

may contribute to chronic kidney disease

63
Q

What are some causes of acute kidney injury?

A

decreased perfusion

nephritis vs nephrosis (swelling, toxin)

post-renal obstruction

64
Q

What is chronic kidney disease?

A

slowly progressive

65
Q

What is protein-losing nephropathy?

A

glomerular disease results in increased permeability in the membrane

albumin crosses into the urine

66
Q

Albumin crossing into the urine with Protien-losing nephropathy leads to [hyperalbuminemia/hypoalbuminemia]

A

hypoalbuminemia

67
Q

What is nephrotic syndrome?

A

protein-losing nephropathy that is characterized by:

proteinuria
hypoalbuminemia
hypercholesterolemia
ascites due to low oncotic pressure

68
Q

Go over cases

A

Clinical Pathology (28 decks)

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