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Renal Flashcards

1
Q

Why is the left kidney taken during donor transplantation?

A

Because it has a longer renal vein

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2
Q

Path of renal blood flow, beginning with the renal artery?

A

Renal artery -> segmental artery -> interlobar artery -> arcuate artery -> interlobular artery -> afferent arteriole -> glomerulus -> efferent arteriole -> vasa recta/peritubular capillaries -> enous outflow

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3
Q

Explain the fluid compartments of the body.

A
  1. Total body water (TBW - 60% of body mass) + non water mass (NWM - 40% of body mass) = Body mass
  2. Total body water = Intracellular fluid (ICF - 2/3 TBW) + Extracellular fluid (ECF - 1/3 TBW)
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4
Q

What is the 60-40-20 rule?

A

% of body weight for average person:
60% total body water
40% ICF
20% ECF

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5
Q

What are the components of ECF?

A 
Interstitial fluid (75% ECF)
Plasma (25% ECF)
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6
Q

How can plasma volume be measured?

A

Radiolabeling albumin

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7
Q

How can ECF volume be measured?

A

With inulin or mannitol

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8
Q

What is normal osmolality?

A

285-295 mOsm/kg H2O

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9
Q

What are the components of the glomerular filtration barrier?

A
  1. Fenestrated capillary endothelium
  2. BM with type IV collagen chains and heparan sulfate
  3. Epithelial layer consisting of podocyte foot processes
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10
Q

How does the glomerular filtration barrier select for filtration?

A

Charge and size

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11
Q

What creates the charge barrier?

A

All three layers of the barrier contain negatively charged glycoproteins, preventing negatively charged molecule entry (eg, albumin)

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12
Q

What creates the seize barrier?

A

Fenestrated capillary endothelium prevents entry of >100 nm molecules/blood cells
Podocyte foot processes interpose with BM -> slit diaphragm (prevents entry of molecules >50-60 nm)

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13
Q

Renal clearance of a substance = ?

A

[(Urine concentration of X)(Urine flow rate)]/Plasma concentration of X

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14
Q

What is renal clearance?

A

The volume of plasma from which the substance is completely cleared per unit time (mL/min)

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15
Q

What is happening if clearance does not equal GFR?

A

If clearance is greater than GFR, net tubular secretion

If clearance is less than GFR, net tubular reabsorption

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16
Q

What can be used to calculate GFR? Why?

A

Inulin clearance; it is freely filtered and neither reabsorbed nor secreted

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17
Q

GFR = ?

A

UV/P (of inulin)

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18
Q

Normal GFR = ?

A

~100 mL/min

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19
Q

What is an approximate measure of GFR? Why is it a slight overestimate?

A

Creatinine clearance; slightly overestimates GFR because creatinine is moderately secreted by renal tubules

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20
Q

What is used to estimate effective renal plasma flow (eRPF)?

A

Para-aminohippuric acid (PAH) clearance; between filtration and secretion via the proximal tubule, there is nearly 100% excretion of all PAH that enters the kidney (slight underestimate of the true RPF)

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21
Q

eRPF = ?

A

UV/P (of PAH)

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22
Q

Renal blood flow (RBF) = ?

A

RPF/(1 - Hct)

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23
Q

FF = ?

A

GFR/RPF

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24
Q

Normal FF?

A

20%

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25
Q

Filtered load = ?

A

GFR x plasma concentration

mg/min

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26
Q

What preferentially dilates the afferent arteriole and what medication blocks this?

A

Prostaglandins preferentially dilate the afferent arteriole; NSAIDs block this

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27
Q

What preferentially constricts the efferent arteriolar and what medication blocks this?

A

Angiotensin II preferentially constricts the efferent arteriole; ACEIs block this

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28
Q

Effect of afferent arteriole constriction vs. efferent arteriole constrict on GFR, RPF, and FF?

A

Afferent arteriole constriction - decreased GFR, decreased RPF, no change in FF
Efferent arteriole constriction - increased GFR, decreased RPF, increased FF

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29
Q

Effect of increased plasma protein concentration vs. decreased plasma protein concentration on GFR, RPF, and FF?

A

Increased plasma protein concentration - decreased GFR, no change in RPF, decreased FF
Decreased plasma protein concentration - increased GFR, no change in RPF, increased FF

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30
Q

Effect of constriction of ureter on GFR, RPF, and FF?

A

Decreases GFR, no change in RPF, decrease in FF

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31
Q

Effect of dehydration on GFR, RPF, and FF?

A

Decreases GFR, greatly decreases RPF, increases FF

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32
Q

Filtered load = ?

A

GFR x P

P = plasma concentration of X

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33
Q

Excretion rate = ?

A

V x U

V = urine flow rate
U = urine concentration of X
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34
Q

Reabsorption rate = ?

A

Filtered - excreted

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35
Q

Secretion rate = ?

A

Excreted - filtered

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36
Q

Fe(Na) = ?

A

Na excreted/Na filtered = [P(creatinine) x U(sodium)]/[U(creatinine) x P(sodium)]

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37
Q

What happens to glucose normally in the kidneys?

A

Glucose at a normal plasma level (range 60-120 mg/dL) is completely reabsorbed in the PCT by Na+/glucose

38
Q

When does glucosuria begin in adults?

A

~200 mg/dL (plasma glucose)

39
Q

When are all glucose transports in the kidney fully saturated?

A

~375 mg/min

40
Q

Why can glucosuria and aminoaciduria occur in normal pregnancy?

A

Decreased ability of the PCT to reabsorb glucose and amino acids

41
Q

What are the key regions of the nephron?

A
  1. Early PCT
  2. Thin descending loop of Henle
  3. Thick ascending loop of Henle
  4. Early DCT
  5. Collecting tubule
42
Q

What are the apical transporters of the early PCT? The basolateral?

A

Apical (urine):

  1. Na/glucose co-transporter (into cell)
  2. Na/H exchanger (Na into cell, H into urine)
  3. Cl/base exchanger (Cl into cell, base into urine)
  4. CO2 diffuses into the cell

Basolateral (blood):

  1. Na/K ATPase (Na into blood, K into cell)
  2. HCO3- transporter into blood

In the cell: CO2+H2O -> H2CO3 (by CA) -> H+ + HCO3-

43
Q

What is the role of the early PCT?

A

Reabsorbs all glucose and amino acids
Resorbs most HCO3, Na, Cl, PO4, K, H2O, and uric acid
Generates and secretes NH3 (enables kidney to secrete more H+)

44
Q

How much Na+ is absorbed in each part of the nephron?

A

Early PCT - 65-80%
Thick ascending loop - 10-20%
Early DCT - 5-10%
Collecting tubule - 3-5%

45
Q

Which portion of the nephron contains a brush border?

46
Q

What hormones act on the early PCT?

A
  1. PTH - inhibits Na/PO4 cotransport -> PO4 excretion

2. AT II - stimulates Na/H exchange -> increased Na, H2O, and HCO3 reabsorption (permits contraction alkalosis)

47
Q

Which diuretics act on the early PCT?

A

Acetazolamide (CA inhibitor)

48
Q

What is the role of the thin descending loop of Henle?

A

Passively reabsorbs H2O via medullary hypertonicity
Impermeable to Na
Makes urine hypertonic (concentrates the urine)

49
Q

What are the apical transporters of the thick ascending loop of Henle? The basolateral?

A

Apical:

  1. Na/K/2Cl transporter (all into cell)
  2. K+ channel (diffuses out into lumen)
  3. Mg, Ca paracellular transport (into cell -> blood)

Basolateral:

  1. Na/K ATPase (Na into blood, K into cell)
  2. K+ and Cl- channels (diffuse into blood down gradient)
50
Q

What is the purpose of the thick ascending loop of Henle?

A

Reabsorbs Na, K, Cl
Indirectly induces paracellular reabsorption of Mg and Ca through a positive lumen potential generate by K+ backleak
Impermeable to water (makes urine less concentrated as it ascends)

51
Q

Which portions of the nephron are impermeable and to what substances?

A

Thin descending loop - impermeable to Na+

Thick ascending loop - impermeable to H2O

52
Q

Which diuretics work on the thick ascending loop?

A

Loop diuretics (block Na/K/2Cl transporter)

53
Q

What are the apical transporters of the early DCT? The basolateral?

A

Apical:

  1. Na/Cl cotransporter (into cell)
  2. Calcium channel (diffuses into cell)

Basolateral:

  1. Na/K ATPase (Na into blood, K into cell)
  2. Receptor for PTH
  3. Na/Ca exchanger (Na into cell, Ca into blood)
  4. Chloride channel diffusion (into blood)
54
Q

What is the role of the early DCT?

A

Reabsorbs Na, Cl

Makes urine fully dilute (hypotonic)

55
Q

What hormones act on the early DCT?

A

PTH - increase Ca/Na exchange -> increase Ca reabsorption

56
Q

What diuretic acts on the early DCT?

A

Thiazide diuretics (blocks Na/Cl cotransporter on apical membrane)

57
Q

What ar ethe three types of cells in the collecting tubule?

A
  1. Principal cell
  2. Alpha-intercalated cell
  3. Beta-intercalated cell
58
Q

What are the apical transporters of the principal cells of the collecting tubule? The basolateral?

A

Apical:

  1. H2O channels (into cell)
  2. K+ channels (diffuse into urine)
  3. Na+ channels (diffuse into cell)
  4. Cl- channels (paracellular - diffuse into cell -> blood)

In cell - Aldosterone receptors

Basolateral

  1. V2 receptors
  2. Na/K ATPase
59
Q

What is the role of the collecting tubule?

A

Reabsorbs Na+ in exchange for secreting K+ and H+

60
Q

What are the apical transporters of the alpha-intercalated cells of the collecting tubule? The basolateral?

A

Apical:

  1. H+ ATPase (H+ into urine)
  2. K/H ATPase (K into cell, H into urine)

In cell - Aldosterone receptors

Basolateral:
1. HCO3/Cl exchanger (HCO3 into blood, Cl into cell)

61
Q

What are the apical transporters of the beta-intercalated cells of the collecting tubule? The basolateral?

A

Apical:
1. Cl/HCO3 exchanger (Cl into cell, HCO3 into urine)

Basolateral:
1. H+ ATPase (H+ into blood)

62
Q

What are the effects of aldosterone on principal cells?

A

Increase apical K+ conductance, increase Na/K pump, increase ENaC activity -> lumen negativity -> K+ secretion

63
Q

What are the effects of aldosterone on alpha-intercalated cells?

A

Lumen negativity -> increased H+ ATPase activity -> increased H+ secretion -> incraesed HCO3-/CL- exchanger activity

64
Q

What are the effects of ADH in principal cells?

A

Insertion of aquaporin H2O channels on apical side

65
Q

What diuretics act on the principal cells?

A

Amiloride, triamterene (block ENaC)

66
Q

What are the components of the JGA?

A
  1. Mesangial cells
  2. JG cells (modified smooth muscle of afferent arteriole)
  3. Macular densa (NaCl sensor, part of DCT)
67
Q

What is the role of the JGA?

A

Macula dense cells sense decreased NaCl delivery to DCT -> increase renin release -> efferent arteriole vasoconstriction -> increased GFR

JG cells secrete renin in response to decreased renal blood pressure and increased symapthetic tone (B1)

68
Q

Where is EPO released from in the kidney?

A

Interstitial cells in the peritubular capillary bed

69
Q

Where in the kidney is 25-OH vitamin D3 converted to 1,25-(OH)2 vitamin D3 (calcitriol, active form)?

A

PCT cells (via 1-alpha-hydroxylase enzyme, activated by PTH)

70
Q

What is the role of dopamine in the kidney?

A

Secreted by PCT cells, promotes natriuresis; at low doses, it dilates interlobular arteries, afferent and efferent arterioles -> increased RBF, little or no change in GFR; at high doses, acts as a vasoconstrictor

71
Q

ANP is secreted in response to ___. How does it affect the kidney?

A

Increased atrial pressure; causes increased GFR and increased Na filtration with no compensatory Na reabsorption in distal nephron -> Na and volume loss

72
Q

Ang II is synthesized in response to ___. How does it affect the kidney?

A

Decreased BP; causes efferent arteriole constriction -> increased GFR and increased FF, but with compensatory Na reabsorption in proximal and distal nephron -> preserved renal function in low-volume state with simultaneous Na reabsorption (both proximal and distal) to maintain circulating volume

73
Q

Aldosterone is secreted in response to ___. How does it affect the kidney?

A

Decreased blood volume (via AT II) and increased plasma K+

Causes increased Na reabsorption, and increased H and K secretion

74
Q

ADH is secreted in response to ___. How does it affect the kidney?

A

Increased plasma osmolarity and decreased blood volume

Causes increased water reabsorption

75
Q

Henderson-Hasselbalch equation = ?

A

pH = 6.1 + log([HCO3-]/(0.03xPCO2))

76
Q

DDx - metabolic acidosis with increased anion gap

A 
Methanol (formic acid)
Uremia
Diabetic/alcohol ketoacidosis
Paraldehyde, propylene glycol
Isoniazid, iron tablets
Lactic acidosis
Ethanol/ethylene glycol (metabolized to oxalic acid)
Rhabdomylolysis, renal failure
Salicylates (late)
"MUDPILERS"
77
Q

DDx - metabolic acidosis, non-anion gap

A 
Hyperalimentation
Acetazolamide, Addison disease
Renal tubular acidosis
Diarrhea
Uretero-pelvic junction
Post-hypocapnia
Spironolactone, saline infusion
"HARDUPS"
78
Q

DDx - respiratory acidosis

A

Ultimately, anything that causes hypoventilation:

CNS depression (drugs, CVA)
COPD and restrictive lung disease (causes chronic)
Hemo/pneumothroax
Airway obstruction
Myopathy (weakened respiratory muscles)
Pneumonia
Pulmonary edema
"CCHAMPP"
79
Q

DDx - metabolic alkalosis

A 
Contraction
Licorice
Syndrome of apparent mineralocorticoid excess
Conn's, Cushing's, Bartter's, Gitelman's, Liddle's
Vomiting, NG suction
Excess alkali (antacid use)
Refeeding alkalosis
Post-hypercapnia
Diuretics
80
Q

Which causes of metabolic alkalosis are NOT associated with high urine chloride levels?

A

Vomiting, NG suction

Post-hypercapnia

81
Q

DDx - respiratory alkalosis

A

Ultimately, anything that causes hyperventilation

CNS disease
Hypoxia/hypoxemia
Anxiety
Mechanical ventilators
Progesterone, PE
Salicylates (early), sepsis
Tumor
82
Q

DDx - RBC casts

A

Glomerulonephritis, hypertensive emergency

83
Q

DDx - WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

84
Q

DDx - fatty casts (“oval fat bodies”)

A

Nephrotic syndrome

85
Q

DDx - granular (“muddy brown”) casts

A

Acute tubular necrosis

86
Q

DDx - waxy casts

A

Chronic renal failure/end-stage renal disease

87
Q

DDx - hyaline casts

A

Non-specific finding, often normal, can e seen in concentrated urine

88
Q

The presence of casts indicates what?

A

That the hematuria or pyuria is of glomerular or renal tubular origin

89
Q

Which causes of hematuria present with NO casts?

A

Bladder cancer, kidney stones

90
Q

Which causes of pyuria present with NO casts?

A

Acute cystitis

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