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CAEM Pt. 2 > Renal: Intro & Function > Flashcards

Renal: Intro & Function Flashcards

1
Q

What part of the kidney is most prone to ischemic and toxic injury and why?

A

Renal cortex - receives 20% of cardiac output

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2
Q

Five main functions of the kidney

A

1) Extracellular fluid homeostasis - water, electrolyte, and acid/base balance
2) Eliminate wastes (urea, creatinine), drugs, and toxins
3) Regulate blood pressure - control Na+/water and secrete renin
4) Produce and secrete hormones
4a- Renin in response to hypotension, hypovolemia, or decreased GFR
4b- Erythropoietin
4c- Calcitriol to activate vit-D
5) Gluconeogenesis

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3
Q

Three components of urine formation

A

1) Glomerular ultrafiltration of plasma
2) Tubular reabsorption, Ex: water, Na+, K+, Ca++, Cl-, HCO3, P, glucose, amino acids, some urea
3) Tubular secretion, Ex: H+

> > Urine excreted = filtered + secreted - reabsorbed

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4
Q

Location in the kidney and components of the glomerulus

A

> Located in the renal cortex

  • Tuft of capillaries between afferent and efferent arteriole
  • Epithelial cells of Bowman’s capsule, continuous with proximal tubule
  • Glomerular filtration barrier = fenestrated capillary endothelium, glomerular basement membrane, epithelium of Bowman’s capsule
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5
Q

What determines glomerular filtration (what and how much goes through)? (7)

A

1) Permeability of filtration barrier
2) Surface area available for filtration
3) Charge of molecule (negatively charged is excluded)
4) Size of molecule (large size is excluded)
5) Glomerular hydrostatic pressure (pushing filtrate to Bowman’s)
6) Glomerular capillary oncotic pressure (pulling filtrate to capillary)
7) Bowman’s hydrostatic pressure (pushing filtrate to glomerulus)

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6
Q

What is the blood pressure range that maintains renal blood flow and GFR?

A

80-180 mmg Hg - range the kidneys can adjust to protect themselves

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7
Q

What is the effect of sympathetic tone and norepinephrine and epinephrine on the kidney?

A

Constricts the afferent and efferent arterioles = decrease GFR and RBF (most important during severe and acute disturbances)

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8
Q

What effect does angiotensin II have on the kidney?

A

Powerful renal vasoconstrictor = preferentially constricts the efferent arteriole to maintain glomerular hydrostatic P, GFR, and RBF

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9
Q

What effect does prostaglandins have on the kidneys?

A

Oppose vasoconstriction of the afferent arteriole

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10
Q

What happens NORMALLY, to the afferent and efferent arterioles, during volume depleted states?

A
  • Afferent = vasodilate
  • Efferent = constrict
  • Goal = maintain GFR
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11
Q

What drugs are dangerous to the kidneys in patients in volume depleted states? (3)

A
  • NSAID’s and steroids = no longer able to oppose afferent arteriole constriction
  • ACE inhibitors = no longer able to vasoconstrict the efferent arteriole
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12
Q

What does decreased renal blood flow, hypotension, afferent arteriole vasoconstriction, decreased glomerular hydrostatic P, and increased Bowman’s capsule P cause?

A

Decreased GFR

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13
Q

What does increased renal blood flow, increased glomerular hydrostatic P, or increased efferent arteriole constriction cause?

A

Increased GFR

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14
Q

Things about the proximal tubule - main events

A
  • Extensive brush border
  • Metabolically active - lots of mitochondria
  • Susceptible to toxic and ischemic injury
  • Reabsorbs majority of glucose and amino acids, most of water, Na+, K+, Cl-, bicarb
  • Resorbs some urea, organic acids, H+
  • Making fluid isotonic
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15
Q

Things about the loops of Henle

A
  • Thin descending limb = highly permeable to water
  • Thin ascending limb = impermeable to water, maintains countercurrent gradient between descending limb and vasa recta
  • Thick ascending lim = impermeable to water, resorb electrolytes
  • Making fluid hypotonic
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16
Q

Things about the distal tubule

A
  • Early = resorb electrolytes (impermeable to water)
  • Specialized cells = macula densa
  • Late = similar to cortical collecting ducts
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17
Q

Things about the collecting ducts

A
  • Determine final excretion of water and Na+, K+, H+

- Transport is finely tuned by hormones = aldosterone (Na+, K+), ADH (aquaporins)

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18
Q

Three components required for urine concentration

A

1) Renal medullary gradient
2) Functional ADH-R in medullary collecting ducts
3) ADH secretion

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19
Q

Where is the glomerular apparatus located?

A

Where the distal tubule nestles between the afferent and efferent tubules of the glomerulus

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20
Q

What does the macula densa sense and do?

A
  • Senses osmolality of the tubular fluid

- Stimulates renin production if its high

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21
Q

What does the extraglomerular mesangial do?

A

Transmit info from the macular densa to the JG cells

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22
Q

What do the juxtaglomerular cells sense and do?

A
  • Specialized vascular smooth m. cells located in the afferent arterioles
  • Detects blood flow and pressure
  • Synthesize renin
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23
Q

What are the major functions of angiotensin II (4)?

A

*Activated by renin and the RAAS in response to hypotension, hypovolemia, decreased GFR, or decreased NaCl in the distal tubules

1) Stimulate aldosterone secretion = secrete K+ and resorb Na+
2) Stimulate ADH production from the pituitary
3) Create efferent arteriole constriction to increase BP
4) Increase sympathetic drive

24
Q

What may persistent renal proteinuria indicate and what can it lead to?

A
  • Hallmark of glomerular disease

- Can play a role in the progression of chronic kidney failure by causing tubular damage

25
Q

Three semi-quantitative methods to detect proteinuria

A
  • Needs to be interpreted in the light of the USG and sediment
    1) Urine colometric dipstick = primarily detects albumin
    2) SSA = reading turbidity, primarily detects albumins, globulins, Tamm-Horsfall, and Bence Jones proteins
    3) ERD Healthscreen urine test = uses anti-canine and feline antibiodies, detects microalbuminemia (threshold greater than normal in urine but small enough to be missed by dipstick)
26
Q

Quantitative method to detect proteinuria

A

Urine protein-creatinine ratio (UPC) = primarily measures albumin

27
Q

Normal canine UPC

A

< 0.5

28
Q

Normal feline UPC

A

< 0.4

29
Q

What UPC reading is indicative of glomerular disease?

A

> 2.0

30
Q

Pre-renal cause of proteinuria

A

> Increased amounts of low MW proteins in the plasma = myoglobin and hemoglobin, or Bence Jones proteins
- Freely filtered at the glomerulus, overwhelm the proximal tubular reabsorption

31
Q

Renal causes of proteinuria (4)

A

1) Physiologic/functional = mild and transient following strenuous exercise, seizures, fever, exposure to hot/cold
2) Glomerular = pathologic, structural glomerular damage or glomerular hypertension (may be from systemic hypertension) = MILD to SEVERE
3) Tubular = pathologic, decreased reabsorption with normal glomerular filtration = MILD
4) Interstitial = pathologic, inflammatory process leading to exudation of proteins into the urinary space w/ signs of active nephritis (tender kidneys, fever, azotemia)

32
Q

Post-renal cause of proteinuria

A

Protein added to the urine after it leaves the renal pelvis - from the urinary tract (ureter, bladder, uretha from infection, neoplasia, calculi) or genital tract (infection, neoplasia)

33
Q

How do we rule out a post-renal proteinuria?

A

Examine protein content of urine from cystocentesis

34
Q

How do we rule out a pre-renal proteinuria? (2)

A
  • Check for pigmented urine after centrifugation (RBC’s would separate out)
  • Check out plasma globulin and protein levels (ruling out Bence Jones proteins)
35
Q

How do we rule out inflammatory causes of proteinuria (renal and post-renal)? (2)

A
  • Check urine sediment for signs of inflammation = hematuria, WBC’s
    + Clinical signs = stranguira and pollakuria for post-renal, tender kidneys and azotemia for renal
36
Q

How do we rule out physiologic proteinuria?

A
  • Measure multiple times to confirm if it’s persistent or not
  • Are they also azotemic?
37
Q

What can the magnitude of UPC tell us?

A

> Is it glomerular or tubular proteinuria

  • Glomerular > 2.0
  • Tubular = 0.4/0.5-2.0
38
Q

When do we intervene when we see proteinuria? (3)

A
  • Non-azotemic dogs with UPC’s > 2.0
  • Azotemic dogs with UPC > 0.5
  • Azotemic cats with UPC > 0.4
  • Start renoprotective therapy to slow rate of renal disease progression
39
Q

What range of USG is considered isosthenuric?

A
  • 1.008-1.012 in the dog

< 1.020 or 1.025 in the cat

40
Q

How many nephrons must be lost to see isosthenuria?

A

2/3 or 60% of nephrons

41
Q

What is the first clinical sign of renal dysfunction?

A

PU/PD due to isosthenuria

42
Q

What is azotemia?

A

Increased plasma concentrations of nitrogenous solutes - urea, BUN, etc.

43
Q

How many nephrons must be lost to see azotemia?

A

3/4 or 75% of nephrons

44
Q

Which is a better estimate of GFR - BUN or creatinine?

A

Creatinine - a portion of the BUN that is filtered is reabsorbed

45
Q

If GFR increases, what happens to BUN?

A

Decreases (in the blood) = INVERSELY proportional

46
Q

Causes for increased BUN (3)

A

1) High protein diet
2) GI bleeding (upper GI)
3) Increased catabolic states - fever, starvation, infection

47
Q

Causes for decreased BUN (3)

A

1) Malnutrition
2) Low protein diet
3) Synthetic liver failure - PSS, cirrhosis

48
Q

What happens to creatinine when GFR decreases?

A

Increases - filtration is INVERSELY proportional to GFR

49
Q

Causes of decreased and increased creatinine in the blood?

A
  • Increased = increased muscle mass (greyhounds, athletes)

- Decreased = decreased muscle mass (cachexia, younger animals)

50
Q

True or false - degree of the increase of BUN/Cr is not predictive of the cause (pre, renal, post), acute vs. chronic, progressive vs. non-progressive, or reversibility with kidney injuries

A

TRUE

51
Q

Clinical signs of azotemia

A 
\+ Decreased appetite
\+ Anorexia
\+ Vomiting
\+ Oral ulcerations
>> UREMIA
52
Q

Cause of pre-renal azotemia

A

Decreased renal perfusion and blood flow - dehydration, hypovolemia (Addison’s), decreased cardiac output (CHF), shock

*NO intrinsic kidney disease at the moment, but could progress

53
Q

Causes of renal azotemia

A
  • Implies intrinsic disease of the kidney
  • Acute = ischemic, toxic, infectious, immune-mediated, neoplastic, obstructive
  • Chronic = progressive loss of nephrons
54
Q

Causes of post-renal azotemia (2)

A

1) Blockage of urine flow distal to the kidney = obstruction by tumors or extramural compression
2) Leakage of urine into the peritoneum - rupture distal to kidney

*No intrinsic kidney disease at the moment, but could progress

55
Q

What USG’s indicate that the kidneys are functioning?

A
  • Concentration = > 1.030 in the dog and > 1.035 in the cat

- Dilute = hypostheuric

56
Q

How do we differentiate pre-renal from post-renal azotemia? (5)

A

1) USG = hypersthenuria in the face of dehydration is pre-renal, isostheuria in the face of dehydration is renal
2) Response to fluid therapy = pre-renal
3) History and PE - evidence of obstruction
4) PCV/TP = increase = pre-renal
5) Abdominal imaging = stones, abdominal urine effusion, hydronephrosis

57
Q

What is the exception to isosthenuria that is not indicative of renal azotemia?

A

> > Lacking one of the things that allow you to have concentrated urine:

1) Addisons = no gradient
2) Hypercalcemia = block ADH-R
3) DKA = no gradient, osmotic diuresis
4) Drugs - glucocorticoids, diuretics, phenobarbitol, etc.

*Fluid therapy results in a rapid improvement

CAEM Pt. 2 (27 decks)

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